Priti Patel had defended Boris Johnson after he was branded a "racist" by rapper Dave on stage at the 2020 Brit Awards.

The PM has had two life-changing events in just three weeks - a new family and a brush with death

Labour leader Sir Keir Starmer will hold virtual meetings with members of the public over Zoom as he tries to resuscitate the party after its historic electoral defeat.

He has now been absent from the front line of the Government response for a month, after his three-week recovery period at the Chequers official residence in Buckinghamshire.

It seems like a lifetime ago that Boris Johnson announced that he and his partner were engaged and expecting a baby.

Britain will not enjoy a "V-shaped bounce" out of the crisis caused by coronavirus but will take years to recover fully, two former chancellors today warned.

Read the full interview HERE

Boris Johnson has said he feared he would not live to see his son born as he battled coronavirus in hospital last month.

Cabinet Office minister says Government does not want the UK to continue with its 'European Union-lite membership' beyond December 2020

Sir Keir Starmer has urged the Prime Minister to form a "national consensus" on the next phase of the Government's coronavirus response as ministers work on plans to ease the lockdown.

Downing Street has replaced a trade minister who resigned when an investigation found he threatened a company chairman over a financial dispute with his father.

Theresa May has hit out at world leaders for failing "to forge a coherent international response" to the coronavirus pandemic.

Admission that faster testing might have helped as UK hit by top death toll in Europe

Matt Hancock has slammed Professor Neil Ferguson for his "extraordinary" breach of coronavirus lockdown rules, adding he was left "speechless" by his actions.

EXCLUSIVE: Independent candidate withdraws after difficult decision over job 'I really, really dreamed of'

Scotland Yard has said Professor Neil Ferguson's behaviour is "plainly disappointing" but officers do not intend to take any further action.

Boris Johnson has set out a new target of 200,000 coronavirus tests a day by the end of May, as he admitted he "bitterly regrets" the crisis in care homes.

He also said he "bitterly regrets" the crisis in care homes, where staff have hit out at a lack of testing and PPE. The latest figures show that nursing home fatalities are continuing to rise, standing at 2,794 in the week to April 24, despite deaths in all settings beginning to fall.

It should have been the first litmus test of Sir Keir Starmer's appeal - as well as a verdict on whether Boris Johnson's general election earthquake in former Red Wall regions translated into long term local success

The Government has failed to meet its 100,000 coronavirus daily testing target for the fifth day running as criticism mounts on ministers to bolster supplies.

In a video that first surfaced on Reddit over the weekend, Ezra Miller appears to choke a female fan who approaches the artist on the street.

Canadian actors, musicians and public figures came together on Saturday night for a televised special to support frontline and essential workers, and to raise funds for Food Banks Canada.

Justin Bieber and Ariana Grande’s new video for “Stuck With U” features a variety of celebs and their significant others – and also confirms a few rumoured relationships.

I’m no stranger to forced isolation. For the better part of my 20s, I served as a nuclear submarine officer running secret missions for the United States Navy. I deployed across the vast Pacific Ocean with a hundred other sailors on the USS Connecticut, a Seawolf-class ship engineered in the bygone Cold War era to be one of the fastest, quietest, and deepest-diving submersibles ever constructed. The advanced reactor was loaded with decades of enriched uranium fuel that made steam for propulsion and electrical power so we could disappear under the waves indefinitely without returning to port. My longest stint was for two months, when I traveled under the polar ice cap to the North Pole with a team of scientists studying the Arctic environment and testing high frequency sonar and acoustic communications for under-ice operations. During deployments, critical-life events occur without you: holidays with loved ones, the birth of a child, or in my case, the New York Giants 2011-2012 playoff run to beat Tom Brady’s Patriots in the Super Bowl for the second time. On the bright side, being cut off from the outside world was a great first job for an introvert.

It’s been a month since COVID-19 involuntarily drafted me into another period of isolation far away from home. I’m in Turkey, where a two-week trip with my partner to meet her family has been extended indefinitely. There were no reported cases here and only a few in California in early March when we left San Francisco, where I run a business design studio. I had a lot of anticipation about Turkey because I’d never been here. Now I’m sheltering in a coastal town outside of Izmir with my partner, her parents, their seven cats, and a new puppy.

Shuttered in a house on foreign soil where I don’t speak the language, I have found myself snapping back into submarine deployment mode. Each day I dutifully monitor online dashboards of data and report the status of the spread at the breakfast table to no one in particular. I stay in touch with friends and family all over the world who tell me they’re going stir crazy and their homes are getting claustrophobic. But if there is one thing my experience as a submarine officer taught me, it’s that you get comfortable being uncomfortable.

OFFICER OF THE DECK: Author Steve Weiner in 2011, on the USS Connecticut, a nuclear submarine. Weiner was the ship’s navigator. Submarine and crew, with a team of scientists, were deployed in the Arctic Ocean, studying the Arctic environment and testing high frequency sonar and acoustic communications for under-ice operations.Courtesy of Steve Weiner

My training began with psychological testing, although it may not be what you think. Evaluating mental readiness for underwater isolation isn’t conducted in a laboratory by clipboard-toting, spectacled scientists. The process to select officers was created by Admiral Hyman Rickover—the engineering visionary and noted madman who put the first nuclear reactor in a submarine—to assess both technical acumen and composure under stress. For three decades as the director of the Navy’s nuclear propulsion program, Rickover tediously interviewed every officer, and the recruiting folklore is a true HR nightmare: locking candidates in closets for hours, asking obtuse questions such as “Do something to make me mad,” and sawing down chair legs to literally keep one off balance.

Rickover retired from the Navy as its longest-serving officer and his successors carried on the tradition of screening each officer candidate, but with a slightly more dignified approach. Rickover’s ghost, though, seemed to preside over my interview process when I applied to be a submariner as a junior at the U.S. Naval Academy in Annapolis, Maryland. I was warned by other midshipmen that I would fail on the spot if I initiated a handshake. So, dressed in my formal navy blue uniform and doing my best to avoid tripping into accidental human contact, I rigidly marched into the Admiral’s office, staring straight ahead while barking my resume. When I took a seat on the unaltered and perfectly level chair in front of his desk, the Admiral asked me bluntly why I took so many philosophy classes and if I thought I could handle the technical rigors of nuclear power school. My response was a rote quip from John Paul Jones’ “Qualifications of a Naval Officer.” “Admiral, an officer should be a gentleman of liberal education, refined manners, punctilious courtesy, and the nicest sense of personal honor.” My future boss looked at me, shook his head like he thought I’d be a handful, and told me I got the job.

Confinement opened something up in my psyche and I gave myself permission to let go of my anxieties.

Nuclear power training is an academic kick in the face every day for over a year. The curriculum is highly technical and the pedagogy resembles a cyborg assembly-line without even a hint of the Socratic method. Our grades were conspicuously posted on the classroom wall and a line was drawn between those who passed and those who failed. I was below the line enough to earn the distinguished dishonor of 25 additional study hours each week, which meant I was at school at 5 a.m. and every weekend. This is how the Nuclear Navy builds the appropriate level of knowledge and right temperament to deal with shipboard reactor operations.

I finally sat down for a formal psychological evaluation a few months before my first deployment. I was ushered into a room no bigger than a broom closet and instructed to click through a computer-based questionnaire with multiple-choice questions about my emotions. I never did  learn the results, so I assume my responses didn’t raise too many red flags.

During my first year onboard, I spent all my waking hours either supervising reactor operations or learning the intricacies of every inch of the 350-foot tube and the science behind how it all worked. The electrolysis machine that split water molecules to generate oxygen was almost always out of commission, so instead we burned chlorate candles that produced breathable air. Seawater was distilled each day for drinking and shower water. Our satellite communications link had less bandwidth than my dial-up modem in the 1990s and we were permitted to send text-only emails to friends and family at certain times and in certain locations so as not to risk being detected. I took tests every month to demonstrate proficiency in nuclear engineering, navigation, and the battle capabilities of the ship. When I earned my submarine warfare qualification, the Captain pinned the gold dolphins insignia on my uniform and gave me the proverbial keys to the $4 billion warship. At that point, I was responsible for coordinating missions and navigating the ship as the Officer of the Deck.

Modern submarines are hydrodynamically shaped to have the most efficient laminar flow underwater, so that’s where we operated 99 percent of the time. The rare exception to being submerged is when we’d go in and out of port. The most unfortunate times were long transits tossing about in heavy swells, which made for a particularly nauseated cruise. To this day, conjuring the memory of some such sails causes a reflux flashback. A submariner’s true comfort zone is beneath the waves so as soon as we broke ties with the pier we navigated toward water that was deep enough for us to dive.

It’s unnatural to stuff humans, torpedoes, and a nuclear reactor into a steel boat that’s intentionally meant to sink. This engineering marvel ranks among the most complex, and before we’d proceed below and subject the ship and its inhabitants to extreme sea pressures, the officers would visually inspect thousands of valves to verify the proper lineup of systems that would propel us to the surface if we started flooding uncontrollably and sinking—a no-mistakes procedure called rigging for dive. Once we’d slip beneath the waves, the entire crew would walk around to check for leaks before we’d settle into a rotation of standing watch, practicing our casualty drills, engineering training, eating, showering (sometimes), and sleeping (rarely). The full cycle was 18 hours, which meant the timing of our circadian cycles were constantly changing. Regardless of the amount of government-issued Folger’s coffee I’d pour down my throat, I’d pass out upon immediate contact with my rack (the colloquialism for a submarine bunk in which your modicum of privacy was symbolized by a cloth curtain).

As an officer, I lived luxuriously with only two other grown men in a stateroom no bigger than a walk-in closet. Most of the crew slept stacked like lumber in an 18-person bunk room and they all took turns in the rack. This alternative lifestyle is known as hot-racking, because of the sensation you get when you crawl into bedding that’s been recently occupied. The bunk rooms are sanctuaries where silence is observed with monastic intensity. Slamming the door or setting an alarm clock was a cardinal sin so wakeups were conducted by a junior sailor who gently coaxed you awake when it was time to stand watch. Lieutenant Weiner, it’s time to wake up. You’ve got the midnight watch, sir. Words that haunt my dreams.

The electrolysis machine was out of commission, so we burned chlorate candles that produced breathable air.

I maintained some semblance of sanity and physical fitness by sneaking a workout on a rowing erg in the engine room or a stationary bike squeezed between electronics cabinets. The rhythmic beating of footsteps on a treadmill was a noise offender—the sound could be detected on sonar from miles away—so we shut it off unless we were in friendly waters where we weren’t concerned with counter-detection.

Like a heavily watered-down version of a Buddhist monk taking solitary retreat in a cave, my extended submarine confinements opened something up in my psyche and I gave myself permission to let go of my anxieties. Transiting underneath a vast ocean in a vessel with a few inches of steel preventing us from drowning helps put things into perspective. Now that I’m out of the Navy, I have more appreciation for the freedoms of personal choice, a fresh piece of fruit, and 24 hours in a day. My only regrets are not keeping a journal or having the wherewithal to discover the practice of meditation under the sea.

Today, I’m learning Turkish so I can understand more about what’s happening around me. I’m doing Kundalini yoga (a moving meditation that focuses on breathwork) and running on the treadmill (since I’m no longer concerned about my footsteps being detected on sonar). On my submarine, I looked at photos to stay connected to the world I left behind, knowing that I’d return soon enough. Now our friend who is isolating in our apartment in San Francisco sends us pictures of our cat and gives us reports about how the neighborhood has changed.

It’s hard to imagine that we’ll resume our lifestyles exactly as they were. But the submariner in me is optimistic that we have it in us to adapt to whatever conditions are waiting for us when it’s safe to ascend from the depths and return to the surface.

Steve Weiner is the founder of Very Scarce, a business design studio. He used to lead portfolio companies at Expa and drive nuclear submarines in the U.S. Navy. He has an MBA from The Wharton School and a BS from the U.S. Naval Academy. Instagram: @steve Twitter: @weenpeace

Lead image: Mike H. / Shutterstock

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My mother-in-law, Carol, lives alone. It was her 75th birthday the other day. Normally, I send flowers. Normally, she spends some part of the day with the family members who live nearby and not across the country as my husband, Mark, and I do. And normally, she makes plans to celebrate with a friend. But these are not normal times. I was worried about sending a flower delivery person. Social distancing means no visiting with friends or family, no matter how close they are. So, my sister-in-law dropped off a gift and Mark and I sang “Happy Birthday” down the phone line with our kids. But I could hear the loneliness in Carol’s voice.

This was hardly the worst thing anyone experienced in America on that particular April day. We are fortunate that Carol is healthy and safe. But it upset me anyway. People over 60 are more vulnerable to COVID-19 than anyone else. They are also vulnerable to loneliness, especially when they live alone. By forcing us all into social isolation, one public health crisis—the coronavirus—is shining a bright light on another, loneliness. It will be some time before we have a vaccine for the coronavirus. But the antidote to loneliness is accessible to all of us: friendship.

Those who valued friendship as much as family had higher levels of health and happiness.

All too often we fail to appreciate what we have until it’s gone. And this shared global moment has illuminated how significant friends are to day-to-day happiness. Science has been accumulating evidence that friendship isn’t just critical for our happiness but our health and longevity. Its presence or absence matters at every point in life, but the cumulative effects of either show up most starkly in the later stages of life. That is also the moment when demographics and health concerns can conspire to make friendships harder to find or sustain. As the world hits pause, it’s worth reminding ourselves why friendship is more important now than ever.

Friendship has long been understood to be valuable and pleasurable. Ancient Greek philosophers enjoyed debating its virtues, in the company of friends. But friendship has largely been considered a cultural phenomenon, a pleasant by-product of the human capacity for language and living in groups. In the 1970s and 1980s, a handful of epidemiologists and sociologists began to establish a link between social relationships and health. They showed those who were more socially isolated were more likely to die over the course of the studies. In 2015, a meta-analysis of more than 3 million people whose average age was 66 showed that social isolation and loneliness increased the risk of early mortality by up to 30 percent.1 Yet loneliness and social isolation are not the same thing. Social isolation is an objective measure of the number and extent of social contact a person has day to day. Loneliness is a subjective feeling of mismatch between how much social connection you want and how much you have.

Once the link between health and relationships was established in humans, it was noticed in other species as well. Primatologists studying baboons in Africa remarked that when female baboons lost their primary grooming partners to lions or drought, they worked to build bonds with other animals in place of the one they’d lost. When the researchers analyzed the social behavior of the animals and their outcomes over generations, they found in multiple studies that the animals with the strongest social networks live longer and have more and healthier babies than those that are more isolated.2 Natural selection has resulted in survival of the friendliest.

Since baboons don’t drive each other to the hospital, something deeper than social support must be at work. Friendship is getting “under the skin,” as biologists say. Some of the mechanisms by which it works have yet to be explained, but studies have demonstrated that social connection improves cardiovascular functioning, reduces susceptibility to inflammation and viral disease, sharpens cognition, reduces depression, lowers stress, and even slows biological aging.3

We also now have a clearer definition of what friendship is. Evolutionary biologists concluded that friendship in monkeys—as well as people—required at least three things: it had to be long-lasting, positive, and cooperative. When an anthropologist looked for consistent definitions of friendship across cultures, he found something similar. Friendships were described as positive, and they nearly always include a willingness to help, especially in times of crisis. What friendship is about at the end of the day is creating intensely bonded groups that act as protection against life’s stresses.4

Social connection reduces depression, lowers stress, and even slows biological aging.

That buffering effect is particularly powerful as we age. Those first epidemiology studies focused on people in the middle of life. In 1987, epidemiologist Teresa Seeman of the University of California, Los Angeles, wondered if age and type of relationship mattered for health.5 She found that for those under 60, whether or not they were married mattered most. Being unmarried in midlife put people at greater risk of dying earlier than normal. But that did not turn out to be true for the oldest groups. For those over 60, close ties with friends and relatives mattered more than having a spouse. “That was a real lightbulb that went on,” Seeman says.

In a 2016 study, researchers at the University of North Carolina found that in both adolescence and old age, having friends was associated with a lower risk of physiological problems.6 The more friends you had, the lower the risk. By contrast, adults in middle age were less affected by variation in how socially connected they were. But the quality of their social relationships—whether friendships provided support or added strain—mattered more. Valuing friendship also proved increasingly important with age in a 2017 study by William Chopik of Michigan State University. He surveyed more than 270,000 adults from 15 to 99 years of age and found that those who valued friendship as much as family had higher levels of health, happiness, and subjective well-being across the lifespan. The effects were especially strong in those over 65. As you get older, friendships become more important, not less; whether you’re married is relatively less significant.7

There’s a widespread sense, especially among younger people, that people are lonely post-retirement. The truth is more complicated. Social networks do get smaller later in life for a variety of reasons. In retirement, people lose regular interaction with colleagues. Most diseases, and the probability of getting them, worsen with age. It’s more likely you will lose a spouse. Friends start to die as well. Mental and physical capacities may diminish, and social lives may be limited by hearing loss or reduced mobility.

Yet some of this social-narrowing is intentional. If time is of the essence, the motivation to derive emotional meaning from life increases, says Laura Carstensen, director of the Stanford Center for Longevity. She found that people choose to spend time with those they really care about. They emphasize quality of relationships over quantity. While family members fill much of a person’s inner social circle, friends are there, too, and regularly fill in in the absence of family. A related, more optimistic perspective on retirement is that with fewer professional and family obligations, there are more hours for the things we want to do and the people with whom we want to do them.

At all stages of life, how we do friendship—whether we focus on one or two close friends or socialize more widely—has to do with our natural levels of sociability and motivation. Those vary, of course. I recently spoke with a man who had retired to Las Vegas. When he and his wife moved to their new house, his wife began baking cookies and distributing them to neighbors. She started throwing block parties for silly holidays and those neighbors showed up. No one had bothered to organize such a thing before. Even in retirement, this woman is what psychologists call a “social broker”—someone who brings people together. She has most likely always been friendly.

What best predicted health wasn’t cholesterol levels, but satisfaction in relationships.

How you live your life before you reach 60 makes a difference, experts on aging say. Friendship is a lifelong endeavor, but not everyone treats it that way. Think of relationships the way we do smoking, says epidemiologist Lisa Berkman of Harvard University. “If you start smoking when you’re 14, and stop smoking when you’re 65, in many ways, the damage is done,” she says “It’s not undoable. Stopping makes some things better. It’s worth doing but it’s very late in the game.” Similarly, if you only focus on friendships when your family and professional obligations slow, you will be at a disadvantage. Damage will have been done. The payoff in making friendship a priority was born out in the long-running Harvard Study of Adult Development, which followed more than 700 men for the entire course of their lives. What best predicted how healthy those men were at 80 wasn’t middle-aged cholesterol levels, it was how satisfied they were in their relationships at 50.8

Fortunately, it is possible to make new friends at every stage of life. In Los Angeles, I met a group of 70-something women who bonded as volunteers for Generation Xchange, an educational and community health nonprofit. The program places older adults in early elementary classrooms as teachers’ aids for a school year. As a result of the extra adult attention in class, the children’s reading scores have gone up and behavioral problems have gone down. The volunteers’ health has improved—they’ve lost weight, and lowered blood pressure and cholesterol. But they have also become friends, which is just what UCLA’s Seeman had in mind when she started the program. “One of the reasons our program may be successful is that we are motivating them to get engaged through their joint interest in helping the kids,” Seeman says. “It takes the pressure off of making friends. You can start getting to know each other in the context of the school and our team. Hopefully, the friendships can grow out of that.”

Concerns about loneliness among the elderly are well-founded. Demographics are not working in favor of the fight against loneliness. By 2035, older adults are projected to outnumber children for the first time in American history. Because of drops in marriage and childbearing, more of those older adults will be unmarried and childless than ever before. The percentage of older adults living alone rose steadily through the 20th century, and now hovers at 27 percent. And a digital divide still exists between older adults and their children and grandchildren, according to recent studies. That means older adults are less able to use virtual technology like Zoom to stay connected during the COVID-19 pandemic—though some are learning. Laura Fisher, a personal trainer in New York City, found that putting her business online meant training older clients one-on-one in videoconferencing. She now works out with one of her young clients in New York City and her client’s grandmother in Israel. Generally, older adults who use social media report more support from both their grown children and their friends. “For older people, social media is a real avenue of connection, of relational well-being,” says psychologist Jeff Hancock who runs the social media lab at Stanford University.

That is good news in this moment of enforced social isolation. So is the fact that being apart has reminded so many of us of how much we enjoy being together. For my part, I sent those flowers to my mother-in-law after all when I discovered contactless delivery. When the flowers arrived, we spoke again. And then I called her again two days later. “It’s great to talk to you,” she said.

Lydia Denworth is a contributing editor for Scientific American and the author of Friendship: The Evolution, Biology, and Extraordinary Power of Life’s Fundamental Bond.

Lead image: SanaStock / Shutterstock

References

1 Holt-Lunstad, J., et al. Loneliness and social isolation as risk factors for mortality: a meta-analytic review. Perspectives on Psychological Science 10, 227-237 (2015).

2 Silk, J.B., Alberts, S.C., & Altmann, J. Social bonds of female baboons enhance infant survival. Science 302, 1231-1234 (2003).

3 Holt-Lunstad, J., Uchino, B.N., Smith, T.W., & Hicks, A. On the importance of relationship quality: The impact of ambivalence in friendships on cardiovascular functioning. Annals of Behavioral Medicine 33, 278-290 (2007).

4 Uchino, B.N., Kent de Grey, R.G., & Cronan, S. The quality of social networks predicts age-related changes in cardiovascular reactivity to stress. Psychology and Aging 31, 321–326 (2016).

5 Seeman, T.E., et al. Social network ties and mortality among tile elderly in the Alameda County Study. American Journal of Epidemiology 126, 714-723 (1987).

6 Yang, Y.C., et al. Social relationships and physiological determinants of longevity across the human life span. Proceedings of the National Academy of Sciences 113, 578-583 (2016).

7 Chopik, W.J. Associations among relational values, support, health, and well‐being across the adult lifespan. Personal Relationships 24, 408-422 (2017).

8 Vaillant, G.E. & Mukamal, K. Successful aging. American Journal of Psychiatry 158, 839-847 (2001).

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Early in the morning on April 5, 2020, an article appeared on the website Medium with the title “Covid-19 had us all fooled, but now we might have finally found its secret.” The article claimed that the pathology of COVID-19 was completely different from what public health authorities, such as the World Health Organization, had previously described. According to the author, COVID-19 strips the body’s hemoglobin of iron, preventing red blood cells from delivering oxygen and damaging the lungs in the process. It also claimed to explain why hydroxychloroquine, an experimental treatment often hyped by President Trump, should be effective.

The article was published under a pseudonym—libertymavenstock—but the associated account was linked to a Chicagoland man working in finance, with no medical expertise. (His father is a retired M.D., and in a follow-up note posted on a blog called “Small Dead Animals,” the author claimed that the original article was a collaboration between the two of them.) Although it was not cited, the claims were apparently based on a single scientific article that has not yet undergone peer-review or been accepted for publication, along with “anecdotal evidence” scraped from social media.1

While Medium allows anyone to post on their site and does not attempt to fact-check content, this article remained up for less than 24 hours before it was removed for violating Medium’s COVID-19 content policy. Removing the article, though, has not stopped it from making a splash. The original text continues to circulate widely on social media, with users tweeting or sharing versions archived by the Wayback Machine and re-published by a right-wing blog. As of April 12, the article had been tweeted thousands of times.

There is a pandemic of misinformation about COVID-19 spreading on social media sites. Some of this misinformation takes well-understood forms: baseless rumors, intentional disinformation, and conspiracy theories. But much of it seems to have a different character. In recent months, claims with some scientific legitimacy have spread so far, so fast, that even if it later becomes clear they are false or unfounded, they cannot be laid to rest. Instead, they become information zombies, continuing to shamble on long after they should be dead.

POOR STANDARD: The antiviral drug hydroxychloroquine has been hyped as an effective treatment for COVID-19, notably by President Trump. The March journal article that kicked off the enthusiasm was later followed by a lesser-read news release from the board of its publisher, the International Society of Antimicrobial Chemotherapy, which states the “Board believes the article does not meet the Society’s expected standard.”Marc Bruxelle / Shutterstock

It is not uncommon for media sources like Medium to retract articles or claims that turn out to be false or misleading. Neither are retractions limited to the popular press. In fact, they are common in the sciences, including the medical sciences. Every year, hundreds of papers are retracted, sometimes because of fraud, but more often due to genuine errors that invalidate study findings.2 (The blog Retraction Watch does an admirable job of tracking these.)

Reversing mistakes is a key part of the scientific process. Science proceeds in stops and starts. Given the inherent uncertainty in creating new knowledge, errors will be made, and have to be corrected. Even in cases where findings are not officially retracted, they are sometimes reversed— definitively shown to be false, and thus no longer valid pieces of scientific information.3

Researchers have found, however, that the process of retraction or reversal does not always work the way it should. Retracted papers are often cited long after problems are identified,4 sometimes at a rate comparable to that before retraction. And in the vast majority of these cases, the authors citing retracted findings treat them as valid.5 (It seems that many of these authors pull information directly from colleagues’ papers, and trust that it is current without actually checking.) Likewise, medical researchers have bemoaned the fact that reversals in practice sometimes move at a glacial pace, with doctors continuing to use contraindicated therapies even though better practices are available.6

For example, in 2010, the anesthesiologist Scott Reuben was convicted of health care fraud for fabricating data and publishing it without having performed the reported research. Twenty-one of Reuben’s articles were ultimately retracted. And yet, an investigation four years later found half of these articles were still consistently cited, and that only one-fourth of these citations mentioned that the original work was fraudulent.7 Given that Reuben’s work focused on the use of anesthetics, this failure of retraction is seriously disturbing.

Claims with some scientific legitimacy continue to shamble on long after they should be dead.

But why don’t scientific retractions always work? At the heart of the matter lies the fact that information takes on a life of its own. Facts, beliefs, and ideas are transmitted socially, from person to person to person. This means that the originator of an idea soon loses control over it. In an age of instant reporting and social media, this can happen at lightning speed.

The first models of the social spread of information were actually epidemiological models, developed to track the spread of disease. (Yes, these are the very same models now being used to predict the spread of COVID-19.) These models treat individuals as nodes in a network and suppose that information (or disease) can propagate between connected nodes.

Recently, one of us, along with co-authors Travis LaCroix and Anders Geil, repurposed these models to think specifically about failures of retraction and reversal.8 A general feature of retracted information, understood broadly, is that it is less catchy than novel information in the following way. People tend to care about reversals or retractions only when they have already heard the original, false claim. And they tend to share retractions only when those around them are continuing to spread the false claim. This means that retractions actually depend on the spread of false information.

We built a contagion model where novel ideas and retractions can spread from person to person, but where retractions only “infect” those who have already heard something false. Across many versions of this model, we find that while a false belief spreads quickly and indiscriminately, its retraction can only follow in the path of its spread, and typically fails to reach many individuals. To quote Mark Twain, “A lie can travel halfway around the world while the truth is putting on its shoes.” In these cases it’s because the truth can’t go anywhere until the lie has gotten there first.

Another problem for retractions and reversals is that it can be embarrassing to admit one was wrong, especially where false claims can have life or death consequences. While scientists are expected to regularly update their views under normal circumstances, under the heat of media and political scrutiny during a pandemic they too may be less willing to publicize reversals of opinion.

The COVID-19 pandemic has changed lives around the world at a startling speed—and scientists have raced to keep up. Academic journals, accustomed to a comparatively glacial pace of operations, have faced a torrent of new papers to evaluate and process, threatening to overwhelm a peer-review system built largely on volunteer work and the honor system.9 Meanwhile, an army of journalists and amateur epidemiologists scour preprint archives and university press releases for any whiff of the next big development in our understanding of the virus. This has created a perfect storm for information zombies—and although it also means erroneous work is quickly scrutinized and refuted, this often makes little difference to how those ideas spread.

Many examples of COVID-19 information zombies look like standard cases of retraction in science, only on steroids. They originate with journal articles written by credentialed scientists that are later retracted, or withdrawn after being refuted by colleagues. For instance, in a now-retracted paper, a team of biologists based in New Delhi, India, suggested that novel coronavirus shared some features with HIV and was likely engineered.10 It appeared on an online preprint archive, where scientists post articles before they have undergone peer review, on January 31; it was withdrawn only two days later, following intense critique of the methods employed and the interpretation of the results by scientists from around the world. Days later, a detailed analysis refuting the article was published in the peer-reviewed journal Emerging Microbes & Infections.11 But a month afterward, the retracted paper was still so widely discussed on social media and elsewhere that it had that highest Altmetric score—a measure of general engagement with scientific research—of any scientific article published or written in the previous eight years. Despite a thorough rejection of the research by the scientific community, the dead information keeps walking.

Other cases are more subtle. One major question with far-reaching implications for the future development of the pandemic is to what extent asymptomatic carriers are able to transmit the virus. The first article reporting on asymptomatic transmission was a letter published in the prestigious New England Journal of Medicine claiming that a traveler from China to Germany transmitted the disease to four Germans before her symptoms appeared.12 Within four days, Science reported that the article was flawed because the authors of the letter had not actually spoken with the Chinese traveler, and a follow-up phone call by public health authorities confirmed that she had had mild symptoms while visiting Germany after all.13 Even so, the article has subsequently been cited nearly 500 times according to Google Scholar, and has been tweeted nearly 10,000 times, according to Altmetric.

Media reporting on COVID-19 should be linked to authoritative sources that are updated as information changes.

Despite the follow-up reporting on this article’s questionable methods, the New England Journal of Medicine did not officially retract it. Instead, a week after publishing the letter, the journal added a supplemental appendix describing the progression of the patient’s symptoms while in Germany, leaving it to the reader to determine whether the patient’s mild early symptoms should truly count. Meanwhile, subsequent research14, 15 involving different cases has suggested that asymptomatic transmission may be possible after all—though as of April 13, the World Health Organization considers the risk of infection from asymptomatic carriers to be “very low.” It may turn out that transmission of the virus can occur before any symptoms appear, or while only mild symptoms are present, or even in patients who will never go on to present symptoms. Even untangling these questions is difficult, and the jury is still out on their answers. But the original basis for claims of confirmed asymptomatic transmission was invalid, and those sharing them are not typically aware of the fact.

Another widely discussed article, which claims that the antiviral drug hydroxychloroquine and the antibiotic azithromycin, when administered together, are effective treatments for COVID-19 has drawn enormous amounts of attention to these particular treatments, fueled in part by President Trump.16 These claims, too, may or may not turn out to be true—but the article with which they apparently originated has since received a statement of concern from its publisher, noting that its methodology was problematic. Again, we have a claim that rests on shoddy footing, but which is spreading much farther than the objections can.17 And in the meantime, the increased demand for these medications has led to dangerous shortages for patients who have an established need for them.18

The fast-paced and highly uncertain nature of research on COVID-19 has also created the possibility for different kinds of information zombies, which follow a similar pattern as retracted or refuted articles, but with different origins. There have been a number of widely discussed arguments to the effect that the true fatality rate associated with COVID-19 may be ten or even a hundred times lower than early estimates from the World Health Organization, which pegged the so-called “case fatality rate” (CFR)—the number of fatalities per detected case of COVID-19—at 3.4 percent.19-21

Some of these arguments have noted that the case fatality rate in certain countries with extensive testing, such as Iceland, Germany, and Norway, is substantially lower. References to the low CFR in these countries have continued to circulate on social media, even though the CFR in all of these locations has crept up over time. In the academic realm, John Ioannidis, a Stanford professor and epidemiologist, noted in an editorial, “The harms of exaggerated information and non‐evidence‐based measures,” published on March 19 in the European Journal of Clinical Investigation, that Germany’s CFR in early March was only 0.2 percent.21 But by mid-April it had climbed to 2.45 percent, far closer to the original WHO estimate. (Ioannidis has not updated the editorial to reflect the changing numbers.) Even Iceland, which has tested more extensively than any other nation, had a CFR of 0.47 percent on April 13, more than 4 times higher than it was a month ago. None of this means that the WHO figure was correct—but it does mean some arguments that it is wildly incorrect must be revisited.

What do we do about false claims that refuse to die? Especially when these claims have serious implications for decision-making in light of a global pandemic? To some degree, we have to accept that in a world with rapid information sharing on social media, information zombies will appear. Still, we must combat them. Science journals and science journalists rightly recognize that there is intense interest in COVID-19 and that the science is evolving rapidly. But that does not obviate the risks of spreading information that is not properly vetted or failing to emphasize when arguments depend on data that is very much in flux.

Wherever possible, media reporting on COVID-19 developments should be linked to authoritative sources of information that are updated as the information changes. The Oxford-based Centre for Evidence-Based Medicine maintains several pages that review the current evidence on rapidly evolving questions connected to COVID-19—including whether current data supports the use of hydroxychloroquine and the current best estimates for COVID-19 fatality rates. Authors and platforms seeking to keep the record straight should not just remove or revise now-false information, but should clearly state what has changed and why. Platforms such as Twitter should provide authors, especially scientists and members of the media, the ability to explain why Tweets that may be referenced elsewhere have been deleted. Scientific preprint archives should encourage authors to provide an overview of major changes when articles are revised.

And we should all become more active sharers of retraction. It may be embarrassing to shout one’s errors from the rooftops, but that is what scientists, journals, and responsible individuals must do to slay the information zombies haunting our social networks.

Cailin O’Connor and James Owen Weatherall are an associate professor and professor of logic and philosophy at the University of California, Irvine. They are coauthors of The Misinformation Age: How False Beliefs Spread.

Lead image: nazareno / Shutterstock

References

1. Liu, W. & Li, H. COVID-19 attacks the 1-beta chain of hemoglobin and captures the porphyrin to inhibit human heme metabolism. ChemRxiv (2020).

2. Wager, E. & Williams, P. Why and how do journals retract articles? An analysis of Medline retractions 1988-2008. Journal of Medical Ethics 37, 567-570 (2011).

3. Prasad, V., Gall, V., & Cifu, A. The frequency of medical reversal. Archives of Internal Medicine 171, 1675-1676 (2011).

4. Budd, J.M., Sievert, M., & Schultz, T.R. Phenomena of retraction: Reasons for retraction and citations to the publications. The Journal of the American Medical Association 280, 296-297 (1998).

5. Madlock-Brown, C.R. & Eichmann, D. The (lack of) impact of retraction on citation networks. Science and Engineering Ethics 21, 127-137 (2015).

6. Prasad, V. & Cifu, A. Medical reversal: Why we must raise the bar before adopting new technologies. Yale Journal of Biology and Medicine 84, 471-478 (2011).

7. Bornemann-Cimenti, H., Szilagyi, I.S., & Sandner-Kiesling, A. Perpetuation of retracted publications using the example of the Scott S. Reuben case: Incidences, reasons and possible improvements. Science and Engineering Ethics 22, 1063-1072 (2016).

8. LaCroix, T., Geil, A., & O’Connor, C. The dynamics of retraction in epistemic networks. Preprint. (2019).

9. Jarvis, C. Journals, peer reviewers cope with surge in COVID-19 publications. The Scientist (2020).

10. Pradhan, P., et al. Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag. bioRxiv (2020).

11. Xiao, C. HIV-1 did not contribute to the 2019-nCoV genome. Journal of Emerging Microbes and Infections 9, 378-381 (2020).

12. Rothe, C., et al. Transmission of 2019-nCoV infection from an asymptomatic contact in Germany. New England Journal of Medicine 382, 970-971 (2020).

13. Kupferschmidt, K. Study claiming new coronavirus can be transmitted by people without symptoms was flawed. Science (2020).

14. Hu, Z., et al. Clinical characteristics of 24 asymptomatic infections with COVID-19 screened among close contacts in Nanjing, China. Science China Life Sciences (2020). Retrieved from doi: 10.1007/s11427-020-1661-4.

15. Bai, R., et al. Presumed asymptomatic carrier transmission of COVID-19. The Journal of the American Medical Association 323, 1406-1407 (2020).

16. Gautret, P., et al. Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial. International Journal of Antimicrobial Agents (2020).

17. Ferner, R.E. & Aronson, J.K. Hydroxychloroquine for COVID-19: What do the clinical trials tell us? The Centre for Evidence-Based Medicine (2020).

18. The Arthritis Foundation. Hydroxychloroquine (Plaquenil) shortage causing concern. Arthritis.org (2020).

19. Oke, J. & Heneghan, C. Global COVID-19 case fatality rates. The Centre for Evidence-Based Medicine (2020).

20. Bendavid, E. & Bhattacharya, J. Is the coronavirus as deadly as they say? The Wall Street Journal (2020).

21. Ionnidis, J.P.A. Coronavirus disease 2019: The harms of exaggerated information and non-evidence-based measures. European Journal of Clinical Investigation 50, e13222 (2020).

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It seems like people who get infected with SARS-CoV-2 retain immunity, but we can’t be sure how long that immunity will last. We still lack the testing capabilities to be certain.eamesBot / Shutterstock

This story was updated post-publication to include information from a study published on the preprint server medRxiv on April 17, 2020.

With more than half a million cases of COVID-19 in the United States1 and the number of deaths increasing daily, it remains unclear when and how we might return to some semblance of pre-pandemic life. This leaves many grappling with an important question: Do you become immune after SARS-CoV-2 infection? And, if so, how long might that immunity last?

In 2019, the virus SARS-CoV-2 jumped to a human host for the first time, causing the disease COVID-19. When you become infected with a new virus, your body does not possess the antibodies necessary to mount a targeted immune response. Antibodies, proteins belonging to the immunoglobulin family, consist of four chains of amino acids that form a characteristic Y-shaped structure. Antibodies are manufactured by the immune system to bind to antigens (viral proteins) to neutralize viral infectivity.

When you inhale an aerosolized droplet containing SARS-CoV-2, the virus encounters the cells of the mucous membrane lining the respiratory tract. If effective contact is made, the virus binds to a particular receptor on these cells called ACE-2. After binding ACE-2, a host enzyme is co-opted to cleave the virus’ surface protein, called the spike protein, allowing the virus to enter the cell.

It appears that individuals with COVID-19 do create neutralizing antibodies—the basis of immunity.

Within the first few hours of infection, the body’s first line of defense—the innate immune response—is activated. The innate immune response is non-specific. When a “foreign” molecule is detected, innate immune cells signal to other cells to alter their response or prepare to combat infection.

In the following days, the adaptive immune response is activated, which is more specific. The adaptive immune response will peak one to two weeks post-infection and consists of antibodies and specialized immune cells. It is called the “adaptive” immune response because of its ability to tailor the response to a specific pathogen. Antibodies can neutralize viral infectivity by preventing virus from binding to receptors, blocking cell entry, or causing virus particles to aggregate.2 Once an infection has resolved, some of these antibodies remain in the body as immunological memory to be recruited for protection in the case of reinfection. To be immune to a virus is to possess this immunological memory.

Many vaccines work by activating the adaptive immune response. Inactivated virus, viral protein, or some other construct specific to a particular virus are introduced into the body as vaccines to initiate an immune response. Ideally, the body creates antibodies against the viral construct so that it can mount a succinct response when infected by the virus. However, in order to work effectively, a vaccine must provoke an immune response that is sufficiently robust. If the body only produces low concentrations of neutralizing antibodies, adequate immunological memory may not be sustained.

While there is still much that we have to learn about SARS-CoV-2, it appears that individuals with COVID-19 do create neutralizing antibodies—the basis of immunity. However, we don’t know for certain how long that immunity might offer protection. On the question of COVID-19 re-infection, Matt Frieman, a coronavirus researcher at the University of Maryland School of Medicine, commented in a recent interview with NPR: “We don’t know very much … I think there’s a very likely scenario where the virus comes through this year, and everyone gets some level of immunity to it, and if it comes back again, we will be protected from it—either completely or if you do get reinfected later, a year from now, then you have much less disease. That’s the hope, but there is no way to know that.”3

Immunity to a virus is measured by serological testing—patient blood is collected and analyzed for the presence of antibodies against a particular virus. Serological data is most informative when collected long-term, so the data we have been able to obtain on SARS-CoV-2 is limited. However, data on other coronaviruses that we’ve had the opportunity to study in more depth can inform our estimations on how this outbreak may evolve.

First, we can look to the coronaviruses that are known to cause the common cold. Following infection with one of these coronaviruses, disease is often mild; therefore, the concentration of antibodies detected in the blood is low. This is because mild disease often indicates a less robust immune response. Interestingly, it is not the virus itself that causes us to feel sick, but, rather, our body’s response to it. Typically, the sicker we feel, the stronger the immune response; therefore, after a cold, we are often only protected for a year or two against the same virus.4 While SARS-CoV-2 wouldn’t necessarily act like these common coronaviruses, the body’s response to these coronaviruses serves as a point of reference upon which to make predictions in the absence of virus-specific data.

We can also look to coronaviruses that are known to cause severe disease, such as SARS-CoV, which caused the 2002-2003 outbreak of SARS in China. One study discovered that antibodies against SARS-CoV remained in the blood of healthcare workers for 12 years after infection.5 While it is not certain that SARS-CoV-2 will provoke a response similar to that of SARS-CoV, this study provides us with information that can inform our estimates on immunity following COVID-19 and provide hope that immunity will provide long-term protection.

If immunity to SARS-CoV-2 diminishes as it does for common cold coronaviruses, it is likely that wintertime outbreaks will recur.

Scientists have also been working to analyze antibodies in samples from individuals infected with SARS-CoV-2. A research group in Finland recently published a study detailing the serological data collected from a COVID-19 patient over the course of their illness.6 Antibodies specific to SARS-CoV-2 were present within two weeks from the onset of symptoms. Similarly, another recent report analyzing patients with confirmed COVID-19 indicated that it took approximately 11-14 days for neutralizing antibodies to be detected in blood.7 Both of these studies, while preliminary, suggest that the basis for immunity is present in patients infected with SARS-CoV-2.

Another report looked at the possibility for recurrence of COVID-19 following re-infection with SARS-CoV-2.8 In this study, rhesus macaques were infected with SARS-CoV and allowed to recover after developing mild illness. Once blood samples were collected and confirmed to test positive for neutralizing antibodies, half of the infected macaques were re-challenged with the same dose of SARS-CoV-2. The re-infected macaques showed no significant viral replication or recurrence of COVID-19. While macaques “model” human immunity, not predict it, these data further support the possibility that antibodies manufactured in response to SARS-CoV-2 are protective against short-term re-infection.

We can also analyze a virus’ structure, and the information gained from sequencing the viral genome, when trying to predict its behavior. All viruses continually undergo mutation in the process of rapid replication. They lack the necessary machinery to repair changes incurred to the genetic sequence (we as humans also incur mutations to our genetic sequence daily, but we have more sophisticated genetic repair mechanisms in place). The occurrence of significant genetic changes to the viral genome that result in viable genetic changes to a virus is termed antigenic variation. We see a lot of antigenic variation in influenza viruses (thus the need to create new vaccines each year); but the coronaviruses seem to be relatively stable antigenically.4 This is because most coronaviruses have an enzyme that allows them to correct genetic errors sustained during replication. The more stable a virus remains over time, the more likely that antibodies manufactured in response to infection or vaccination will remain effective at neutralizing viral infectivity.

All this considered, it appears that immunity is retained following SARS-CoV-2 infection. So too, that immunity might persist long enough to warrant the implementation of vaccination. However, we still have much to learn about this virus, and whether there may be some cross-immunity between SARS-CoV-2 and other coronaviruses. The widespread variation in patient immune responses adds an additional layer of complexity. We still don’t have a good understanding of why people have different responses to viral infection—some of this variation is owed to genetic variation, but how and why some people have more robust immune responses and more severe disease is still unknown.4 In some cases, individuals show a high immune response because the concentration of virus is high. In other cases, individuals show a high immune response because they differ in some aspect of immune regulation or efficiency. However, as levels of immunity increase generally across a population, the population approaches what is called “herd immunity”—when the percentage of a population immune to a particular virus is sufficiently high that viral load drops below the threshold required to sustain the infection in that population.9

How the pandemic will evolve in the coming months is uncertain. Outcomes depend on a myriad of factors—the duration of immunity, the dynamics of transmission and how we mitigate those dynamics through social distancing, the development of therapeutics and or vaccines, and the ability of healthcare systems to handle COVID-19 caseloads. If immunity to SARS-CoV-2 diminishes as it does for common cold coronaviruses, it is likely that wintertime outbreaks will recur in coming years.10 Whether immunity to other coronaviruses might offer some cross protective immunity to SARS-CoV-2 will also play a role, albeit to a lesser extent. Widespread serological testing to assess the duration of immunity to SARS-CoV-2 is imperative, but many countries still lack this capability.

A recent study looking at serological data from 3,300 symptomatic and asymptomatic individuals in California estimates that there may be as many as 48,000-81,000 people who have been infected with SARS-Cov-2 in Santa Clara County, which is 50- to 85-fold more cases than we previously thought.11 This small-scale survey emphasizes the importance of serological testing in determining the true extent of infection.

The continuation of rigid social distance also hangs in a balance—one-time social distancing measures may drive the SARS-CoV-2 epidemic peak into the fall and winter months, especially if there is increased wintertime transmissibility.10 New therapeutics, vaccines, or measures such as contact tracing and quarantine—once caseloads have been reduced and testing capacity increased—might reduce the need for rigid social distancing. However, if such measures are not put in place, mathematical models predict that surveillance and recurrent social distancing may be required through 2022.10 Only time will tell.

Helen Stillwell is a research associate in immunobiology at Yale University.

References

1. The COVID Tracking Project https://covidtracking.com/data/us-daily (2020).

2. Virology Blog: About Viruses and Viral Disease. Virus neutralization by antibodies. virology.ws (2009).

3. GreenfieldBoyce, N. Do you get immunity after recovering from a case of coronavirus? NPR (2020).

4. Racaniello, V., Langel, S., Leifer, C., & Barker, B. Immune 29: Immunology of COVID-19. Immune Podcast. microbe.tv (2020).

5. Guo, X., et al. Long-Term persistence of IgG antibodies in SARS-CoV infected healthcare workers. bioRxiv (2020). Retrieved from doi: 10.1101/20202/02/12/20021386

6. Haveri, A., et al. Serological and molecular findings during SARS-CoV-2 infection: the first case study in Finland, January to February 2020. Euro Surveillance 25, (2020).

7. Zhao, J., et al. Antibody responses to SARS-CoV-2 in patients of novel coronavirus disease 2019. Clinical Infectious Diseases (2020). Retrieved from doi: 10.1093/cid/ciaa344

8. Bao, L., et al. Reinfection could not occur in SARS-CoV-2 infected rhesus macaques. bioRxiv (2020). Retrieved from doi: 10.1101/20202.03.13.990226

9. Virology Blog: About Viruses and Viral Disease. Herd immunity. virology.ws (2008).

10. Kissler, S.M. Tedijanto, C., Goldstein, E., Grad, Y.H., & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the post-pandemic period. Science eabb5793 (2020).

11. Bendavid, E., et al. COVID-19 antibody seroprevalence in Santa Clara County, California. medRxiv (2020). Retrieved from doi: 10.1101/2020.04.14.20062463

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Like most of us, Adam Tooze is stuck at home. The British-born economic historian and Columbia University professor of history had been on leave this school year to write a book about climate change. But now he’s studying a different global problem. There are more than 700,000 cases of COVID-19 in the United States and over 2 million infections worldwide. It’s also caused an economic meltdown. More than 18 million Americans have filed for unemployment in recent weeks, and Goldman Sachs analysts predict that U.S. gross domestic product will decline at an annual rate of 34 percent in the second quarter.

Tooze is an expert on economic catastrophes. He wrote the book Crashed: How a Decade of Financial Crises Changed the World, about the 2008 economic crisis and its aftermath. But even he didn’t see this one coming. He hadn’t thought much about how pandemics could impact the economy—few economists had. Then he watched as China locked down the city of Wuhan, in a province known for auto manufacturing, on January 23; as northern Italy shut down on February 23; and as the U.S. stock market imploded on March 9. By then, he knew he had another financial crisis to think about. He’s been busy writing ever since. Tooze spoke with Nautilus from his home in New York City.

INEQUALITY FOR ALL: Adam Tooze (above) says a crisis like this one, “where you shut the entire economy down in a matter of weeks” highlights the “profound inequality” in American society.Wikimedia

What do you make of the fact that, in three weeks, more than 16 million people in the U.S. have filed for unemployment?

The structural element here—and this is quite striking, when you compare Europe, for instance, to the U.S.—is that America has and normally celebrates the flexibility and dynamism of its labor market: The fact that people move between jobs. The fact that employers have the right to hire and fire if they need to. The downside is that in a shock like this, the appropriate response for an employer is simply to let people go. What America wasn’t able to do was to improvise the short-time working systems that the Europeans are trying to use to prevent the immediate loss of employment to so many people.

The disadvantage of the American system that reveals itself in a crisis like this is that hiring and firing is not easily reversible. People who lose jobs don’t necessarily easily get them back. There is a fantasy of a V-shaped recovery. We literally have never done this before, so we don’t know one way or another how this could happen. But it seems likely that many people who have lost employment will not immediately find reemployment over the summer or the fall when business activity resumes something like its previous state. In a situation with a lot of people with low qualifications in precarious jobs at low income, the damage from that kind of interruption of employment in sectors notably which are already teetering on the edge—the chain stores, which are quite likely closing anyway, and fragile malls, which were on the edge of dying—it’s quite likely that this shock will also induce disproportionately large amounts of scarring.

What role has wealth and income inequality played during this crisis?

The U.S. economic system is bad enough in a regular crisis. In one like this, where you shut the entire economy down in a matter of weeks, the damage is barely conceivable. There are huge disparities, all of which ultimately are rooted in social structures of race and class, and in the different types of jobs that people have. The profound inequality in American society has been brought home for us in everyone’s families, where there is a radical disparity between the ability of some households to sustain the education of their children and themselves living comfortably at home. Twenty-five percent of kids in the United States appear not to have a stable WiFi connection. They have smartphones. That seems practically universal. But you can’t teach school on a smartphone. At least, that technology is not there.

Presumably by next year something like normality returns. But forever after we’ll live under the shadow of this having happened.

President Trump wants the economy to reopen by May. Would that stop the economic crisis?

Certainly that is presumably what drives that haste to restart the economy and to lift intense social distancing provisions. There is a sense that we can’t stand this. And that has a lot to do with deep fragilities in the American social system. If all Americans live comfortably in their own homes, with the safety of a regular paycheck, with substantial savings, with health insurance that wasn’t conditional on precarious employment, and with unemployment benefits that were adequate and that were rolled out to most people in this society if they needed them, then there wouldn’t be such a rush. But that isn’t America as we know it. America is a society in which half of families have virtually no financial cushion; in which small businesses, which are so often hailed as the drivers of job creation, the vast majority of owners of them live hand-to-mouth; in which the unemployment insurance system really is a mockery; and with health insurance directly tied to employment for the vast majority of the people. A society like that really faces huge pressures if the economy is shut down.

How is the pandemic-induced economic collapse we’re facing now different from what we faced in 2008?

This is so much faster. Early this year, America had record-low unemployment numbers. And last week or so already we probably broke the record for unemployment in the United States in the period since World War II. This story is moving so fast that our statistical systems of registration can’t keep up. So we think probably de facto unemployment in the U.S. right now is 13, 14, 15 percent. That’s never happened before. 2007 to 2008 was a classic global crisis in the sense that it came out of one particular over-expanded sector, a sector which is very well known for its volatility, which is real estate and construction. It was driven by a credit boom.

What we’re seeing this time around is deliberately, government-ordered, cliff edge, sudden shutdown of the entire economy, hitting specifically the face-to-face human services—retail, entertainment, restaurants—sector, which are, generally speaking, lagging in cyclical terms and are not the kind of sectors that generate boom-bust cycles.

Are we better prepared this time than in 2008?

You’d find it very hard to point to anyone in the policymaking community at the beginning of 2020 who was thinking of pandemic risk. Some people were. Former Treasury Secretary and former Director of the National Economic Council Larry Summers, for example, wrote a paper about pandemic flu several years ago, because of MERS and SARS, previous respiratory illnesses caused by coronaviruses. But it wasn’t top of stack at the beginning of this year. So we weren’t prepared in that sense. But do we know what to do now if we see the convulsions in the credit markets that we saw at the beginning of March? Yes. Have the central banks done it? Yes. Did they use some of the techniques they employed in ’08? Yes. Did they know that you had to go in big and you had to go in heavy and hard and quickly? Yes. And they have done so on an even more gigantic scale than in ’08, which is a lesson learned in ’08, too: There’s no such a thing as too big. And furthermore, the banks, which were the fragile bit in ’08, have basically been sidelined.

You’ve written that the response to the 2008 crisis worked to “undermine democracy.” How so, and could we see that again with this crisis?

The urgency that any financial crisis produces forces governments’ hands—it strips the legislature, the ordinary processes of democratic deliberation. When you’re forced to make very dramatic, very rapid decisions—particularly in a country as chronically divided as the U.S. is on so many issues—the risk that you create opportunities for demagogues of various types to take advantage of is huge. We know what the response of the Tea Party was to the ’08, ’09 economic crisis. They created an extraordinarily distorted vision of what had happened and then rode that to see extraordinary influence over the Republican party in the years that followed. And there is every reason to think that we might be faced with similar stresses in the American political system in months to come.

The U.S. economic system is bad enough in a regular crisis. In one like this, where you shut the entire economy down in a matter of weeks, the damage is barely conceivable.

How should we be rethinking the economy to buffer against meltdowns like this in the future?

We clearly need to have a far more adequate and substantial medical capacity. There’s no alternative to a comprehensive publicly backstopped or funded health insurance system. Insofar as you haven’t got that, your capacity to guarantee the security in the most basic and elementary sense of your population is not there. When you have a system in which one of the immediate side effects, in a crisis like this, is that large parts of your hospital system go bankrupt—one of the threats to the American medical system right now—that points to something extraordinarily wrong, especially if you’re spending close to 18 percent of GDP on health, more than any other society on the planet.

What about the unemployment insurance system?

America needs to have a comprehensive unemployment insurance system. It can be graded by local wage rates and everything else. But the idea that you have the extraordinary disparities that we have between a Florida and a Georgia at one end, with recipiency rates in the 11, 12, 13, 14, 15 percent, and then states which actually operate an insurance system, which deserve the name—this shouldn’t be accepted in a country like the U.S. We would need to look at how short-time working models might be a far better way of dealing with shocks of this kind, essentially saying that there is a public interest in the continuity of employment relationships. The employer should be investing in their staff and should not be indifferent as to who shows up for work on any given day.

What does this pandemic teach us about living in a global economy?

There are a series of very hard lessons in the recent history of globalization into which the corona shock fits—about the peculiar inability of American society, American politics, and the American labor market to cushion shocks that come from the outside in a way which moderates the risk and the damage to the most vulnerable people. If you look at the impact of globalization on manufacturing, industry, inequality, the urban fabric in the U.S., it’s far more severe than in other societies, which have basically been subject to the same shock. That really needs to raise questions about how the American labor market and welfare system work, because they are failing tens of millions of people in this society.

You write in Crashed not just about the 2008 crisis, but also about the decade afterward. What is the next decade going to look like, given this meltdown?

I have never felt less certain in even thinking about that kind of question. At this point, can either you or I confidently predict what we’re going to be doing this summer or this autumn? I don’t know whether my university is resuming normal service in the fall. I don’t know whether my daughter goes back to school. I don’t know when my wife’s business in travel and tourism resumes. That is unprecedented. It’s very difficult against that backdrop to think out over a 10-year time horizon. Presumably by next year something like normality returns. But forever after we’ll live under the shadow of this having happened. Every year we’re going to be anxiously worrying about whether flu season is going to be flu season like normal or flu season like this. That is itself something to be reckoned with.

How will anxiety and uncertainty about a future pandemic-like crisis affect the economy?

When we do not know what the future holds to this extent, it makes it very difficult for people to make bold, long-term financial decisions. This previously wasn’t part of the repertoire of what the financial analysts call tail risk. Not seriously. My sister works in the U.K. government, and they compile a list every quarter of the top five things that could blow your departmental business up. Every year pandemics are in the top three. But no one ever acted on it. It’s not like terrorism. In Britain, you have a state apparatus which is geared to address the terrorism risk because it’s very real—it’s struck many times. Now all of a sudden we have to take the possibility of pandemics that seriously. And their consequences are far more drastic. How do we know what our incomes are going to be? A very large part of American society is not going to be able to answer that question for some time to come. And that will shake consumer confidence. It will likely increase the savings rate. It’s quite likely to reduce the desire to invest in a large part of the U.S. economy.

Max Kutner is a journalist in New York City. He has written for Newsweek, The Boston Globe, and Smithsonian. Follow him on Twitter @maxkutner.

Lead image: Straight 8 Photography / Shutterstock

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The marquee on my closed neighborhood movie theater reads, “See you on the other side.” I like reading it every day as I pass by on my walk. It causes me to envision life after the coronavirus pandemic. Which is awfully hard to envision now. But it’s out there. When you have a disease and are in a hospital, alone and afraid, intravenous tubes and sensor wires snaking from your body into digital monitors, all you want is to be normal again. You want nothing more than to have a beer in a dusky bar and read a book in amber light. At least that’s all I wanted last year when I was in a hospital, not from a coronavirus. When, this February, I had that beer in a bar with my book, I was profoundly happy. The worst can pass.

With faith, you can ask how life will be on the other side. Will you be changed personally? Will we be changed collectively? The knowledge we’re gaining now is making us different people. Pain demands relief, demands we don’t repeat what produced it. Will the pain of this pandemic point a new way forward? It hasn’t before, as every war attests. This time may be no different. But the pandemic has slipped a piece of knowledge into the body public that may not be easy to repress. It’s an insight scientists and poets have voiced for centuries. We’re not apart from nature, we are nature. The environment is not outside us, it is us. We either act in concert with the environment that gives us life, or the environment takes life away.

Guess which species is the bully? No animal has had the capacity to modify its niche the way we have.

Nothing could better emphasize our union with nature than the lethal coronavirus. It’s crafted by a molecule that’s been omnipresent on Earth for 4 billion years. Ribonucleic acid may not be the first bridge from geochemical to biochemical life, as some scientists have stated. But it’s a catalyst of biological life. It wrote the book on replication. RNA’s signature molecules, nucleotides, code other molecules, proteins, the building blocks of organisms. When RNA’s more chemically stable kin, DNA, arrived on the scene, it outcompeted its ancestor. Primitive organisms assembled into cells and DNA set up shop in their nucleus. It employed its nucleotides to code proteins to compose every tissue in every multicellular species, including us. A shameless opportunist, RNA made itself indispensable in the cellular factory, shuttling information from DNA into the cell’s power plant, where proteins are synthesized.

RNA and DNA had other jobs. They could be stripped down to their nucleotides, swirled inside a sticky protein shell. That gave them the ability to infiltrate any and all species, hijack their reproductive machinery, and propagate in ways that make rabbits look celibate. These freeloading parasites have a name: virus. But viruses are not just destroyers. They wear another evolutionary hat: developers. Viruses “may have originated the DNA replication system of all three cellular domains (archaea, bacteria, eukarya),” writes Luis P. Villareal, founding director of the Center for Virus Research at the University of California, Irvine.1 Their role in nature is so successful that DNA and RNA viruses make up the most abundant biological entities on our planet. More viruses on Earth than stars in the universe, scientists like to say.

Today more RNA than DNA viruses thrive in cells like ours, suggesting how ruthless they’ve remained. RNA viruses generally reproduce faster than DNA viruses, in part because they don’t haul around an extra gene to proofread their molecular merger with others’ DNA. So when the reckless RNA virus finds a new place to dwell, organisms become heartbreak hotels. Once inside a cell, the RNA virus slams the door on the chemical saviors dispatched by cells’ immunity sensors. It hijacks DNA’s replicative powers and fans out by the millions, upending cumulative cellular functions. Like the ability to breathe.

Humans. We love metaphors. They allow us to compare something as complex as viral infection to something as familiar as an Elvis Presley hit. But metaphors for natural processes are seldom accurate. The language is too porous, inviting our anthropomorphic minds to close the gaps. We imagine viruses have an agenda, are driven by an impetus to search and destroy. But nature doesn’t act with intention. It just acts. A virus lives in a cell like a planet revolves around a sun.

Biologists debate whether a virus should be classified as living because it’s a deadbeat on its own; it only comes to life in others. But that assumes an organism is alive apart from its environment. The biochemist and writer Nick Lane points out, “Viruses use their immediate environment to make copies of themselves. But then so do we: We eat other animals or plants, and we breathe in oxygen. Cut us off from our environment, say with a plastic bag over the head, and we die in a few minutes. One could say that we parasitize our environment—like viruses.”2

Our inseparable accord with the environment is why the coronavirus is now in us. Its genomic signature is almost a perfect match with a coronavirus that thrives in bats whose habitats range across the globe. Humans moved into the bats’ territory and the bats’ virus moved into humans. The exchange is just nature doing its thing. “And nature has been doing its thing for 3.75 billion years, when bacteria fought viruses just as we fight them now,” says Shahid Naeem, an upbeat professor of ecology at Columbia University, where he is director of the Earth Institute Center for Environmental Sustainability. If we want to assign blame, it lies with our collectively poor understanding of ecology.

FLYING LESSON: Bats don’t die from the same coronavirus that kills humans because the bat’s anatomy fights the virus to a draw, neutralizing its lethal moves. What’s the deal with the human immune system? We don’t fly.Martin Pelanek / Shutterstock

Organisms evolve with uniquely adaptive traits. Bats play many ecological roles. They are pollinators, seed-spreaders, and pest-controllers. They don’t die from the same coronavirus that kills humans because the bat’s anatomy fights the virus to a draw, neutralizing its lethal moves. What’s the deal with the human immune system? We don’t fly. “Bats are flying mammals, which is very unusual,” says Christine K. Johnson, an epidemiologist at the One Health Institute at the University of California, Davis, who studies virus spillover from animals to humans. “They get very high temperatures when they fly, and have evolved immunological features, which humans haven’t, to accommodate those temperatures.”

A viral invasion can overstimulate the chemical responses from a mammal’s immune system to the point where the response itself causes excessive inflammation in tissues. A small protein called a cytokine, which orchestrates cellular responses to foreign invaders, can get over-excited by an aggressive RNA virus, and erupt into a “storm” that destroys normal cellular function—a process physicians have documented in many current coronavirus fatalities. Bats have genetic mechanisms to inhibit that overreaction. Similarly, bat flight requires an increased rate of metabolism. Their wing-flapping action leads to high levels of oxygen-free radicals—a natural byproduct of metabolism—that can damage DNA. As a result, states a 2019 study in the journal Viruses, “bats probably evolved mechanisms to suppress activation of immune response due to damaged DNA generated via flight, thereby leading to reduced inflammation.”3

Bats don’t have better immune systems than humans; just different. Our immune systems evolved for many things, just not flying. Humans do well around the cave fungus Pseudogymnoascus destructans, source of the “white-nose syndrome” that has devastated bats worldwide. Trouble begins when we barge into wildlife habitats with no respect for differences. (Trouble for us and other animals. White-nose syndrome spread in part on cavers’ shoes and clothing, who tracked it from one site to the next.) We mine for gold, develop housing tracts, and plow forests into feedlots. We make other animals’ habitats our own.

Our moralistic brain sees retribution. Karma. A viral outbreak is the wrath that nature heaps on us for bulldozing animals out of their homes. Not so. “We didn’t violate any evolutionary or ecological laws because nature doesn’t care what we do,” Naeem says. Making over the world for ourselves is just humans being the animals we are. “Every species, if they had the upper hand, would transform the world into what it wants,” Naeem says. “Birds build nests, bees build hives, beavers build dams. It’s called niche construction. If domestic cats ruled the world, they would make the world in their image. It would be full of litter trays, lots of birds, lots of mice, and lots of fish.”

But nature isn’t an idyllic land of animal villages constructed by evolution. Species’ niche-building ways have always brought them into contact with each other. “Nature is ruled by processes like competition, predation, and mutualism,” Naeem says. “Some of them are positive, some are negative, some are neutral. That goes for our interactions with the microbial world, including viruses, which range from super beneficial to super harmful.”

Nature has been doing its thing for 3.75 billion years, when bacteria fought viruses as we fight them now.

Ultimately, nature works out a truce. “If the flower tries to short the hummingbird on sugar, the hummingbird is not going to provide it with pollination,” Naeem says. “If the hummingbird sucks up all the nectar and doesn’t do pollination well, it’s going to get pinged as well. Through this kind of back and forth, species hammer out an optimal way of getting along in nature. Evolution winds up finding some middle ground.” Naeem pauses. “If you try to beat up everybody, though, it’s not going to work.”

Guess which species is the bully? “There’s never been any species on this planet in its entire history that has had the capacity to modify its niche the way we have,” Naeem says. Our niche—cities, farms, factories—has made the planet into a zoological Manhattan. Living in close proximity with other species, and their viruses, means we are going to rub shoulders with them. Dense living isn’t for everyone. But a global economy is. And with it comes an intercontinental transportation system. A virus doesn’t have a nationality. It can travel as easily from Arkansas to China as the other way around. A pandemic is an inevitable outcome of our modified niche.

Although nature doesn’t do retribution, our clashes with it have mutual consequences. The exact route of transmission of SARS-CoV-2 from bat to humans remains unmapped. Did the virus pass directly into a person, who may have handled a bat, or through an intermediate animal? What is clear is the first step, which is that a bat shed the virus in some way. University of California, Davis epidemiologist Johnson explains bats shed viruses in their urine, feces, and saliva. They might urinate on fruit or eat a piece of it, and then discard it on the ground, where an animal may eat it. The Nipah virus outbreak in 1999 was spurred by a bat that left behind a piece of fruit that came in contact with a domestic pig and humans. The Ebola outbreaks in the early 2000s in Central Africa likely began when an ape, who became bushmeat for humans, came in contact with a fruit bat’s leftover. “The same thing happened with the Hendra virus in Australia in 1994,” says Johnson. “Horses got infected because fruit bats lived in trees near the horse farm. Domesticated species are often an intermediary between bats and humans, and they amplify the outbreak before it gets to humans.”

Transforming bat niches into our own sends bats scattering—right into our backyards. In a study released this month, Johnson and colleagues show the spillover risk of viruses is the highest among animal species, notably bats, that have expanded their range, due to urbanization and crop production, into human-run landscapes.4 “The ways we’ve altered the landscape have brought a lot of great things to people,” Johnson says. “But that has put wildlife at higher pressures to adapt, and some of them have adapted by moving in with us.”

Pressures on bats have another consequence. Studies indicate physiological and environmental stress can increase viral replication in them and cause them to shed more than they normally do. One study showed bats with white-nose syndrome had “60 times more coronavirus in their intestines” as uninfected bats.5 Despite evidence for an increase in viral replication and shedding in stressed bats, “a direct link to spillover has yet to be established,” concludes a 2019 report in Viruses.3 But it’s safe to say that bats being perpetually driven from their caves into our barns is not ideal for either species.

As my questions ran out for Columbia University’s Naeem, I asked him to put this horrible pandemic in a final ecological light for me.

“We think of ourselves as being resilient and robust, but it takes something like this to realize we’re still a biological entity that’s not capable of totally controlling the world around us,” he says. “Our social system has become so disconnected from nature that we no longer understand we still are a part of it. Breathable air, potable water, productive fields, a stable environment—these all come about because we’re part of this elaborate system, the biosphere. Now we’re suffering environmental consequences like climate change and the loss of food security and viral outbreaks because we’ve forgotten how to integrate our endeavors with nature.”

A 2014 study by a host wildlife ecologists, economists, and evolutionary biologists lays out a plan to stem the tide of emergent infectious diseases, most of which spawned in wildlife. Cases of emergent infectious diseases have practically quadrupled since 1940.6 World leaders could get smart. They could pool money for spillover research, which would identify the hundreds of thousands of potentially lethal viruses in animals. They could coordinate pandemic preparation with international health regulations. They could support animal conservation with barriers that developers can’t cross. The scientists give us 27 years to cut the rise of infectious diseases by 50 percent. After that, the study doesn’t say what the world will look like. I imagine it will look like a hospital right now in New York City.

Patients lie on gurneys in corridors, swaddled in sheets, their faces shrouded by respirators. They’re surrounded by doctors and nurses, desperately trying to revive them. In pain, inconsolable, and alone. I know they want nothing more than to see their family and friends on the other side, to be wheeled out of the hospital and feel normal again. Will they? Will others in the future? It will take tremendous political will to avoid the next pandemic. And it must begin with a reckoning with our relationship with nature. That tiny necklace of RNA tearing through patients’ lungs right now is the world we live in. And have always lived in. We can’t be cut off from the environment. When I see the suffering in hospitals, I can only ask, Do we get it now?

Kevin Berger is the editor of Nautilus.

References

1. Villareal, L.P. The Widespread Evolutionary Significance of Viruses. In Domingo, E., Parrish, C.R., & Hooland, J. (Eds.) Origin and Evolution of Viruses Elsevier, Amsterdam, Netherlands (2008).

2. Lane, N. The Vital Question: Energy, Evolution, and the Origins of Complex Life W.W. Norton, New York, NY (2015).

3. Subudhi, S., Rapin, N., & Misra, V. Immune system modulation and viral persistence in Bats: Understanding viral spillover. Viruses 11, E192 (2019).

4. Johnson, C.K., et al. Global shifts in mammalian population trends reveal key predictors of virus spillover risk. Proceedings of The Royal Society B 287 (2020).

5. Davy, C.M., et al. White-nose syndrome is associated with increased replication of a naturally persisting coronaviruses in bats. Scientific Reports 8, 15508 (2018).

6. Pike, J., Bogich, T., Elwood, S., Finnoff, D.C., & Daszak, P. Economic optimization of a global strategy to address the pandemic threat. Proceedings of the National Academy of Sciences 111, 18519-18523 (2014).

Lead image: AP Photo / Mark Lennihan

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There are many challenges to developing a vaccine that will be successful against COVID-19.eamesBot / Shutterstock

Wayne Koff is one of the world’s experts on vaccine development, the president and CEO of the Human Vaccines Project. He possesses a deep understanding of the opportunities and challenges along the road to a safe and effective vaccine against COVID-19. He has won prestigious awards, published dozens of scientific papers, held major positions in academia, government, industry, and nonprofit organizations. But Koff, 67, has never produced a successful vaccine.

“I have been an abject failure,” he says. He smiles with a charming, self-deprecating sense of humor. “That’s what the message is.”

The real reason for Koff’s lack of success is that he spent most of his career searching for a vaccine against HIV, the virus that causes AIDS. It remains, as he and many others put it, “the perfect storm” of a viral infection resistant to a vaccine development. Almost 40 years after doctors first recognized the disease in five men in Los Angeles—and 70 million people have been infected worldwide—there are no adequate animal models. Neutralizing antibodies, the backbone of many vaccines, do not stop it, and most importantly, HIV begins its assault on the body by attacking CD4 T cells, which serve as the command center of much of the immune system.

As for COVID-19, “We’re all hoping this one is going to be easier,” says Koff, a slight, bearded man with thick, curly salt-and-pepper hair. “There are research issues that still have to be addressed on a COVID vaccine. But they are a lot more straightforward than what we were dealing with in HIV.”

Let’s say we have a vaccine in 18 months. How do you make 1 billion doses or 4 billion doses or whatever it’s going to take to immunize everybody?

Koff and others started the Human Vaccines Project in 2016, modeled on the Human Genome Project. The project works with industry and academia to study the human immune system and develop vaccines, incorporating every modern-day tool, including artificial intelligence, computational biology, and big data sets. Today it is partnered with the Harvard T.H. Chan School of Public Health.

With COVID-19, Koff says, scientists “know the target is the spike protein binding site.” This is where the proteins sticking out from the virus attach to the cells in the human respiratory system. “If you can elicit antibodies against those proteins, they should be neutralizing.” He puts a strong emphasis on should. To prove antibodies will prevent infection, scientists must watch a population of people who’ve been infected for months or longer. It’s a good bet, based on similar viruses, that antibodies will appear and protect—although no one right now can predict how long and how well.

Depending on which count you use, more than 70 companies, universities, and other institutions are offering candidate vaccines. Koff says the real number of companies is lower. During the AIDS crisis, he says, “a lot of people claimed they had an experimental HIV vaccine in development. Some of those were a one-person lab who had created a paper company to attract investors.”

But even with a lower number, almost everyone involved in the search for a vaccine agrees that several different approaches from different research organizations need to proceed in parallel. The world does not have the time to bet on one horse. The race will be neither simple nor cheap.

“The probability of success, depending on whose metric is used in vaccines, is somewhere between 6 and 10 percent of candidate vaccines that make it from the animal model through licensure,” Koff says. “That process costs $1 billion or more. So you can do the math.”

Koff sees big potential problems at the outset. “In the best of all worlds, let’s say we have a vaccine in 18 months. Who knows where the epidemic is going to be then and what its impact is going to be? How do you make 1 billion doses or 4 billion doses or whatever it’s going to take to immunize everybody? Will we need one dose or two or three? These are issues people just haven’t faced before.”

COVID-19 also presents some unique dangers for vaccine safety. Based on how the virus behaves when it infects some people, there’s a chance a vaccine could dangerously overstimulate the immune system, a reaction called immune enhancement. “I’m hoping it’s more theoretical than real,” Koff says. “But that has to be addressed and it may slow down the entire process.” To ensure safety, he says, “It may mean we have to test the vaccine in a larger number of people. It’s one thing to do a 50-person trial in healthy adults as a safety signal. It’s another thing to run a trial of 4,000 or 5000 or more individuals.”

The world does not have the time to bet on one horse. The race will be neither simple nor cheap.

A virus also sometimes causes mysterious, potentially deadly blood clots. This means an experimental vaccine could hypothetically induce the same damage. “This is a bad bug,” Koff says. “We’re just starting to understand that pathogenesis.”

A big question is who should be the first volunteers for widespread vaccine testing. “Who are the high-risk groups?” asks Koff. “Is it nursing-home residents and staff, health-care workers and people on the front lines, or people someplace else like grocery stores? We must also make sure a vaccine is effective for the elderly and people in the developing world.”

Many vaccines work well in young and healthy people but not in older adults because immunity declines with age. Influenza vaccine is a prime example. Rotavirus vaccine, which protects against the deadliest killer—diarrheal disease in children—works better in the developed world. In the developing world, the virus often circulates year-round. Infants get antibodies from breast milk but not enough to prevent disease. Worse, those antibodies can make the vaccine less effective.

Another hypothetical obstacle is that a mutation in the COVID-19 virus could render a vaccine designed today less effective in the future. While the virus mutates frequently, so far there has been little change in the critical part of the spike that binds to human cells.

Of course, neither Koff nor all the others working for a COVID-19 vaccine focus solely on the potential obstacles. At one time, all vaccines against viruses either killed viruses, such as the Salk polio vaccine, or rendered them harmless, such as the Sabin polio vaccine. Now there is a multiplicity of ways to stimulate an immune response to prevent infection or reduce the consequences. These include genetically engineered protein subunits (peptides) or virus-like particles. Such approaches have led to successful vaccines against hepatitis B and human papilloma virus, which causes cervical cancer. Researchers now use “vectors”—harmless viruses attached to the protein subunits and virus particles to transmit them into the body. There are also many new adjuvants, chemicals that boost immune response to a vaccine.

Newer platforms include direct injection of messenger-RNA. M-RNA is the chemical used to translate the information in DNA into proteins in all cells. The Moderna Company, which received a $483 million grant from the U.S. government, and has begun early clinical trials, uses m-RNA to try to make the body produce proteins to protect against the COVID-19 virus. INOVIO Pharmaceuticals uses pieces of DNA called plasmids to achieve the same objective. It has also begun phase 1 studies.

“There are about eight platforms, and it would be good to see a couple vaccines in each of those advance,” Koff says. Predicting which of these most likely to succeed or fail he says would be “simply foolish.”

Many groups, including the Human Vaccines Initiative, are plotting routes to test any possible vaccine more quickly than tradition dictates with an “adaptive trial design.” Usually trials begin with a phase 1 study of some 50 healthy people to search for any immediate signs of toxicity, then moves onto about 200 people in a phase 2, still looking for hazards and a signal of immunity, and then to phase 3 in thousands of people. But the plan here is to start phases 2 and 3 even before its predecessors are finished, and keep recruiting additional volunteers so long as no danger signals arise.

Good animal models are appearing almost daily. Macaque monkeys, hamsters, and genetically engineered mice have all been infected in the laboratory and could determine whether potential vaccines exhibit various types of immunity. Members of Congress from both sides of the aisle have suggested that healthy human volunteers should be allowed to agree to be test subjects, allowing themselves to be infected. Stanley Plotkin, a vaccine researcher at the University of Pennsylvania, was among the first to suggest the idea.

Arthur Caplan, a bioethicist at New York University, says that “deliberately causing disease in humans is normally abhorrent.” But COVID-19 is anything but a normal circumstance. In this case, Caplan says, “asking volunteers to take risks without pressure or coercion is not exploitation but benefitting from altruism.” At least 1,500 people have already volunteered to be such human guinea pigs, although none of the experimental vaccines is far enough along to try such challenging experiments.

Koff says the key to a successful vaccine is a cooperative effort. “It’s going to take a whole different way of thinking to move this onto the expedited train,” he says. “The old dog-eat-dog, ‘I’m going to beat you to the end of the game,’ isn’t going to help us with this.” Seth Berkley, who worked with Koff at the International AIDS Vaccine Initiative, and now heads GAVI, an international vaccine organization, agrees that a COVID-19 vaccine needs a Manhattan Project approach. “An initiative of this scale won’t be easy,” Berkley says. “Extraordinary sharing of information and resources will be critical, including data on the virus, the various vaccine candidates, vaccine adjuvants, cell lines, and manufacturing advances.”

Koff has no regrets about spending so many years on an AIDS vaccine without results. He learned a great deal, he says, which he’s putting to work in the COVID-19 crisis. “The reason COVID-19 vaccines should be a lot easier is because most of the platforms, the novel approaches, and the clinical infrastructure for the testing of vaccines, came out of HIV.” He pauses. “We’re far better prepared.”

Robert Bazell is an adjunct professor of molecular, cellular, and developmental biology at Yale. For 38 years, he was chief science correspondent for NBC News.

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The final outcome of COVID-19 is still unclear. It will ultimately be decided by our patience and the financial bottom line.Castleski / Shutterstock

On January 5, six days after China officially announced a spate of unusual pneumonia cases, a team of researchers at Shanghai’s Fudan University deposited the full genome sequence of the causal virus, SARS-CoV-2, into Genbank. A little more than three months later, 4,528 genomes of SARS-CoV-2 have been sequenced,1 and more than 883 COVID-related clinical trials2 for treatments and vaccines have been established. The speed with which these trials will deliver results is unknown—the delicate bаlance of efficacy and safety can only be pushed so far before the risks outweigh the benefits. For this reason, a long-term solution like vaccination may take years to come to market.3

The good news is that a lack of treatment doesn’t preclude an end to the ordeal. Viral outbreaks of Ebola and SARS, neither of which had readily available vaccines, petered out through the application of consistent public health strategies—testing, containment, and long-term behavioral adaptations. Today countries that have previously battled the 2002 SARS epidemic, like Taiwan, Hong Kong, and Singapore, have shown exemplary recovery rates from COVID. Tomorrow, countries with high fatality rates like Sweden, Belgium, and the United Kingdom will have the opportunity to demonstrate what they’ve learned when the next outbreak comes to their shores. And so will we.

The first Ebola case was identified in 1976,4 when a patient with hemorrhagic symptoms arrived at the Yambuku Mission Hospital, located in what is now the Democratic Republic of Congo (DRC). Patient samples were collected and sent to several European laboratories that specialized in rare viruses. Scientists, without sequencing technology, took about five weeks to identify the agent responsible for the illness as a new member of the highly pathogenic Filoviridae family.

The first Ebola outbreak sickened 686 individuals across the DRC and neighboring Sudan. 453 of the patients died, with a final case fatality rate (CFR)—the number of dead out of number of sickened—of 66 percent. Despite the lethality of the virus, sociocultural interventions, including lockdowns, contact-tracing, campaigns to change funeral rites, and restrictions on consumption of game meat all proved effective interventions in the long run.

That is, until 2014, when there was an exception to the pattern. Ebola appeared in Guinea, a small country in West Africa, whose population had never before been exposed to the virus. The closest epidemic had been in Gabon, 13 years before and 2,500 miles away. Over the course of two years, the infection spread from Guinea into Liberia and Sierra Leone, sickening more than 24,000 people and killing more than 10,000.

Countries that have previously battled the 2002 SARS epidemic, like Taiwan and Hong Kong, have shown exemplary recovery rates.

During the initial phase of the 2014 Ebola outbreak, rural communities were reluctant to cooperate with government directives for how to care for the sick and the dead. To help incentivize behavioral changes, sociocultural anthropologists like Mariane Ferme of the University of California, Berkeley, were brought in to advise the government. In a recent interview with Nautilus, Ferme indicated that strategies that allowed rural communities to remain involved with their loved ones increased cooperation. Villages located far from the capital, she said, were encouraged to “deputize someone to come to the hospital, to come to the burial, so they could come back to the community and tell the story of the body.” For communities that couldn’t afford to send someone to the capital, she saw public health officials adopt a savvy technological solution—tablets to record video messages that were carried between convalescent patients and their families.

However, there were also systemic failures that, in Ferme’s opinion, contributed to the severity of the 2014 West African epidemic. In Sierra Leone, she said, “the big mistake early on was to distribute [weakly causal] information about zoonotic transmission, even when it was obviously community transmission.” In other words, although there had been an instance of zoonotic transmission—the virus jumping from a bat to a human—that initiated the epidemic, the principle danger was other contagious individuals, not game meat. Eventually, under pressure from relief groups, the government changed its messaging to reflect scientific consensus.

But the retraction shook public faith in the government and bred resentment. The mismatch between messaging and reality mirrors the current pandemic. Since the COVID outbreak began, international and government health officials have issued mixed messages. Doubts initially surfaced about the certainty of the virus being capable of spreading from person to person, and the debate over the effectiveness of masks in preventing infection continues.

Despite the confused messaging, there has been general compliance with stay-at-home orders that has helped flatten the curve. Had the public been less trusting of government directives, the outcome could have been disastrous, as it was in Libera in 2014. After a two-week lockdown was announced, the Liberian army conducted house-to-house sweeps to check for the sick and collect the dead. “It was a draconian method that made people hide the sick and dead in their houses,” Ferme said. People feared their loved ones would be buried without the proper rites. A direct consequence was a staggering number of active cases, and an unknown extent of community transmission. But in the end, the benchmark for the end of Ebola and SARS was the same. The WHO declared victory when the rate of new cases slowed, then stopped. By the same measure, when an entire 14-day quarantine period passes with no new cases of COVID-19, it can be declared over.

It remains possible that even if we manage to end the epidemic, it will return again. Driven by novel zoonotic transmissions, Ebola has flared up every few years. Given the extent of COVID-19’s spread, and the potential for the kind of mutations that allow for re-infection, it may simply become endemic.

Two factors will play into the final outcome of COVID-19 are pathogenicity and virulence. Pathogenicity is the ability of an infectious agent to cause disease in the host, and is measured by R0—the number of new infections each patient can generate. Virulence, on the other hand, is the amount of harm the infectious agent can cause, and is best measured by CFR. While the pathogenicity of Ebola, SARS, and SARS-CoV-2 is on the same order—somewhere between 1 to 3 new infections for each patient, virulence differs greatly between the two SARS viruses and Ebola.

The case fatality rate for an Ebola infection is between 60 to 90 percent. The spread in CFR is due to differences in infection dynamics between strains. The underlying cause of the divergent virulence of Ebola and SARS is largely due to the tropism of the virus, meaning the cells that it attacks. The mechanism by which the Ebola virus gains entry into cells is not fully understood, but it has been shown the virus preferentially targets immune and epithelial cells.5 In other words, the virus first destroys the body’s ability to mount a defense, and then destroys the delicate tissues that line the vascular system. Patients bleed freely and most often succumb to low blood pressure that results from severe fluid loss. However, neither SARS nor SARS-CoV-2 attack the immune system directly. Instead, they enter lung epithelial cells through the ACE2 receptor, which ensures a lower CFR. What is interesting about these coronaviruses is that despite their similar modes of infection, they demonstrate a range of virulence: SARS had a final CFR of 10 percent, while SARS-CoV-2 has a pending CFR of 1.4 percent. Differences in virulence between the 2002 and 2019 SARS outbreaks could be attributed to varying levels of care between countries.

The chart above displays WHO data of the relationship between the total number of cases in a country and the CFR during the 2002-2003 SARS-CoV epidemic. South Africa, on the far right, had only a single case. The patient died, which resulted in a 100 percent CFR. China, on the other hand, had 5,327 cases and 349 deaths, giving a 7 percent CFR. The chart below zooms to the bottom left corner of the graph, so as to better resolve critically affected countries, those with a caseload of less than 1,000, but with a high CFR.

Here is Hong Kong, with 1,755 cases and a 17 percent CFR. There is also Taiwan, with 346 cases and an 11 percent CFR. Finally, nearly tied with Canada is Singapore with 238 cases and a 14 percent CFR.

With COVID-19, it’s apparent that outcome reflects experience. China has 82,747 cases of COVID, but has lowered their CFR to 4 percent. Hong Kong has 1,026 cases and a 0.4 percent CFR. Taiwan has 422 cases at 1.5 percent CFR, and Singapore with 8,014 cases, has a 0.13 percent CFR.

It was the novel coronavirus identification program established in China in the wake of the 2002 SARS epidemic that alerted authorities to SARS-CoV-2 back in November of 2019. The successful responses by Taiwan, Hong Kong, and Singapore can also be attributed to a residual familiarity with the dangers of an unknown virus, and the sorts of interventions that are necessary to prevent a crisis from spiraling out of control.

In West Africa, too, they seem to have learned the value of being prepared. When Ferme returned to Liberia on March 7, she encountered airport staff fully protected with gowns, head covers, face screens, masks, and gloves. By the time she left the country, 10 days later, she said, “Airline personnel were setting up social distancing lines, and [rural vendors] hawking face masks. Motorcycle taxis drivers, the people most at risk after healthcare workers—all had goggles and face masks.”

The sheer number of COVID-19 cases indicates the road to recovery will take some time. Each must be identified, quarantined, and all contacts traced and tested. Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars. Northwestern University economists Martin Eichenbaum et al. modeled6 the cost of a yearlong shutdown to be $4.2 trillion, a cost that proactive countries will not face. A recent Harvard study7 published in Science suggests the virus will likely make seasonal appearances going forward, potentially requiring new waves of social distancing. In other words, initial hesitancy will have repercussions for years. In the future, smart containment principles,6 where restrictions are applied on the basis of health status, may temper the impact of these measures.

Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars.

Inaction was initially framed as promoting herd immunity, where spread of the virus is interrupted once everyone has fallen sick with it. This is because getting the virus results in the same antibody production process as getting vaccinated—but doesn’t require the development of a vaccine. The Johns Hopkins Bloomberg School of Public Health estimates that 70 percent of the population will need to be infected with or vaccinated against the virus8 for herd immunity to work. Progress toward it has been slow, and can only be achieved through direct infection with the virus, meaning many will die. A Stanford University study in Santa Clara County9 suggests only 2.5 percent to 4.2 percent of the population have had the virus. Another COVID hotspot in Gangelt, Germany, suggests 15 percent10—higher, but still nowhere near the 70 percent necessary for herd immunity. Given the dangers inherent in waiting on herd immunity, our best hope is a vaccine.

A key concern for effective vaccine development is viral mutation. This is because vaccines train the immune system to recognize specific shapes on the surface of the virus—a composite structure called the antigen. Mutations threaten vaccine development because they can change the shape of the relevant antigen, effectively allowing the pathogen to evade immune surveillance. But, so far, SARS-CoV-2 has been mutating slowly, with only one mutation found in the section most accessible to the immune system, the spike protein. What this suggests is that the viral genome may be sufficiently stable for vaccine development.

What we know, though, is that Ebola was extinguished due to cooperation between public health officials and community leaders. SARS-CoV ended when all cases were identified and quarantined. The Spanish Flu in 1918 vanished after two long, deadly seasons.

The final outcome of COVID-19 is still unclear. It will ultimately be decided by our patience and the financial bottom line. With 26 million unemployed and protests erupting around the country, it seems there are many who would prefer to risk life and limb rather than face financial insolvency. Applying smart containment principles in the aftermath of the shutdown might be the best way to get the economy moving again, while maintaining the safety of those at greatest risk. Going forward, vigilance and preparedness will be the watchwords of the day, and the most efficient way to prevent social and economic ruin.

Anastasia Bendebury and Michael Shilo DeLay did their PhDs at Columbia University. Together they created Demystifying Science, a science literacy organization devoted to providing clear, mechanistic explanations for natural phenomena. Find them on Twitter @DemystifySci.

References

1. Genomic epidemiology of novel coronavirus - Global subsampling. Nextstrain www.nextstrain.org.

2. Covid-19 TrialsTracker. TrialsTracker www.trialstracker.net.

3. Struck, M. Vaccine R&D success rates and development times. Nature Biotechnology 14, 591-593 (1996).

4. Breman, J. & Johnson, K. Ebola then and now. The New England Journal of Medicine 371 1663-1666 (2014).

5. Baseler, L., Chertow, D.S., Johnson, K.M., Feldmann, H., & Morens, D.M. THe pathogenesis of Ebola virus disease. The Annual Review of Pathology 12, 387-418 (2017).

6. Eichenbaum, M., Rebell, S., & Trabandt, M. The macroeconomics of epidemics. The National Bureau of Economic Research Working Paper: 26882 (2020).

7. Kissler, S., Tedijanto, C., Goldstein, E., Grad, Y., & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the postpandemic period. Science eabb5793 (2020).

8. D’ Souza, G. & Dowdy, D. What is herd immunity and how can we achieve it with COVID-19? Johns Hopkins COVID-19 School of Public Health Insights www.jhsph.edu (2020).

9. Digitale, E. Test for antibodies against novel coronavirus developed at Stanford Medicine. Stanford Medicine News Center Med.Stanford.edu (2020).

10. Winkler, M. Blood tests show 14%of people are now immune to COVID-19 in one town in Germany. MIT Technology Review (2020).

Read More…

On January 5, six days after China officially announced a spate of unusual pneumonia cases, a team of researchers at Shanghai’s Fudan University deposited the full genome sequence of the causal virus, SARS-CoV-2, into Genbank. A little more than three months later, 4,528 genomes of SARS-CoV-2 have been sequenced,1 and more than 883 COVID-related clinical trials2 for treatments and vaccines have been established. The speed with which these trials will deliver results is unknown—the delicate bаlance of efficacy and safety can only be pushed so far before the risks outweigh the benefits. For this reason, a long-term solution like vaccination may take years to come to market.3

The good news is that a lack of treatment doesn’t preclude an end to the ordeal. Viral outbreaks of Ebola and SARS, neither of which had readily available vaccines, petered out through the application of consistent public health strategies—testing, containment, and long-term behavioral adaptations. Today countries that have previously battled the 2002 SARS epidemic, like Taiwan, Hong Kong, and Singapore, have shown exemplary recovery rates from COVID. Tomorrow, countries with high fatality rates like Sweden, Belgium, and the United Kingdom will have the opportunity to demonstrate what they’ve learned when the next outbreak comes to their shores. And so will we.

The first Ebola case was identified in 1976,4 when a patient with hemorrhagic symptoms arrived at the Yambuku Mission Hospital, located in what is now the Democratic Republic of Congo (DRC). Patient samples were collected and sent to several European laboratories that specialized in rare viruses. Scientists, without sequencing technology, took about five weeks to identify the agent responsible for the illness as a new member of the highly pathogenic Filoviridae family.

The first Ebola outbreak sickened 686 individuals across the DRC and neighboring Sudan. 453 of the patients died, with a final case fatality rate (CFR)—the number of dead out of number of sickened—of 66 percent. Despite the lethality of the virus, sociocultural interventions, including lockdowns, contact-tracing, campaigns to change funeral rites, and restrictions on consumption of game meat all proved effective interventions in the long run.

That is, until 2014, when there was an exception to the pattern. Ebola appeared in Guinea, a small country in West Africa, whose population had never before been exposed to the virus. The closest epidemic had been in Gabon, 13 years before and 2,500 miles away. Over the course of two years, the infection spread from Guinea into Liberia and Sierra Leone, sickening more than 24,000 people and killing more than 10,000.

Countries that have previously battled the 2002 SARS epidemic, like Taiwan and Hong Kong, have shown exemplary recovery rates.

During the initial phase of the 2014 Ebola outbreak, rural communities were reluctant to cooperate with government directives for how to care for the sick and the dead. To help incentivize behavioral changes, sociocultural anthropologists like Mariane Ferme of the University of California, Berkeley, were brought in to advise the government. In a recent interview with Nautilus, Ferme indicated that strategies that allowed rural communities to remain involved with their loved ones increased cooperation. Villages located far from the capital, she said, were encouraged to “deputize someone to come to the hospital, to come to the burial, so they could come back to the community and tell the story of the body.” For communities that couldn’t afford to send someone to the capital, she saw public health officials adopt a savvy technological solution—tablets to record video messages that were carried between convalescent patients and their families.

However, there were also systemic failures that, in Ferme’s opinion, contributed to the severity of the 2014 West African epidemic. In Sierra Leone, she said, “the big mistake early on was to distribute [weakly causal] information about zoonotic transmission, even when it was obviously community transmission.” In other words, although there had been an instance of zoonotic transmission—the virus jumping from a bat to a human—that initiated the epidemic, the principle danger was other contagious individuals, not game meat. Eventually, under pressure from relief groups, the government changed its messaging to reflect scientific consensus.

But the retraction shook public faith in the government and bred resentment. The mismatch between messaging and reality mirrors the current pandemic. Since the COVID outbreak began, international and government health officials have issued mixed messages. Doubts initially surfaced about the certainty of the virus being capable of spreading from person to person, and the debate over the effectiveness of masks in preventing infection continues.

Despite the confused messaging, there has been general compliance with stay-at-home orders that has helped flatten the curve. Had the public been less trusting of government directives, the outcome could have been disastrous, as it was in Libera in 2014. After a two-week lockdown was announced, the Liberian army conducted house-to-house sweeps to check for the sick and collect the dead. “It was a draconian method that made people hide the sick and dead in their houses,” Ferme said. People feared their loved ones would be buried without the proper rites. A direct consequence was a staggering number of active cases, and an unknown extent of community transmission. But in the end, the benchmark for the end of Ebola and SARS was the same. The WHO declared victory when the rate of new cases slowed, then stopped. By the same measure, when an entire 14-day quarantine period passes with no new cases of COVID-19, it can be declared over.

It remains possible that even if we manage to end the epidemic, it will return again. Driven by novel zoonotic transmissions, Ebola has flared up every few years. Given the extent of COVID-19’s spread, and the potential for the kind of mutations that allow for re-infection, it may simply become endemic.

Two factors will play into the final outcome of COVID-19 are pathogenicity and virulence. Pathogenicity is the ability of an infectious agent to cause disease in the host, and is measured by R0—the number of new infections each patient can generate. Virulence, on the other hand, is the amount of harm the infectious agent can cause, and is best measured by CFR. While the pathogenicity of Ebola, SARS, and SARS-CoV-2 is on the same order—somewhere between 1 to 3 new infections for each patient, virulence differs greatly between the two SARS viruses and Ebola.

The case fatality rate for an Ebola infection is between 60 to 90 percent. The spread in CFR is due to differences in infection dynamics between strains. The underlying cause of the divergent virulence of Ebola and SARS is largely due to the tropism of the virus, meaning the cells that it attacks. The mechanism by which the Ebola virus gains entry into cells is not fully understood, but it has been shown the virus preferentially targets immune and epithelial cells.5 In other words, the virus first destroys the body’s ability to mount a defense, and then destroys the delicate tissues that line the vascular system. Patients bleed freely and most often succumb to low blood pressure that results from severe fluid loss. However, neither SARS nor SARS-CoV-2 attack the immune system directly. Instead, they enter lung epithelial cells through the ACE2 receptor, which ensures a lower CFR. What is interesting about these coronaviruses is that despite their similar modes of infection, they demonstrate a range of virulence: SARS had a final CFR of 10 percent, while SARS-CoV-2 has a pending CFR of 1.4 percent. Differences in virulence between the 2002 and 2019 SARS outbreaks could be attributed to varying levels of care between countries.

The chart above displays WHO data of the relationship between the total number of cases in a country and the CFR during the 2002-2003 SARS-CoV epidemic. South Africa, on the far right, had only a single case. The patient died, which resulted in a 100 percent CFR. China, on the other hand, had 5,327 cases and 349 deaths, giving a 7 percent CFR. The chart below zooms to the bottom left corner of the graph, so as to better resolve critically affected countries, those with a caseload of less than 1,000, but with a high CFR.

Here is Hong Kong, with 1,755 cases and a 17 percent CFR. There is also Taiwan, with 346 cases and an 11 percent CFR. Finally, nearly tied with Canada is Singapore with 238 cases and a 14 percent CFR.

With COVID-19, it’s apparent that outcome reflects experience. China has 82,747 cases of COVID, but has lowered their CFR to 4 percent. Hong Kong has 1,026 cases and a 0.4 percent CFR. Taiwan has 422 cases at 1.5 percent CFR, and Singapore with 8,014 cases, has a 0.13 percent CFR.

It was the novel coronavirus identification program established in China in the wake of the 2002 SARS epidemic that alerted authorities to SARS-CoV-2 back in November of 2019. The successful responses by Taiwan, Hong Kong, and Singapore can also be attributed to a residual familiarity with the dangers of an unknown virus, and the sorts of interventions that are necessary to prevent a crisis from spiraling out of control.

In West Africa, too, they seem to have learned the value of being prepared. When Ferme returned to Liberia on March 7, she encountered airport staff fully protected with gowns, head covers, face screens, masks, and gloves. By the time she left the country, 10 days later, she said, “Airline personnel were setting up social distancing lines, and [rural vendors] hawking face masks. Motorcycle taxis drivers, the people most at risk after healthcare workers—all had goggles and face masks.”

The sheer number of COVID-19 cases indicates the road to recovery will take some time. Each must be identified, quarantined, and all contacts traced and tested. Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars. Northwestern University economists Martin Eichenbaum et al. modeled6 the cost of a yearlong shutdown to be $4.2 trillion, a cost that proactive countries will not face. A recent Harvard study7 published in Science suggests the virus will likely make seasonal appearances going forward, potentially requiring new waves of social distancing. In other words, initial hesitancy will have repercussions for years. In the future, smart containment principles,6 where restrictions are applied on the basis of health status, may temper the impact of these measures.

Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars.

Inaction was initially framed as promoting herd immunity, where spread of the virus is interrupted once everyone has fallen sick with it. This is because getting the virus results in the same antibody production process as getting vaccinated—but doesn’t require the development of a vaccine. The Johns Hopkins Bloomberg School of Public Health estimates that 70 percent of the population will need to be infected with or vaccinated against the virus8 for herd immunity to work. Progress toward it has been slow, and can only be achieved through direct infection with the virus, meaning many will die. A Stanford University study in Santa Clara County9 suggests only 2.5 percent to 4.2 percent of the population have had the virus. Another COVID hotspot in Gangelt, Germany, suggests 15 percent10—higher, but still nowhere near the 70 percent necessary for herd immunity. Given the dangers inherent in waiting on herd immunity, our best hope is a vaccine.

A key concern for effective vaccine development is viral mutation. This is because vaccines train the immune system to recognize specific shapes on the surface of the virus—a composite structure called the antigen. Mutations threaten vaccine development because they can change the shape of the relevant antigen, effectively allowing the pathogen to evade immune surveillance. But, so far, SARS-CoV-2 has been mutating slowly, with only one mutation found in the section most accessible to the immune system, the spike protein. What this suggests is that the viral genome may be sufficiently stable for vaccine development.

What we know, though, is that Ebola was extinguished due to cooperation between public health officials and community leaders. SARS-CoV ended when all cases were identified and quarantined. The Spanish Flu in 1918 vanished after two long, deadly seasons.

The final outcome of COVID-19 is still unclear. It will ultimately be decided by our patience and the financial bottom line. With 26 million unemployed and protests erupting around the country, it seems there are many who would prefer to risk life and limb rather than face financial insolvency. Applying smart containment principles in the aftermath of the shutdown might be the best way to get the economy moving again, while maintaining the safety of those at greatest risk. Going forward, vigilance and preparedness will be the watchwords of the day, and the most efficient way to prevent social and economic ruin.

Anastasia Bendebury and Michael Shilo DeLay did their PhDs at Columbia University. Together they created Demystifying Science, a science literacy organization devoted to providing clear, mechanistic explanations for natural phenomena. Find them on Twitter @DemystifySci.

References

1. Genomic epidemiology of novel coronavirus - Global subsampling. Nextstrain www.nextstrain.org.

2. Covid-19 TrialsTracker. TrialsTracker www.trialstracker.net.

3. Struck, M. Vaccine R&D success rates and development times. Nature Biotechnology 14, 591-593 (1996).

4. Breman, J. & Johnson, K. Ebola then and now. The New England Journal of Medicine 371 1663-1666 (2014).

5. Baseler, L., Chertow, D.S., Johnson, K.M., Feldmann, H., & Morens, D.M. THe pathogenesis of Ebola virus disease. The Annual Review of Pathology 12, 387-418 (2017).

6. Eichenbaum, M., Rebell, S., & Trabandt, M. The macroeconomics of epidemics. The National Bureau of Economic Research Working Paper: 26882 (2020).

7. Kissler, S., Tedijanto, C., Goldstein, E., Grad, Y., & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the postpandemic period. Science eabb5793 (2020).

8. D’ Souza, G. & Dowdy, D. What is herd immunity and how can we achieve it with COVID-19? Johns Hopkins COVID-19 School of Public Health Insights www.jhsph.edu (2020).

9. Digitale, E. Test for antibodies against novel coronavirus developed at Stanford Medicine. Stanford Medicine News Center Med.Stanford.edu (2020).

10. Winkler, M. Blood tests show 14%of people are now immune to COVID-19 in one town in Germany. MIT Technology Review (2020).

Lead image: Castleski / Shutterstock

Read More…

Plants are intelligent beings with profound wisdom to impart—if only we know how to listen. And Monica Gagliano knows how to listen. The evolutionary ecologist has done groundbreaking experiments suggesting plants have the capacity to learn, remember, and make choices. That’s not all. Gagliano, a senior research fellow at the University of Sydney in Australia, talks to plants. And they talk back. Plants summon her with instructions on how to live and work. Some of Gagliano’s conversations happened in prophetic dreams, which led her to study with a shaman in Peru while tripping on psychoactive plants.

Along with forest scientists like Suzanne Simard and Peter Wohlleben, Gagliano raises profound scientific and philosophical questions about the nature of intelligence and the possibility of “vegetal consciousness.” But what’s unusual about Gagliano is her willingness to talk about her experiences with shamans and traditional healers, along with her use of psychedelics. For someone who’d already received fierce pushback from other scientists, it was hardly a safe career move to reveal her personal experiences in otherworldly realms.

Gagliano considers her explorations in non-Western ways of seeing the world to be part of her scientific work. “Those are important doors that you need to open and you either walk through or you don’t,” she told me. “I simply decided to walk through.” Sometimes, she said, certain plants have given her precise directions on how to conduct her experiments, even telling her which plant to study. But it hasn’t been easy. “Like Alice, [I] found myself tumbling down a rather strange rabbit hole,” she wrote in a 2018 memoir, Thus Spoke the Plant. “I did doubt my own sanity many times, especially when all these odd occurrences started—and yet I know I do not suffer from psychoses.”

Shortly before the COVID-19 lockdown, I talked with Gagliano at Dartmouth College, where she was a visiting scholar. We spoke about her experiments, the new field of plant intelligence, and her own experiences of talking with plants.

PAVLOV’S PEAS: Monica Gagliano sketches a pea plant in her lab at the University of Sydney (above). She conducted experiments with pea plants to determine if, like Pavlov’s famous dogs, the plants learned to anticipate food. They did. “Although they do not salivate,” Gagliano says.Scene from the upcoming documentary, AWARE ©umbrellafilms.org

You are best known for an experiment with Mimosa pudica, commonly known as the “sensitive plant,” which instantly closes its leaves when it’s touched. Can you describe your experiment?

I built a little contraption that allowed me to drop the plants from a height of maybe 15 centimeters. So it’s not too high. When they fall, they land in a softly padded base. This plant closes its leaves when disturbed, especially if the disturbance is a potential predator. When the leaves are closed, big, spiny, pointy things stick out, so they might deter a predator. In fact, they not only close the leaf, but literally droop, like, “Look, I’m dead. No juice for you here.”

You did this over and over, dropping the plants repeatedly.

Exactly. It makes no sense for a plant or animal to repeat a behavior that is actually useless, so we learn pretty quick that whatever is useless, you don’t do anymore. You’re wasting a lot of energy trying to do something that doesn’t actually help. So, can the plant—in this case, Mimosa—learn not to close the leaves when the potential predator is not real and there are no bad consequences afterward?

After how many drops did they stop closing their leaves?

The test is for a specific type of learning that is called habituation. I decided they would be dropped continuously for 60 times. Then there was a big pause to let them rest and I did it again. But the plants were already re-opening their leaves after the first three to six drops. So within a few minutes, they knew exactly what was going on—like, “Oh my god, this is really annoying but it doesn’t mean anything, so I’m just not going to bother closing. Because when my leaves are open, I can eat light.” So there is a tradeoff between protecting yourself when the threat is real and continuing to feed and grow. I left the plants undisturbed for a month and then came back and repeated the same experiment on those individuals. And they showed they knew exactly what was going on. They were trained.

This is who I am. And nobody has the right to tell me that it’s not real.

You say these plants “understand” and “learn” that there’s no longer a threat. And you’re suggesting they “remember.” You’re not using these words metaphorically. You mean this literally?

Yes, that’s what they’re doing. This is definitely memory. It’s the same kind of experiment we do with a bee or a mouse. So using the words “memory” and “learning” feels totally appropriate. I know that some of my colleagues accuse me of anthropomorphizing, but there is nothing anthropomorphic about this. These are terms that refer to certain processes. Memory and learning are not two separate processes. You can’t learn unless you remember. So if a plant is ticking all the boxes and doing what you would expect a rat or a mouse or a bee to do, then the test is being passed.

Do you think these plants are actually making decisions about whether or not to close their leaves?

This experiment with Mimosa wasn’t designed to test that specific question. But later, I did experiments with other plants, with peas in particular, and yes, there is no doubt the plants make choices in real decision-making. This was tested in the context of a maze, where the test is actually to make a choice between left and right. The choice is based on what you might gain if you choose one side or the other. I did one study with peas that showed the plants can choose the right arm in a maze based on where the sound of water is coming from. Of course, they want water. So they will use the signal to follow that arm of the maze as they try to find the source of water.

So plants can hear water?

Oh, yeah, of course. And I’m not talking about electrical signals. We have also discovered that plants emit their own sounds. The acoustic signal comes out of the plant.

What kind of sounds do they make?

We call them clicks, but this is where language might fail because we are trying to describe something we’re not familiar enough with to create the language that really describes the picture. We worked out that, yes, plants not only produce their own sound, which is amazing, but they are listening to sounds. We are surrounded by sound, so there are studies, like my own study, of plants moving toward certain frequencies and then responding to sounds of potential predators chewing on leaves, which other plants that are not yet threatened can hear. “Oh, that’s a predator chewing on my neighbor’s leaves. I better put my defenses up.” And more recently, there was some work done in Israel on the sound of bees and how flowers prepared themselves and become very nice and sweet, literally, to be more attractive to the bee. So the level of sugars gets increased as a bee passes by.

SECRET LIFE OF PLANTS: Monica Gagliano says her experiences with indigenous people, such as the Huichol in Mexico (above), informed her view that plants have a range of feelings. “I don’t know if they would use those words to describe joy or sadness, but they are feeling bodies,” she says.Scene from the upcoming documentary, AWARE ©umbrellafilms.org

You are describing a surprising level of sophistication in these plants. Do you have a working definition of “intelligence?”

That’s one of those touchy subjects. I use the Latin etymology of the word and “intelligere” literally means something like “choosing between.” So intelligence really underscores decision-making, learning, memory, choice. As you can imagine, all those words are also loaded. They belong in the cognitive realm. That’s why I define all of this work as “cognitive ecology.”

Do you see parallels between this kind of intelligence in plants and the collective intelligence that we associate with social insects in ant colonies or beehives?

That kind of intelligence might be referred to as “distributed intelligence” or “collective intelligence.” We are testing those questions right now. Plants don’t have neurons. They don’t have a brain, which is often what we assume is the base for all of these behaviors. But like slime molds and other basal animals that don’t have neural systems, they seem to be doing the same things. So the short answer is yes.

What you’re saying is very controversial among scientists. The common criticism of your views is that an organism needs a brain or at least a nervous system to be able to learn or remember. Are you saying neurons are not required for intelligence?

Science is full of assumptions and presuppositions that we don’t question. But who said the brain and the neurons are essential for any form of intelligence or learning or cognition? Who decided that? And when I say neurons and brains are not required, it’s not to say they’re not important. For those organisms like ourselves and many animals who do have neurons and brains, it’s amazing. But if we look at the base of the animal kingdom, sponges don’t have neurons. They look like plants because when they’re adults, they settle on the bottom of the ocean and pretty much just sit there forever. Yet if you look at the sponge’s genome, they have the genetic code for the neural system. It’s almost like from an evolutionary perspective, they simply decided that developing a neural system was not useful. So they went a different way. Why would you invest that energy if you don’t need it? You can achieve the same task in different ways.

Your food is psychedelic. It changes your brain chemistry all the time.

Your critics say these are just automatic adaptive responses. This is not really learning.

You know, they just say plants do not learn and do not remember. Then you do this study and stumble on something that actually shows you otherwise. It’s the job of science to be humble enough to realize that we actually make mistakes in our thinking, but we can correct that. Science grows by correcting and modifying and adjusting what we once thought was the fact. I went and asked, can plants do Pavlovian learning? This is a higher kind of learning, which Pavlov did with his dogs salivating, expecting dinner. Well, it turns out plants actually can do it, but in a plant way. So plants do not salivate and dinner is a different kind of dinner. Can you as a scientist create the space for these other organisms to express their own, in this case, “plantness,” instead of expecting them to become more like you?

There’s an emerging field of what’s called “vegetal consciousness.” Do you think plants have minds?

What is the mind? [Laughs] You see, language is very inadequate at the moment in describing this field. I could ask you the same question in referring to humans. Do you think humans have a mind? And I could answer again, what is the mind? Of course, I have written a paper with the title “The Mind of Plants” and there is a book coming called The Mind of Plants. In this context, language is used to capture aspects of how plants can change their mind, and also whether they have agency. Is there a “person” there? These questions are relevant beyond science because they have ethical repercussions. They demand a change in our social attitude toward the environment. But I already have a problem with the language we are using because the question formulated in that way demands a yes or no answer. And what if the answer cannot be yes or no?

Let me ask the question a different way. Do you think plants have emotional lives? Can they feel pain or joy?

It’s the same question. Where do feelings arise from, and what are feelings? These are yes or no questions, usually. But to me, they are yes and no. It depends on what you mean by “feeling” and “joy.” It also depends on where you are expecting the plant to feel those things, if they do, and how you recognize them in a human way. I mean, plants might have more joy than we do. It’s just that we don’t know because we’re not plants.

We have only talked about this from the scientific perspective, which is the Western view of the world. But I’ve also had a close relationship with plants from a very different perspective, the indigenous world view. Why is that less valuable? And when you actually do explore those perspectives, they require your experience. You can’t just understand them by thinking about them. My own personal experience tells me that plants definitely feel many things. I don’t know if they would use those words to describe joy or sadness, but they are feeling bodies. We are feeling bodies.

Science is full of assumptions and presuppositions that we don’t question.

You’ve studied with shamans in indigenous cultures and you’ve taken ayahuasca and other psychoactive plants. Why did you seek out those experiences?

I didn’t. They sought me. So I just followed. They just arrived in my life. You know, those are important doors that you need to open and you either walk through or you don’t. I simply decided to walk through. I had this weird series of three dreams while I was in Australia doing my normal life. By the time the third dream came, it was very clear that the people that I was dreaming of were real people. They were waiting somewhere in this reality, in this world. And the next thing, I’m buying a ticket and going to Peru and my partner at the time is looking at me like, “What are you doing?” [laughs] I have no idea, but I need to go. As a scientist, I find this is the most scientific approach that I’ve ever had. It’s like there is something asking a question and is calling you to meet the answer. The answer is already there and is waiting for you, if you are prepared to open the door and cross through. And I did.

What did you do in Peru?

The first time I went, I found this place that was in my dream. It was just exactly the same as what I saw in my dream. It was the same man I saw in my dream, grinning in the same way as he was in my dream. So I just worked with him, trying to learn as much as I could about myself with his support.

This was a local shaman whom you identify as Don M. And there was a particular plant substance, a hallucinogen, that you took.

I did what they call a “dieta,” which is basically a quiet, intense time in isolation that you do on your own in a little hut. You are just relating with the plant that the elder is deciding on. So for me, the plant that I worked with wasn’t by itself a psychedelic in the normal way of thinking about it. But of course, all plants are psychedelic. Even your food is psychedelic because it changes your brain chemistry and your neurobiology all the time you eat. Sugars, almonds, all sorts of neurotransmitters are flying everywhere. So, again, even the idea of what a psychedelic experience is needs to be revised, because a lot of people might think that it’s only about certain plants that they have a very strong, powerful transformation. And I find that all plants are psychedelic. I can sit in my garden. I don’t have to ingest anything and I can feel very altered by that experience.

You’ve said the plant talked to you. Did you actually hear words?

When you’re trying to describe this to people haven’t had the experience, it probably doesn’t make much sense because this kind of knowledge requires your participation. I don’t hear someone talking to me as if from the outside, talking to me in words and sound. But even that is not correct because inside my head it does sound exactly like a conversation. Not only that, but I know it’s not me. There is no way that I would know about some of the information that’s been shared with me.

Are you saying these plants had specific information to tell you about your life and your work?

Yeah, I mean, some of the plants tell me exactly how wrong I was in thinking about my experiments and how I should be doing them to get them to work. And I’m like, “Really?” I’m scribbling down without really understanding. Then I go in the lab and try what they say. And even then, there is a part of me that doesn’t really believe it. For one experiment, the one on the Pavlovian pea, I was trying to address that question the year before with a different plant. I was using sunflowers. And while I was doing my dieta with a different tree back in Peru, the plant just turned up and said, “By the way, not sunflowers, peas.” And I’m like, “what?” People always think that when you have these experiences, you’re supposed to understand the secrets of the universe. No, my plants are usually quite practical. [laughs] And they were right.

Do you think you are really encountering the consciousness of that plant? Maybe your imagination has opened up to see the world in new ways, but it’s all just a projection of your own mind. How do you know you are actually encountering another intelligence?

If you had this experience of connecting with plants the way I have described—and there are plenty of people who have—the experience is so clear that you know that it’s not you; it’s someone else talking. If you haven’t had that experience, then I can totally see it’s like, “No way, it must be your mind that makes it up.” But all I can say is that I have had exchanges with plants who have shared things about topics and asked me to do things that I have really no idea about.

What have plants asked you to do?

I’m not a medical scientist, but I’ve been given information by plants about their medical properties. And these are very specific bits of information. I wrote them in my diary. I would later check and I did find them in the medical literature: “This plant is for this and we know this.” I just didn’t know. So maybe I’m tapping into the collective consciousness.

What do you do with these kinds of personal experiences? You are a scientist who’s been trained to observe and study and measure the physical world. But this is an entirely different kind of reality. Can you reconcile these two different realities?

I think there are some presuppositions that a scientist should just explore the consensus reality that most of us experience in more or less the same way. But I don’t really have a conflict because I find this is just part of experimenting and exploring. If anything, I found that it has enriched and expanded the science I do. This is a work in progress, obviously, but I think I’m getting better at it. And in the writing of my book, which for a scientist was a very scary process because it was laying bare some parts of me that I knew would likely compromise my career forever, it also became liberating because once it was written, now the world knows. And it’s my truth. This is how I operate. This is who I am. And nobody has the right or the authority to tell me that it’s not real.

Steve Paulson is the executive producer of Wisconsin Public Radio’s nationally syndicated show “To the Best of Our Knowledge.” He’s the author of Atoms and Eden: Conversations on Religion and Science. You can subscribe to TTBOOK’s podcast here.

Lead image: kmeds7 / Shutterstock

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