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

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

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

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

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

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

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

Cardi B invited Bernie Sanders to join her on Instagram Live last night to talk politics, coronavirus and manicures.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Lead image: SanaStock / Shutterstock

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kevin Berger is the editor of Nautilus.

References

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

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

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

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

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

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

Lead image: AP Photo / Mark Lennihan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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