If I was ever going to ‘come out’, I should have done it when I was younger

If anyone ever offers me a cigarette, I always reply: “No thanks, I don’t smoke.” But I’m lying.

I started smoking at 16. I thought it made me look grown-up, but I was shy so I’d do it on my own. I would go into the woods near my home, or occasionally “bravely” have one in the house if nobody was else in.

The singer-songwriter, formerly of Moloko, picks songs from folk to rock and electronica that will transport you to Ireland

“This reminds me of home. I first heard about John McCormack through my grandma,” Murphy says. “It’s about Avoca, which is near Arklow in County Wicklow, where I’m from. I got a bit misty-eyed when I was listening to it this morning. It made me want to be out walking around Avoca and down to the water. Of course the pubs wouldn’t be open, which would be a tragedy.” McCormack, a renowned operatic tenor from Athlone, recorded the song in 1940, with lyrics from a poem by Irish poet Thomas Moore. “My da used to sing this song too. He has a lovely voice and knows hundreds of songs. He used to play a game with us: ‘Name anything and I bet you I know a song about it,’ he’d say.”

The actor on walking the red carpet while having an allergic reaction, her controversial Calvin Klein campaign and dressing like Michael Jackson

I’m not known for wearing outfits that are as completely covered up as this. Often, you are uncomfortable on the red carpet, worried that something is going to pop out, unzip or break. There was something about this look that felt like protection and armour to me. I wore it to the 2018 CFDA fashion awards and I loved how extreme it felt: chic and strong, slightly androgynous but with a femininity to it. It came together nicely with no stress – until I was in the car, when I realised I was having some kind of allergic reaction to my makeup! One of my eyes swelled up right before I was stepping out on to the red carpet. I panicked and put on my reading glasses to camouflage the fact that one eye was almost completely shut!

As a teenager, my relationship with apparel was fraught because I never cultivated my own style. My mom and I bought everything from thrift shops – I would wear the same jeans all year and then cut them into shorts – but every time I would go on a set I would be decked out in designer clothes. There was a disconnect: clothes were just something belonging to other people that I would embody, and then shed.

From Matilda the Hun to the first fleet, test your knowledge with the Weekend quiz

1 Which South American was the world’s first female president?
2 What was the destination of the First Fleet?
3 Who lived at 308 Negra Arroyo Lane, Albuquerque?
4 Which epic poem is based on the Battle of Roncevaux?
5 What animal is a sarcastic fringehead?
6 What German car was last made in Mexico in 2019?
7 Pollex is the medical name for what part of the body?
8 Thomas Neuwirth won Eurovision under what stage persona?
What links:
9 Norwich; Newlyn; St Ives; Camden Town; Bloomsbury?
10 Platypus and four species of echidna?
11 Renren; QQ; Sina Weibo; WeChat?
12 Sydenstricker; Stearns; Staples; Surajprasad?
13 Colonel Ninotchka; Mt Fiji; Zelda the Brain; Matilda the Hun?
14 Harmost; satrap; voivode; bey; subahdar?
15 Ridley Scott; James Cameron; David Fincher; Jean-Pierre Jeunet?

We can expect psychological difficulties to follow as we come out of lockdown. But we have an opportunity to remake our relationship with our bodies, and the social body we belong to. By Susie Orbach

When lockdown started, I was confused by bodies on television. Why weren’t they socially distancing? Didn’t they know not to be so close? The injunction to be separate was unfamiliar and irregular, and for me, self-isolating alone, following this government directive was peculiar. It made watching dramas and programmes produced under normal filming conditions feel jarring.

Seven weeks in, the disjuncture has passed. I, like all of us, am accommodating to multiple corporeal realities: bodies alone, bodies distant, bodies in the park to be avoided, bodies of disobedient youths hanging out in groups, bodies in lines outside shops, bodies and voices flattened on screens and above all, bodies of dead health workers and carers. Black bodies, brown bodies. Working-class bodies. Bodies not normally praised, now being celebrated.

A trio of Senate Democrats wants to give $2,000 per month to individuals through the end of the health emergency. One Senate Republican suggests covering payroll for companies that rehire workers.

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The Canadian military is still determining how to raise the wreckage of a military helicopter that crashed into the Mediterranean Sea last week, Defence Minister Harjit Sajjan said Thursday.

Labour was embroiled in recriminations today over the leak of an internal report that apparently exonerated Jeremy Corbyn's team of failing to crack down on anti-Semitism and instead blamed his opponents for stoking up controversy to damage him.

Coronavirus: The symptoms

The Speaker is presiding over his first virtual PMQs. Susannah Butter meets him (on FaceTime)

The pair announced the exciting news this morning

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

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

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

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