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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Lead image: nazareno / Shutterstock

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

After how many drops did they stop closing their leaves?

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

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

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

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

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

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

So plants can hear water?

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

What kind of sounds do they make?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

What did you do in Peru?

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

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

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

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

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

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

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

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

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

What have plants asked you to do?

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

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

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

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

Lead image: kmeds7 / Shutterstock

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