Celebrities have backed calls for Home Secretary Priti Patel to end restrictions that prevent thousands of migrants in the UK from accessing financial support during the coronavirus crisis.

A row has broken out over Boris Johnson's chief adviser Dominic Cummings attending meetings of the senior scientists advising the Government on the coronavirus outbreak.

Securing more personal protective equipment was top of the agenda for the Prime Minister as he returned to work, his official spokesman said.

Boris Johnson will not take part in Prime Minister's Questions today following the birth of his son.

The pair announced the exciting news this morning

Sir Keir Starmer has urged the Government to publish an exit strategy for the coronavirus lockdown amid warnings the country could "fall behind" without one.

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

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.

It is "too early" to begin easing any lockdown measures "in any meaningful way", Nicola Sturgeon has said.

Prime Minister Boris Johnson led the sixth national applause for frontline workers as his fiancee Carrie Symonds tweeted she had "another wonderful reason to thank the NHS this week too".

Read the full interview HERE

A pandemic, UK lockdown and virtual PMQs — it's not what he imagined, but Keir Starmer has come out all guns blazing. He talks to Ayesha Hazarika and Joe Murphy about challenging the Government and uniting Labour

Too many workers are still falling through cracks in the Covid rescue package, a former cabinet minister warned today as he called for the lockdown to be eased "as quickly as possible".

Asked by LBC's Nick Ferrari if he would join them, Mr Jenrick said: "No, I don't think I would do. But I'm not going to pass judgement on other people and what they're choosing to do.

The UK will begin the first round of post-Brexit trade deal talks with the US this week.

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

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.

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

Lockdown measures may start to be lifted on Monday "if we possibly can", Boris Johnson has announced.

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.

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.

Netflix has capitalized on the huge success of their docuseries Tiger King by releasing an “aftershow” special. Here are 5 things we learned.

Celebrities from across the globe came together Saturday night to lift their fans’ spirits as the world continues to cope with the coronavirus pandemic.

Drake dropped a surprise 14-track mixtape and announced his next studio album will be released this summer.

Adele posted a rare photo of herself to celebrate her birthday, unveiling a dramatically altered appearance.

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.

Needing to clear my head, I went down to the Penobscot River. There they were, swimming with the mergansers, following an early pulse of river herring to the mouth of Kenduskeag stream: two harbor seals, raising sleek round heads for a few long breaths before rolling under the waves.

Evidently it’s not uncommon for seals to swim the couple dozen miles between Bangor, Maine, and the Atlantic Ocean, but I’d never seen them here before. They were a balm to my buzzing thoughts: What happens next? Will I become a vector of death to my elderly mother? Is the economy going to implode? For a precious few minutes there were only the seals and mergansers and the fish who drew them there, arriving as the Penobscot’s winter icepack broke and flowed to sea, a ritual enacted ever since glaciers retreated from this continental shelf.

In the months ahead we can look to nature for these respites. The nonhuman world is free of charge; sunlight is a disinfectant, physical distance easily maintained, and no pandemic can suspend it. Nature offers not just escape but reassurance.

The nonhuman world is free of charge; sunlight is a disinfectant, and physical distance is easily maintained.

In 1946, in the aftermath of World War II, with the Nazi threat vanquished but the Cold War looming, George Orwell welcomed spring’s arrival in London’s bombed-out heart. “After the sorts of winters we have had to endure recently, the spring does seem miraculous, because it has become gradually harder and harder to believe that it is actually going to happen,” he wrote in “Some Thoughts on the Common Toad.” “Every February since 1940 I have found myself thinking that this time Winter is going to be permanent. But Persephone, like the toads, always rises from the dead at about the same moment.”

So she does. And so the slumbering earth warms to life. Two nights before the seals, two nights before World Health Organization declared a pandemic, before the NBA shut down with teams on the floor and fans in the seats, before the fright went beyond viral into logarithmic, was the Worm Moon: the full moon named for the imminent stir of earthworms in thawing soil.

In burrows beneath leaf litter, hibernating toads prepare to open what Orwell called “the most beautiful eye of any living creature,” resembling “the golden-colored semi-precious stone which one sometimes sees in signet rings, and which I think is called a chrysoberyl.” Nearly as beautiful are the eyes of painted turtles waiting on pond bottoms here in eastern Maine, the ice above now retreating from shore, mallard couples dabbling in newly open water.

The birds are the surest sign of spring’s imminence. Downtown the house finches are holding daily concerts. Starlings are starting to replace their gold-streaked winter plumes with more iridescent garb. In the street today I saw two male mockingbirds joust above the pavement, their white wing-bars fluttering territorial semaphores, abandoning the contest only when a car nearly ran them down. 

There are many quieter signs, too: pale tips of shrubs poised to grow, a spider rappelling off a low branch, fresh fox scat in the driveway. It’s red from apples preserved under snow and lined with the fur of field mice and meadow voles whose secret winter tunnels are now revealed in the grass. Somewhere soon mother fox will give birth, nursing her blind hairless charges in underground peace.

Eastern comma butterflies will gather on the trunks of those apple trees and sip their rising sap. Not long after the first orange-belted bumblebee queens will appear, inspecting potential nest sites under fallen leaves and decomposing logs. Warm rainy nights will bring salamanders and newts, just a few spotted glistening inches long, some of them decades old, out from woodland hidey-holes and down ancient paths to vernal pool bacchanals held amidst a chorus of spring peepers. Woodland ephemerals will bloom in sunshine unfiltered by still-bare treetops. My favorite are trout lilies, colonies of which illuminate forest floors with a sea of bright yellow blossoms, petals falling once the canopy unfurls.

“The atom bombs are piling up in the factories, the police are prowling through the cities, the lies are streaming from the loudspeakers,” Orwell wrote, “but the earth is still going round the sun.”

At this point there’s no end of studies showing how nature is good for our health, how patients recover faster in hospital rooms with windows overlooking trees, how a mindful walk in the woods will lower stress and raise moods. All true, but at this moment something deeper and more urgent is offered. An affirmation of life.

Will the nightmare scenes out of Italy and Spain and now New York City spread across the land? How long will the pandemic last? Will it completely rend our already tattered social fabric? When can I again play hockey or go to a coffee shop or use a credit card machine without feeling like I’m risking my own and other lives? Who will die? Nobody knows for sure, but in a few weeks the swallows will arrive, and tonight above the fields at dusk I heard the cries of woodcock.

Secretive, ground-dwelling birds with limpid black eyes and long, slender beaks attuned to the frequencies of earthworm-rustles, their feathers blend perfectly with leaf litter and old grass. They rely on this camouflage, going still rather than fleeing a walker’s approach, taking wing only as a last resort.

When they do, their flight is notable for its slowness and the quavering whistle of their wings. At no other time than in spring do they dare draw attention, much less put on a show: calling out, with an urgent nasal buzz best described as a peent, and flying straight upward before spiraling against a darkening sky.

Brandon Keim is a freelance nature and science journalist. The author of The Eye of the Sandpiper: Stories from the Living World, he’s now writing Meet the Neighbors, forthcoming from W.W. Norton & Company, about what it means to think of wild animals as fellow persons—and what that means for the future of nature.

Lead image: Tim Zurowski / Shutterstock

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.

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

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.

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).

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

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.

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

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).

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

What is this pandemic doing to our minds? Polls repeatedly show it’s having an adverse effect on our mental health. Physical distancing, for some, means social isolation, which has long been shown to encourage depression. Previous disasters have been followed by waves of depression, exacerbated by financial distress. The situation also puts us in a state of fear and anxiety—anxiety about financial strain, about being lonely, about the very lives of ourselves and our loved ones.

This fear can also bring out some of the everyday irrationalities we all struggle with. We have trouble thinking about numbers—magnitudes, probabilities, and the like—and when frightened we tend toward absolutes. Feeling powerless makes people more prone to conspiracy theories. We naturally believe that big effects should have big causes, and we see with the current coronavirus, as we did with AIDS and SARS, conspiracy theories claiming that the virus was engineered as a weapon.

We are seeing the theory of “collective resilience,” an informal solidarity among people, in action.

These psychological ramifications can make us fail to behave as well as we should. We have what psychologists call a “behavioral immune system” that makes us behave in ways that, in general, make us less likely to catch infectious disease. Things we perceive as being risky for disease makes us wary. An unfortunate side effect is that it increases prejudice against foreigners, people with visible sores or deformities, and people we perceive as simply being ugly. Politically, this can result in xenophobia and outgroup distrust. Coronavirus-related attacks, possibly encouraged by the misleading term “Chinese virus,” have plagued some ethnic Asian people.

And yet, in spite of all of the harm the pandemic seems to be wreaking on our minds, there are also encouraging acts of kindness and solidarity. In turbulent times, people come together and help each other.

In the days after the World Trade Center fell, it wasn’t just the police, hospitals, and firefighters who came forward to help, it was normal citizens who often put themselves at risk to help other people out. An equities trader named Sandler O’Neill helped rescue a dozen people and then went back to save more. A tour guide at the Pentagon helped victims outside, and then went back in the burning building to help more. We find these kinds of behaviors in every disaster.

During this pandemic, we see the same thing. Some acts are small and thoughtful, such as putting encouraging signs in windows. Others have made games out of window signs, putting up rainbows for children on walks to count. Some show support for health care and other frontline workers, applauding or banging on pots on their balconies and at windows in a nightly ritual. Others are helping in more substantial ways. In the United Kingdom, over half a million people signed up to be a National Health Volunteer, supporting the most vulnerable people, who have to stay home.

John Drury, a professor of social psychology at the University of Sussex, England, who studies people’s behavior in disasters, has seen these acts of kindness in his own neighborhood over the past month. He and his neighbors set up a WhatsApp group to help one another with shopping. “I think that translates across the country and probably across the world,” Drury says. “People are seeing themselves as an us, a new kind of we, based on the situation that we all find ourselves in. You’ve got this idea of common fate, which motivates our care and concern for others.”

We have always been a social species who rely on each other for happiness and our survival.

Drury is the pioneer of a theory known as “collective resilience,” which he describes as “informal solidarity among people in the public.” Drury’s study of the 2005 London bombing disaster found that mutual helping behaviors were more common than selfish ones. This basic finding has been replicated in other disasters, including the crash of the Ghana football stadium and the 2010 earthquake and tsunami in Chile. In disasters, Drury says, people reach heights of community and cooperation they’ve never reached before.

It turns out that being in a dangerous situation with others fosters a new social identity. Boundaries between us, which seem so salient when things are normal, disappear when we perceive we’re locked in a struggle together, with a common fate, from an external threat. People go from me thinking to we thinking. Respondents in studies about disasters often spontaneously bring up this feeling of group cohesion without being asked. The greater unity they felt, the more they helped.

Popular conceptions of how people respond in a crisis involve helplessness, selfishness, and panic. In practice, though, this rarely happens. “One of the reasons people die in emergencies isn’t overreaction, it’s underreaction,” Drury says. “People die in fires mainly because they’re too slow. They underestimate risk.” The myth of panic can lead to emergency policies that do more harm than good. At one point during Hurricane Katrina, Louisiana governor at the time Kathleen Blanco warned looters that National Guard troops “know how to shoot and kill, and they are more than willing to do so if necessary, and I expect they will.” A few days later, New Orleans police officers shot six civilians, wounding four and killing two.

People revert to selfishness when group identity starts to break down. Drury describes how people acted when the cruise ship, Costa Concordia sank off the coast of Italy in 2012. “There was cooperation until one point, when people got to the lifeboats and there was pushing,” Drury says. “Selfishness isn’t a default because many times people are cooperative. It’s only in certain conditions that people might become selfish and individualistic. Perhaps there isn’t a sense of common fate, people are positioned as individuals against individuals. After a period of time, people run out of energy, run out of emotional energy, run out of resources, and that goodwill, that support, starts to decline. They just haven’t got the resources to help each other.”

Perceptions of group behavior can shape public policy. It’s important that policymakers, rather than seeing groups as problems to be overcome, which can lead to riots and mob behavior, take account of how people in groups help one another. After all, we have always been a social species who rely on each other for happiness and our survival. And groups can achieve things that individuals cannot. This understanding couldn’t be more important than now. We can build on people’s naturally arising feelings of unity by emphasizing that we are all in this together, and celebrating the everyday heroes who, sometimes at great cost, go out of their way to make the pandemic a little less awful.

Jim Davies is a professor of cognitive science at Carleton University and author of Imagination: The Science of Your Mind’s Greatest Power. He is co-host of the Minding the Brain podcast.

Lead image: Franzi / Shutterstock

In the COVID-19 pandemic, numerous models are being used to predict the future. But as helpful as they are, they cannot make sense of themselves. They rely on epidemiologists and other modelers to interpret them. Trouble is, making predictions in a pandemic is also a philosophical exercise. We need to think about hypothetical worlds, causation, evidence, and the relationship between models and reality.1,2

The value of philosophy in this crisis is that although the pandemic is unique, many of the challenges of prediction, evidence, and modeling are general problems. Philosophers like myself are trained to see the most general contours of problems—the view from the clouds. They can help interpret scientific results and claims and offer clarity in times of uncertainty, bringing their insights down to Earth. When it comes to predicting in an outbreak, building a model is only half the battle. The other half is making sense of what it shows, what it leaves out, and what else we need to know to predict the future of COVID-19.

Prediction is about forecasting the future, or, when comparing scenarios, projecting several hypothetical futures. Because epidemiology informs public health directives, predicting is central to the field. Epidemiologists compare hypothetical worlds to help governments decide whether to implement lockdowns and social distancing measures—and when to lift them. To make this comparison, they use models to predict the evolution of the outbreak under various simulated scenarios. However, some of these simulated worlds may turn out to misrepresent the real world, and then our prediction might be off.

In his book Philosophy of Epidemiology, Alex Broadbent, a philosopher at the University of Johannesburg, argues that good epidemiological prediction requires asking, “What could possibly go wrong?” He elaborated in an interview with Nautilus, “To predict well is to be able to explain why what you predict will happen rather than the most likely hypothetical alternatives. You consider the way the world would have to be for your prediction to be true, then consider worlds in which the prediction is false.” By ruling out hypothetical worlds in which they are wrong, epidemiologists can increase their confidence that they are right. For instance, by using antibody tests to estimate previous infections in the population, public health authorities could rule out the hypothetical possibility (modeled by a team at Oxford) that the coronavirus has circulated much more widely than we think.3

One reason the dynamics of an outbreak are often more complicated than a traditional model can predict is that they result from human behavior and not just biology.

Broadbent is concerned that governments across Africa are not thinking carefully enough about what could possibly go wrong, having for the most part implemented coronavirus policies in line with the rest of the world. He believes a one-size-fits-all approach to the pandemic could prove fatal.4 The same interventions that might have worked elsewhere could have very different effects in the African context. For instance, the economic impacts of social distancing policies on all-cause mortality might be worse because so many people on the continent suffer increased food insecurity and malnutrition in an economic downturn.5 Epidemic models only represent the spread of the infection. They leave out important elements of the social world.

Another limitation of epidemic models is that they model the effect of behaviors on the spread of infection, but not the effect of a public health policy on behaviors. The latter requires understanding how a policy works. Nancy Cartwright, a philosopher at Durham University and the University of California, San Diego, suggests that “the road from ‘It works somewhere’ to ‘It will work for us’ is often long and tortuous.”6 The kinds of causal principles that make policies effective, she says, “are both local and fragile.” Principles can break in transit from one place to the other. Take the principle, “Stay-at-home policies reduce the number of social interactions.” This might be true in Wuhan, China, but might not be true in a South African township in which the policies are infeasible or in which homes are crowded. Simple extrapolation from one context to another is risky. A pandemic is global, but prediction should be local.

Predictions require assumptions that in turn require evidence. Cartwright and Jeremy Hardie, an economist and research associate at the Center for Philosophy of Natural and Social Science at the London School of Economics, represent evidence-based policy predictions using a pyramid, where each assumption is a building block.7 If evidence for any assumption is missing, the pyramid might topple. I have represented evidence-based medicine predictions using a chain of inferences, where each link in the chain is made of an alloy containing assumptions.8 If any assumption comes apart, the chain might break.

An assumption can involve, for example, the various factors supporting an intervention. Cartwright writes that “policy variables are rarely sufficient to produce a contribution [to some outcome]; they need an appropriate support team if they are to act at all.” A policy is only one slice of a complete causal pie.9 Take age, an important support factor in causal principles of social distancing. If social distancing prevents deaths primarily by preventing infections among older individuals, wherever there are fewer older individuals there may be fewer deaths to prevent—and social distancing will be less effective. This matters because South Africa and other African countries have younger populations than do Italy or China.10

The lesson that assumptions need evidence can sound obvious, but it is especially important to bear in mind when modeling. Most epidemic modeling makes assumptions about the reproductive number, the size of the susceptible population, and the infection-fatality ratio, among other parameters. The evidence for these assumptions comes from data that, in a pandemic, is often rough, especially in early days. It has been argued that nonrepresentative diagnostic testing early in the COVID-19 pandemic led to unreliable estimates of important inputs in our epidemic modeling.11

Epidemic models also don’t model all the influences of the pathogen and of our policy interventions on health and survival. For example, what matters most when comparing deaths among hypothetical worlds is how different the death toll is overall, not just the difference in deaths due to the direct physiological effects of a virus. The new coronavirus can overwhelm health systems and consume health resources needed to save non-COVID-19 patients if left unchecked. On the other hand, our policies have independent effects on financial welfare and access to regular healthcare that might in turn influence survival.

A surprising difficulty with predicting in a pandemic is that the same pathogen can behave differently in different settings. Infection fatality ratios and outbreak dynamics are not intrinsic properties of a pathogen; these things emerge from the three-way interaction among pathogen, population, and place. Understanding more about each point in this triangle can help in predicting the local trajectory of an outbreak.

In April, an influential data-driven model, developed by the Institute for Health Metrics and Evaluation (IHME) at the University of Washington, which uses a curve-fitting approach, came under criticism for its volatile projections and questionable assumption that the trajectory of COVID-19 deaths in American states can be extrapolated from curves in other countries.12,13 In a curve-fitting approach, the infection curve representing a local outbreak is extrapolated from data collected locally along with data regarding the trajectory of the outbreak elsewhere. The curve is drawn to fit the data. However, the true trajectory of the local outbreak, including the number of infections and deaths, depends upon characteristics of the local population as well as policies and behaviors adopted locally, not just upon the virus.

Predictions require assumptions that in turn require evidence.

Many of the other epidemic models in the coronavirus pandemic are SIR-type models, a more traditional modelling approach for infectious-disease epidemiology. SIR-type models represent the dynamics of an outbreak, the transition of individuals in the population from a state of being susceptible to infection (S) to one of being infectious to others (I) and, finally, recovered from infection (R). These models simulate the real world. In contrast to the data-driven approach, SIR models are more theory-driven. The theory that underwrites them includes the mathematical theory of outbreaks developed in the 1920s and 1930s, and the qualitative germ theory pioneered in the 1800s. Epidemiologic theories impart SIR-type models with the know-how to make good predictions in different contexts.

For instance, they represent the transmission of the virus as a factor of patterns of social contact as well as viral transmissibility, which depend on local behaviors and local infection control measures, respectively. The drawback of these more theoretical models is that without good data to support their assumptions they might misrepresent reality and make unreliable projections for the future.

One reason why the dynamics of an outbreak are often more complicated than a traditional model can predict, or an infectious-disease epidemiology theory can explain, is that the dynamics of an outbreak result from human behavior and not just human biology. Yet more sophisticated disease-behavior models can represent the behavioral dynamics of an outbreak by modeling the spread of opinions or the choices individuals make.14,15 Individual behaviors are influenced by the trajectory of the epidemic, which is in turn influenced by individual behaviors.

“There are important feedback loops that are readily represented by disease-behavior models,” Bert Baumgartner, a philosopher who has helped develop some of these models, explains. “As a very simple example, people may start to socially distance as disease spreads, then as disease consequently declines people may stop social distancing, which leads to the disease increasing again.” These looping effects of disease-behavior models are yet another challenge to predicting.

It is a highly complex and daunting challenge we face. That’s nothing unusual for doctors and public health experts, who are used to grappling with uncertainty. I remember what that uncertainty felt like when I was training in medicine. It can be discomforting, especially when confronted with a deadly disease. However, uncertainty need not be paralyzing. By spotting the gaps in our models and understanding, we can often narrow those gaps or at least navigate around them. Doing so requires clarifying and questioning our ideas and assumptions. In other words, we must think like a philosopher.

Jonathan Fuller is an assistant professor in the Department of History and Philosophy of Science at the University of Pittsburgh. He draws on his dual training in philosophy and in medicine to answer fundamental questions about the nature of contemporary disease, evidence, and reasoning in healthcare, and theory and methods in epidemiology and medical science.

References

1. Walker, P., et al. The global impact of COVID-19 and strategies for mitigation and suppression. Imperial College London (2020).

2. Flaxman, S., et al. Estimating the number of infections and the impact of non-pharmaceutical interventions on COVID-19 in 11 European countries. Imperial College London (2020).

3. Lourenco, J., et al. Fundamental principles of epidemic spread highlight the immediate need for large-scale serological surveys to assess the stage of the SARS-CoV-2 epidemic. medRxiv:10.1101/2020.03.24.20042291 (2020).

4. Broadbent, A., & Smart, B. Why a one-size-fits-all approach to COVID-19 could have lethal consequences. TheConversation.com (2020).

5. United Nations. Global recession increases malnutrition for the most vulnerable people in developing countries. United Nations Standing Committee on Nutrition (2009).

6. Cartwright, N. Will this policy work for you? Predicting effectiveness better: How philosophy helps. Philosophy of Science 79, 973-989 (2012).

7. Cartwright, N. & Hardie, J. Evidence-Based Policy: A Practical Guide to Doing it Better Oxford University Press, New York, New York (2012).

8. Fuller, J., & Flores, L. The Risk GP Model: The standard model of prediction in medicine. Studies in History and Philosophy of Biological and Biomedical Sciences 54, 49-61 (2015).

9. Rothman, K., & Greenland, S. Causation and causal inference in epidemiology. American Journal Public Health 95, S144-S50 (2005).

10. Dowd, J. et al. Demographic science aids in understanding the spread and fatality rates of COVID-19. Proceedings of the National Academy of Sciences 117, 9696-9698 (2020).

11. Ioannidis, J. Coronavirus disease 2019: The harms of exaggerated information and non‐evidence‐based measures. European Journal of Clinical Investigation 50, e13222 (2020).

12. COVID-19 Projections. Healthdata.org. https://covid19.healthdata.org/united-states-of-america.

13. Jewell, N., et al. Caution warranted: Using the Institute for Health metrics and evaluation model for predicting the course of the COVID-19 pandemic. Annals of Internal Medicine (2020).

14. Nardin, L., et al. Planning horizon affects prophylactic decision-making and epidemic dynamics. PeerJ 4:e2678 (2016).

15. Tyson, R., et al. The timing and nature of behavioural responses affect the course of an epidemic. Bulletin of Mathematical Biology 82, 14 (2020).

Lead image: yucelyilmaz / Shutterstock

There’s an old belief that truth will always overcome error. Alas, history tells us something different. Without someone to fight for it, to put error on the defensive, truth may languish. It may even be lost, at least for some time. No one understood this better than the renowned Italian scientist Galileo Galilei.

It is easy to imagine the man who for a while almost single-handedly founded the methods and practices of modern science as some sort of Renaissance ivory-tower intellectual, uninterested and unwilling to sully himself by getting down into the trenches in defense of science. But Galileo was not only a relentless advocate for what science could teach the rest of us. He was a master in outreach and a brilliant pioneer in the art of getting his message across.

Today it may be hard to believe that science needs to be defended. But a political storm that denies the facts of science has swept across the land. This denialism ranges from the initial response to the COVID-19 pandemic to the reality of climate change. It’s heard in the preposterous arguments against vaccinating children and Darwin’s theory of evolution by means of natural selection. The scientists putting their careers, reputations, and even their health on the line to educate the public can take heart from Galileo, whose courageous resistance led the way.

A crucial first step, one that took Galileo a bit of time to take, was to switch from publishing his findings in Latin, as was the custom for scientific writings at the time, to the Italian vernacular, the speech of the common people. This enabled not just the highly educated elite but anyone who was intellectually curious to hear and learn about the new scientific work. Even when risking offense (which Galileo never shied away from)—for instance, in responding to a German Jesuit astronomer who disagreed with him on the nature of sunspots (mysterious dark areas observed on the surface of the sun)—Galileo replied in the vernacular, because, as he explained, “I must have everyone able to read it.” An additional motive may have been that Galileo wanted to ensure that no one would somehow distort the meaning of what he had written.

Galileo also understood that while the Church had the pomp and magic of decades of art and music, science had the enchantment of a new invention—the telescope. Even he wasn’t immune to its seductive powers, writing in his famous booklet The Sidereal Messenger: “In this short treatise I propose great things for inspection and contemplation by every explorer of Nature. Great, I say, because of the excellence of the things themselves, because of their newness, unheard of through the ages, and also because of the instrument with the benefit of which they make themselves manifest to our sight. “ And that gave him his second plan for an ambitious outreach campaign.

With alternative facts acting like real facts, there are Galileo’s heirs, throwing up their hands and attempts to make lies sound like truth.

What if he could distribute telescopes (together with detailed instructions for their use and his booklet about the discoveries) all across Europe, so that all the influential people, that is, the patrons of scientists—dukes and cardinals, could observe with their own eyes far out into the heavens. They would see the stunning craters and mountains that cover the surface of the moon, four previously unseen satellites of Jupiter, dark spots on the surface of the sun, and the vast number of stars that make up the Milky Way.

But telescopes were both expensive and technically difficult to produce. Their lenses had to be of the highest quality, to provide both the ability to see faint objects and high resolution. “Very fine lenses that can show all observations are quite rare and, of the more than sixty I have made, with great effort and expense, I have only been able to retain a very small number,” Galileo wrote on March 19, 1610. Who would front the cost of such a monumental and risky project?

Today the papacy is arguably the single most influential and powerful religious institution in the world. But its power is mostly in the moral and religious realms. In Galileo’s time, the papacy was a political power of significance, gobbling up failed dukedoms elsewhere, merging them into what became known as the “papal states.” The persons with the greatest interest in appearing strong in front of the papacy were the heads of neighboring states at the time.

So it is not surprising that Galileo presented his grandiose scheme to the Tuscan court and the Grand Duke Cosimo II de’ Medici. Nor is it surprising that Cosimo agreed to finance the manufacturing of all the telescopes. On his own, he also instructed the Tuscan ambassadors to all the major European capitals to help publicize Galileo’s discoveries. In doing so he tied the House of Medici, ruler of the foundational city of the Renaissance, Florence, to modern science. A win-win for both the Grand Duke and Galileo.

Last, Galileo instinctively understood what modern PR specialists refer to as the “quick response.” He did not let even one unkind word be said about his discoveries without an immediate reply. And his pen could be sharp.

For example, the Jesuit mathematician Orazio Grassi (hiding behind the pseudonym of Sarsi) published a book entitled The Astronomical and Philosophical Balance, in which he criticized Galileo’s ideas on comets and on the nature of heat. In it, Grassi mistakenly thought that he would strengthen his argument by citing a legendary tale about the ancient Babylonians cooking eggs by whirling them on slings.

Really?

Galileo responded with a stupendous piece of polemic literature entitled The Assayer, in which he pounced on this fabled story like a cat on a mouse.

“If Sarsi wishes me to believe, on the word of Suidas [a Greek historian], that the Babylonians cooked eggs by whirling them rapidly in slings, I shall believe it; but I shall say that the cause of this effect is very far from the one he attributes to it,” he wrote. “ To discover the true cause, I reason as follows: ‘If we do not achieve an effect which others formerly achieved, it must be that we lack something in our operation which was the cause of this effect succeeding, and if we lack one thing only, then this alone can be the true cause. Now we do not lack eggs, or slings, or sturdy fellows to whirl them, and still they do not cook, but rather cool down faster if hot. And since we lack nothing except being Babylonians, then being Babylonian is the cause of the egg hardening.’”

Galileo understood what modern PR specialists refer to as the “quick response.” He did not let one unkind word go without an immediate reply.

Did Galileo’s efforts save science from being cast aside perhaps for decades, even centuries? Unfortunately, not quite. The trial in which he was convicted by the Inquisition for “vehement suspicion of heresy” exerted a chilling effect on progress in deciphering the laws governing the cosmos. The famous French philosopher and scientist René Descartes wrote in a letter: “I inquired in Leiden and Amsterdam whether Galileo’s World System was available, for I thought I had heard that it was published in Italy last year. I was told that it had indeed been published, but that all the copies had immediately been burnt in Rome, and that Galileo had been convicted and fined. I was so astonished at this that I almost decided to burn all my papers, or at least to let no one see them.”

I suspect that there are still too few of us who can tell exactly what Galileo discovered and why he is such an important figure to the birth of modern science. But around the world, in conversations as brittle as today’s politics, with alternative facts acting like real facts, there are Galileo’s heirs, throwing up their hands at such attempts to make lies seem like the truth and worse, the truth like a lie, responding with just four words: “And yet it moves.”

Galileo may have never really uttered these words. He surely didn’t say that phrase in front of the Inquisitors—that would have been insanely dangerous. But whether the motto came first from his own mouth, that of a supporter whom he met during the years the Church put him under house arrest after his trial, or a later historian, we know one thing for sure. That motto represents everything Galileo stood for. It conveys the clear message of: In spite of what you may believe, these are the facts! That science won at the end is not solely because of the methods and rules that Galileo set out for what we accept to be true. Science prevailed because Galileo put his life and his personal freedom on the line to defend it.

Mario Livio is an astrophysicist and author. His new book is Galileo: And the Science Deniers.

Lead image: Mario Breda / Shutterstock

We called Greg Carr the other day to talk about the spread of the coronavirus in Africa. Carr, who has been featured in Nautilus, is the founder of the Gorongosa Restoration Project, a partnership with the Mozambique government to revive Gorongosa National Park, that environmental treasure trove at the southern end of the Rift Valley. The 1,500 square-mile park, about the size of Rhode Island, was first given animal refuge status in the 1920s by the Portuguese, and for years was a favorite of European tourists. But in 1983 civil war broke out and the park became a no-man’s land. The place was poached to death, closed up and didn’t reopen until 1992.

Renewal began in 2004 and in 2008 the government signed a restoration agreement with Carr’s foundation. The agreement, which lasts through 2043, envisions a “human rights park” that will restore both ecosystems and economic vitality. After 11 years of rebuilding infrastructure, reintroducing animals, including hippos and wildebeests, and working with local communities, Gorongosa is thriving again. The park now serves as a model for future conservation. Today some 200,000 people live around the park in a “sustainable development zone” that includes education, employment opportunities, and health service. About 700 people have full time jobs in the park; another 300, part time. Naturalist E.O. Wilson calls Gorongosa “a window on eternity.”

“If there’s one thing the rest of the world can learn from Africans, it would be their resilience.”

Carr is a 60-year-old entrepreneur and philanthropist who grew up in Idaho and in his mid twenties co-founded Boston Technology, a voice mail company. By the time he turned 40 he had amassed his fortune and couldn’t see the fun in doing it all over again, and so turned to philanthropy. These days he’s in Idaho Falls, on the phone six hours a day, getting the latest reports from his staff in the park, now closed until further notice.

The coronavirus news from Mozambique is mixed, as it is in much of sub-Saharan Africa. With the exception of South Africa, with over 7,500 confirmed cases of COVID-19 and 148 deaths, some countries below the Equator have fewer than 100 cases. As of May 6, there were just 81 cases in Mozambique and no deaths. If these numbers don’t blow up, the quick explanation might hold that the median age in Sub Saharan Africa is under 20, just 17.6 in Mozambique; population density is low (103 people per square mile); and there’s relatively limited direct contact with heavily infected countries in other parts of the world. 

Still, many experts fear chaos is inevitable. Underlying conditions in Mozambique include implacable poverty and a 60-year history of colonial and civil wars. On another front, in early April, in northern Mozambique, an Isis group shot or beheaded 52 young people because they refused to be recruited. Add a 48 percent literacy rate for women, 60 percent for men. The country also suffers the world’s eighth-highest incidence of HIV; 1.5 million people have contracted the virus and nearly 40,000 people have died. Finally, a large number of Mozambicans go to South Africa for work and then return. Testing is rare in the entire country.

In March, CDC Africa sent out a national directive requiring social distancing. “People are going to pay more attention to that in the cities than they are in rural Mozambique, at least until the virus really comes,” Carr said the other day. “Now, if you live in rural Mozambique, you don’t have the luxury of saying, ‘I’m isolating at home.’ People have to go out every day, to get food and water, from 40 to 60 liters a day, they have to tend to their farms. The idea of social distancing is a bit impossible for these folks.” He added, “Schools are closed and we are making our own masks for people. We all know there’s no treatment per se or certainly vaccine. If this hits, we’ll only be able to offer people Tylenol and soup.”

Cases in Mozambique could shoot up as mine workers continue to return home from their jobs in South Africa. “In my opinion,” said Carr, “Mozambique does not have the capacity to deal with this type of pandemic, as there are few qualified health personnel and the high level of poverty leads people to resist isolating themselves, as they look for alternatives to take care of their families. Our Gorongosa teams are in the field, spreading prevention messages, distributing masks and water purification.” 

Berta Barros, head nurse at Gorongosa, told Carr recently she has three main worries: lack of COVID-19 test kits, lack of healthcare professionals to respond to sick patients, and shortage of medications for treatment. “Mozambique has a population close to 30 million and we only have 34 ventilators,” Barros said. “It’s beyond impossible to work and choose who to save.”

Carr often talks about Mozambique as though he was Mozambican. “We’re very practical people,” he’ll say. “We’re not really theoretical. We’re just going to work our way through this.” He shies away from broad, open-ended questions about Africa, much less cultural comparisons and grand conclusions. “Africa is more than 1 billion people in 54 countries with, what, 2,500 languages? To make a statement like, ‘Africa is this…’ Frankly, I just think a lot of it is complete baloney.”

At the same time, says Carr, “If there’s one thing the rest of the world can learn from Africans, it would be their resilience. We’ve had five years of war in Mozambique and then last year we had a cyclone that killed nearly 1,000 people. I didn’t even mention the two droughts we had in the last seven years and the armyworm that came through and ate everybody’s maize. These people had their homes washed away in a flood last year, lost everything. So they rebuild their homes and then someone says, ‘Hey, there might be a virus coming through.’ It’s just one thing after another.”

What impact might the pandemic have on animals in the park? What effect will it have on just recovered antelope populations, for example, and the inevitable increase in poaching as tourism subsides? How many resources will need to be taken away from the war on other diseases to fight this? Impossible to say. But an anecdote came to Carr’s mind that suggests the vagaries of death in Southern Africa. “I got a call from a dear friend of mine yesterday, a Mozambique good friend, who said her aunt had just died. I said, ‘Wow, do you think it was COVID?’ She goes, ‘No, she’d been suffering for a while with a bad kidney.’ Life is tough in Africa. Do we know for sure this woman didn’t also have COVID and that contributed? Maybe. The truth about Africa is that disaster is hardly news. Malaria is the most prolific killer. And when they turn 50, people die and often no one knows exactly what the cause was. It’s just the way life is.”

Mark MacNamara is an Asheville, North Carolina-based writer. His articles for Nautilus include “We Need to Talk About Peat” and “The Artist of the Unbreakable Code.”

When I worked as a TV reporter covering health and science, I would often be recognized in public places. For the most part, the interactions were brief hellos or compliments. Two periods of time stand out when significant numbers of those who approached me were seeking detailed information: the earliest days of the pandemic that became HIV/AIDS and during the anthrax attacks shortly following 9/11. Clearly people feared for their own safety and felt their usual sources of information were not offering them satisfaction. Citizens’ motivation to seek advice when they feel they aren’t getting it from official sources is a strong indication that risk communication is doing a substandard job. It’s significant that one occurred in the pre-Internet era and one after. We can’t blame a public feeling misinformed solely on the noise of the digital age.

America is now opening up from COVID-19 lockdown with different rules in different places. In many parts of the country, people have been demonstrating, even rioting, for restrictions to be lifted sooner. Others are terrified of loosening the restrictions because they see COVID-19 cases and deaths still rising daily. The officials deciding what to open, and when, seldom offer thoughtful rationales. Clearly, risk communication about COVID-19 is failing with potentially dire consequences.

A big part of maintaining credibility is to admit to uncertainty—something politicians are loath to do.

Peter Sandman is a foremost expert on risk communication. A former professor at Rutgers University, he was a top consultant with the Centers for Disease Control in designing crisis and emergency risk-communication, a field of study that combines public health with psychology. Sandman is known for the formula Risk = Hazard + Outrage. His goal is to create better communication about risk, allowing people to assess hazards and not get caught up in outrage at politicians, public health officials, or the media. Today, Sandman is a risk consultant, teamed with his wife, Jody Lanard, a pediatrician and psychiatrist. Lanard wrote the first draft of the World Health Organization’s Outbreak Communications Guidelines. “Jody and Peter are seen as the umpires to judge the gold standard of risk communications,” said Michael Osterholm of the Center for Infectious Disease Research and Policy at the University of Minnesota. Sandman and Lanard have posted a guide for effective COVID-19 communication on the center’s website.

I reached out to Sandman to expand on their advice. We communicated through email.

Sandman began by saying he understood the protests around the country about the lockdown. “It’s very hard to warn people to abide by social-distancing measures when they’re so outraged that they want to kill somebody and trust absolutely nothing people say,” he told me. “COVID-19 outrage taps into preexisting grievances and ideologies. It’s not just about COVID-19 policies. It’s about freedom, equality, too much or too little government. It’s about the arrogance of egghead experts, left versus right, globalism versus nationalism versus federalism. And it’s endlessly, pointlessly about Donald Trump.”

Since the crisis began, Sandman has isolated three categories of grievance. He spelled them out for me, assuming the voices of the outraged:

• “In parts of the country, the response to COVID-19 was delayed and weak; officials unwisely prioritized ‘allaying panic’ instead of allaying the spread of the virus; lockdown then became necessary, not because it was inevitable but because our leaders had screwed up; and now we’re very worried about coming out of lockdown prematurely or chaotically, mishandling the next phase of the pandemic as badly as we handled the first phase.”

• “In parts of the country, the response to COVID-19 was excessive—as if the big cities on the two coasts were the whole country and flyover America didn’t need or didn’t deserve a separate set of policies. There are countless rural counties with zero confirmed cases. Much of the U.S. public-health profession assumes and even asserts without building an evidence-based case that these places, too, needed to be locked down and now need to reopen carefully, cautiously, slowly, and not until they have lots of testing and contact-tracing capacity. How dare they destroy our economy (too) just because of their mishandled outbreak!”

• “Once again the powers-that-be have done more to protect other people’s health than to protect my health. And once again the powers-that-be have done more to protect other people’s economic welfare than to protect my economic welfare!” (These claims can be made with considerable truth by healthcare workers; essential workers in low-income, high-touch occupations; residents of nursing homes; African-Americans; renters who risk eviction; the retired whose savings are threatened; and others.)

In their article for the Center for Infectious Disease Research and Policy, Sandman and Lanard point out that coping with a pandemic requires a thorough plan of communication. This is particularly important as the crisis is likely to enter a second wave of infection, when it could be more devastating. The plan starts with six core principles: 1) Don’t over-reassure, 2) Proclaim uncertainty, 3) Validate emotions—your audience’s and your own, 4) Give people things to do, 5) Admit and apologize for errors, and 6) Share dilemmas. To achieve the first three core principles, officials must immediately share what they know, even if the information may be incomplete. If officials share good news, they must be careful not to make it too hopeful. Over-reassurance is one of the biggest dangers in crisis communication. Sandman and Lanard suggest officials say things like, “Even though the number of new confirmed cases went down yesterday, I don’t want to put too much faith in one day’s good news.” 

Sandman and Lanard say a big part of maintaining credibility is to admit to uncertainty—something politicians are loath to do. They caution against invoking “science” as a sole reason for action, as science in the midst of a crisis is “incremental, fallible, and still in its infancy.” Expressing empathy, provided it’s genuine, is important, Sandman and Lanard say. It makes the bearer more human and believable. A major tool of empathy is to acknowledge the public’s fear as well as your own. There is good reason to be terrified about this virus and its consequences on society. It’s not something to hide.

Sandman and Lanard say current grievances with politicians, health officials, and the media, about how the crisis has been portrayed, have indeed been contradictory. But that makes them no less valid. Denying the contradictions only amplifies divisions in the public and accelerates the outrage, possibly beyond control. They strongly emphasize one piece of advice. “Before we can share the dilemma of how best to manage any loosening of the lockdown, we must decisively—and apologetically—disabuse the public of the myth that, barring a miracle, the COVID-19 pandemic can possibly be nearing its end in the next few months.”

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.