Spillover: the powerful, prescient book that predicted the Covid-19 coronavirus pandemic.

by David Quammen

A zoonosis is an animal infection transmissible to humans.

Infectious disease is a kind of natural mortar binding one creature to another, one species to another, within the elaborate biophysical edifices we call ecosystems.

Smallpox could be eradicated because that virus, lacking ability to reside and reproduce anywhere but in a human body (or a carefully watched lab animal), couldn’t hide.

The eradication campaign for poliomyelitis, unlike other well-meant and expensive global health initiatives, may succeed. Why? Because vaccinating humans by the millions is inexpensive, easy, and permanently effective, and because apart from infecting humans, the poliovirus has nowhere to hide. It’s not zoonotic.

Polio success story

By the cold Darwinian logic of natural selection, evolution codifies happenstance into strategy.

To reside undetected within a reservoir host is probably easiest wherever biological diversity is high and the ecosystem is relatively undisturbed. The converse is also true: Ecological disturbance causes diseases to emerge. Shake a tree, and things fall out.

Reservoir host = natural host

Nearly all zoonotic diseases result from infection by one of six kinds of pathogen: viruses, bacteria, fungi, protists (a group of small, complex creatures such as amoebae, formerly but misleadingly known as protozoans), prions, and worms.

Viruses are the most problematic. They evolve quickly, they are unaffected by antibiotics, they can be elusive, they can be versatile, they can inflict extremely high rates of fatality, and they are fiendishly simple, at least relative to other living or quasi-living creatures.

The thing with viruses

the percentage of sampled individuals showing some history of infection, either present or past—is called seroprevalence. It constitutes an estimate, based on finite sampling, of what the percentage throughout an entire population might be.

Seroprevalance

An amplifier host is a creature in which a virus or other pathogen replicates—and from which it spews—with extraordinary abundance.

Human-caused ecological pressures and disruptions are bringing animal pathogens ever more into contact with human populations, while human technology and behavior are spreading those pathogens ever more widely and quickly.

“Spillover” is the term used by disease ecologists (it has a different use for economists) to denote the moment when a pathogen passes from members of one species, as host, into members of another. It’s a focused event.

spillover in the reverse direction—from humans to a nonhuman species—is known as an anthroponosis.

their trapping and hunting efforts, plus the bounties they paid for creatures delivered alive by villagers, yielded more than fifteen hundred animals representing 117 species. There were monkeys, rats, mice, bats, mongooses, squirrels, pangolins, shrews, porcupines, duikers, birds, tortoises, and snakes. Blood was taken from each, and then snips of liver, kidney, and spleen. All these samples, deep-frozen in individual vials, were shipped back to the CDC for analysis. Could any live virus be grown from the sampled tissues? Could any Ebola antibodies be detected in blood serum? The bottom line, reported with candor by Johnson and coauthors in the pages of The Journal of Infectious Diseases, was negatory: “No evidence of Ebola virus infection4 was found.”

The elusive Ebola

Many factors contribute to the case fatality rate during an outbreak, including diet, economic conditions, public health in general, and the medical care available in the location where an outbreak occurs.

Some scientists use the term “dead-end host,” as distinct from “reservoir host,” to describe humanity’s role in the lives and adventures of ebolaviruses. What the term implies is this: Outbreaks have been contained and terminated; in each situation the virus has come to a dead end, leaving no offspring. Not the virus in toto throughout its range, of course, but that lineage of virus, the one that has spilled over, betting everything on this gambit—it’s gone, kaput. It’s an evolutionary loser. It hasn’t caught hold to become an endemic disease within human populations. It hasn’t caused a huge epidemic. Ebolaviruses, judged by experience so far, fit that pattern.

Ebola: An evolutionary loser

Every spillover is like a sweepstakes ticket, bought by the pathogen, for the prize of a new and more grandiose existence. It’s a long-shot chance to transcend the dead end. To go where it hasn’t gone and be what it hasn’t been. Sometimes the bettor wins big. Think of HIV.

Lmao

concerning the five ebolaviruses: “Viruses of each species have genomes that6 are at least 30–40% divergent from one another, a level of diversity that presumably reflects differences in the ecologic niche they occupy and in their evolutionary history.” Towner and company suggested that some of the crucial differences between one ebolavirus and another—including the differences in lethality—might be related to where and how they live, where and how they have lived, within their reservoir hosts.

Ebola: a multifaceted killer

Acholi cultural knowledge dictated a program of special behaviors, some of which were quite appropriate for controlling infectious disease, whether you believed it was caused by spirits or by a virus. These behaviors included quarantining each patient in a house apart from other houses; relying on a survivor of the epidemic (if there were any) to provide care to each patient; limiting movement of people between the affected village and others; abstaining from sexual relations; not eating rotten or smoked meat; and suspending the ordinary burial practices, which would involve an open casket and a final “love touch” of the deceased8 by each mourner, filing up for that purpose. Dancing was also prohibited. Such traditional Acholi strictures (along with intervention by the Uganda Ministry of Health and support from the CDC, Médecins Sans Frontières, and WHO) may have helped suppress the Gulu outbreak.

Wisdom

another aspect of the pathology of Ebola virus disease is a phenomenon called disseminated intravascular coagulation, familiar to the medical community as DIC. It’s also known as consumptive coagulopathy (if that helps you), because it involves consumption of too much of the blood’s coagulating capacity in a misdirected way. Billy Karesh had told me about DIC as we boated down the Mambili River after our gorilla stakeout. Disseminated intravascular coagulation, he explained, is a form of pathological blood sludge, in which the normal clotting factors (coagulation proteins and platelets) are pulled out to form tiny clots along the insides of blood vessels throughout the victim’s body, leaving little or no coagulation capacity to prevent leakage elsewhere. As a result, blood may seep from capillaries into a person’s skin, forming bruiselike purple marks (hematomas); it may dribble from a needle puncture that seems never to heal, or it may leak into the gastrointestinal tract or the urine. Still worse, the mass aggregation of small clots in the vessels may block blood flow to the kidneys or the liver, causing organ failure as often seen with Ebola.

One of the lab people at Porton Down was Geoffrey S. Platt. On November 5, 1976, in the course of an experiment, Platt filled a syringe with homogenized liver from a guinea pig that had been infected with the Sudanese virus. Presumably he intended to inject that fluid into another test animal. Something went amiss, and instead he jabbed himself in the thumb. Platt didn’t know exactly what pathogen he had just exposed himself to, but he knew it wasn’t good. The fatality rate from this unidentified virus, as he must have been aware, was upwards of 50 percent. Immediately he peeled off his medical glove, plunged his thumb into a hypochlorite solution (bleach, which kills virus) and tried to squeeze out a drop or two of blood. None came. He couldn’t even see a puncture. That was a good sign if it meant there was no puncture, a bad sign if it meant a little hole sealed tight. The tininess of Platt’s wound, in light of subsequent events, testifies that even a minuscule dose of an ebolavirus is enough to cause infection, at least if that dose gets directly into a person’s bloodstream. Not every pathogen is so potent. Some require a more sizable foothold. Ebolaviruses have force but not reach. You can’t catch one by breathing shared air, but if a smidgen of the virus gets through a break in your skin (and there are always tiny breaks), God help you. In the terms used by the scientists: It’s not very contagious but it’s highly infectious. Six days after the needle prick, Geoffrey P...

Ebola is relentless

Did you ever consider not going back to Ebola? I asked. “No,” she said. Why do you love this work so much? “I don’t know,” she said, and began to ruminate. “I mean, why Ebola? It only kills maybe a couple hundred people a year.” That is, it hasn’t been a disease of massive global significance and, notwithstanding the lurid scenarios that some people evoke, it’s unlikely ever to become one. But she could cite its attractions in scientific terms. She took deep interest, for instance, in the fact that such a simple organism can be so potently lethal. It contains only a tiny genome, enough to construct just ten proteins, which account for the entire structure, function, and self-replicating capacity of the thing. (A herpesvirus, by contrast, carries about ten times more genetic complexity.) Despite the minuscule genome, Ebola virus is ferocious. It can kill a person in seven days. “How can something that is so small and so simple just be so darn dangerous?” Warfield posed the question and I waited. “That’s just really fascinating to me.”

The allure of Ebola

Ebola virus is not in your habitat. You are in its.

Ebola is difficult to study, Leroy explained, because of the character of the virus. It strikes rarely, it progresses quickly through the course of infection, it kills or it doesn’t kill within just a few days, it affects only dozens or hundreds of people in each outbreak, and those people generally live in remote areas, far from research hospitals and medical institutes—far even from his institute, CIRMF. (It takes about two days to travel, by road and river, from Franceville to Mayibout 2.) Then the outbreak exhausts itself locally, coming to a dead end, or is successfully stanched by intervention. The virus disappears like a band of jungle guerrillas. “There is nothing to do,” Leroy said, expressing the momentary perplexity of an otherwise patient man. He meant, nothing to do except keep trying, keep working, keep sampling from the forest, keep responding to outbreaks as they occur. No one can predict when and where Ebola virus will next spill. “The virus seems to decide for itself.”

What Walsh suggested—to recapitulate in simplest form—is a wave of Ebola virus sweeping across Central Africa by newly infecting some reservoir host or hosts. From its recent establishment in the host, according to Walsh, the virus spilled over, here and there, into ape and human populations. The result of that process is manifest as a sequence of human outbreaks coinciding with clusters of dead chimps and gorillas—almost as though the virus were sweeping through ape populations across Central Africa. Walsh insisted during our Libreville chat, though, that he had never proposed a continental wave of dying gorillas, one group infecting another. His wave of Ebola, he explained, has been traveling mainly through the reservoir populations, not through the apes. Ape deaths have been numerous and widespread, yes, and to some degree amplified by ape-to-ape contagion, but the larger pattern reflects progressive viral establishment in some other group of animals, still unidentified, with which apes frequently come into contact. Leroy, on the other hand, has presented his particle hypothesis of “multiple independent introductions” as a diametric alternative not to Walsh’s idea as here stated but to the notion of a continuous wave among the apes. In other words, one has cried: Apples! The other has replied: Not oranges, no! Either might be right, or not, but in any case their arguments don’t quite meet nose to nose.

there’s a critical minimum size of the host population, below which it can’t persist indefinitely as an endemic, circulating infection. This is known as the critical community size (CCS), an important parameter in disease dynamics. The critical community size for measles seems to be somewhere around five hundred thousand people. That number reflects characteristics specific to the disease, such as the transmission efficiency of the virus, its virulence (as measured by the case fatality rate), and the fact that one-time exposure confers lifelong immunity. Any isolated community of less than a half million people may be struck by measles occasionally, but in a relatively short time the virus will die out. Why? Because it has consumed its opportunities among susceptible hosts. The adults and older children in the population are nearly all immune, having been previously exposed, and the number of babies born each year is insufficient to allow the virus a permanent circulating presence. When the population exceeds five hundred thousand, on the other hand, there will be a sufficient and continuing supply of vulnerable newborns.

On critical community size *Does not apply to zoonotic pathogens

Although the control measures he advocated were effective toward reducing malaria in certain locales (Panama, Mauritius), in other places they failed to do much good (Sierra Leone, India) or the results were transitory. For all his honors, for all his mathematical skills, for all his combative ambition and obsessive hard work, Ronald Ross couldn’t conquer malaria, nor even provide a strategy by which such an absolute victory would eventually be won. He may have understood why: because it’s such an intricate disease, deeply entangled with human social and economic considerations as well as ecological ones, and therefore a problem more complicated than even differential calculus can express.

Why malaria couldn't be arrested by math alone

The four kinds of malaria to which these statements applied are caused by protists of the species Plasmodium vivax, Plasmodium falciparum, Plasmodium ovale, and Plasmodium malariae, all of them belonging to the same diverse genus, Plasmodium, which encompasses about two hundred species. Most of the others infect birds, reptiles, or nonhuman mammals. The four known for targeting humans are transmitted from person to person by Anopheles mosquitoes. These four parasites possess wondrously complicated life histories, encompassing multiple metamorphoses and different forms in series: an asexual stage known as the sporozoite, which enters the human skin during a mosquito bite and migrates to the human liver; another asexual stage known as the merozoite, which emerges from the liver and reproduces in red blood cells; a stage known as the trophozoite, feeding and growing inside the blood cells, each of which fattens as a schizont and then bursts, releasing more merozoites to further multiply in the blood, and causing a spike of fever; a sexual stage known as the gametocyte, differentiated into male and female versions, which emerge from a later round of infected red blood cells, enter the bloodstream en masse, and are taken up within a blood meal by the next mosquito; a fertilized sexual stage known as the ookinete, which lodges in the gut lining of the mosquito, each ookinete ripening into a sort of egg sac filled with sporozoites; and then come the sporozoites again, bursting ou...

The malarial life cycle

It shows evolution’s power, over great lengths of time, to produce structures, tactics, and transformations of majestic intricacy. Alternatively, anyone who favors Intelligent Design in lieu of evolution might pause to wonder why God devoted so much of His intelligence to designing malarial parasites.

Within the Plasmodium family tree, as revealed by molecular phylogenetics over the last two decades, the four human-afflicting kinds don’t cluster on a single branch. They are each more closely related to other kinds of Plasmodium, infecting nonhuman hosts, than to one another. In the lingo of taxonomists, they are polyphyletic. What that suggests, besides the diversity of their genus, is that each of them must have made the leap to humans independently.

Each malaria has a different origin story

the entire genetic range of P. falciparum in humans forms “a monophyletic lineage within the gorilla P. falciparum radiation.”9 In plain talk: The human version is one twig within a gorilla branch, suggesting that it came from a single spillover. That’s one mosquito biting one infected gorilla, becoming a carrier, and then biting one human. By delivering the parasite into a new host, that second bite was enough to account for a zoonosis that still kills more than a half million people each year.

Ek machchar insaan ko...

dR/dt = γI merely means that the number of recovered individuals in the population, at a given moment, reflects the number of infected individuals times the average recovery rate. So much for R, the “recovered” class. The equations for S (“susceptibles”) and I (“infected”) are likewise opaque but sensible. All this became known as an SIR model. It was a handy tool for thinking about infectious outbreaks, still widely used by disease theorists.

A look into the SIR disease model

MacDonald got some of his field experience in Ceylon (now Sri Lanka) during the late 1930s, just after a calamitous malaria epidemic there in 1934–1935, which sickened a third of the Ceylonese populace and killed eighty thousand. The severity of the Ceylon epidemic had been surprising because the disease was familiar, at least in parts of the island, recurring as modest annual outbreaks that mostly affected young children. What happened differently in 1934–1935 was that, after a handful of years with little malaria at all, a drought increased breeding habitat for mosquitoes (standing pools in the rivers, instead of flowing current), whose population then multiplied hugely, carrying malaria into areas where it had been long absent and where most people—especially the young children—possessed no acquired immunity.

Dayum

The ultimate product of MacDonald’s equations was a single number, which he called the basic reproduction rate. That rate represented, in his words, “the number of infections distributed in a community13 as the direct result of the presence in it of a single primary non-immune case.” More precisely, it was the average number of secondary infections produced, at the beginning of an outbreak, when one infected individual enters a population where all individuals are nonimmune and therefore susceptible. MacDonald had identified a crucial index—fateful, determinative. If the basic reproduction rate was less than 1, the disease fizzled away. If it was greater than 1 (greater than 1.0, to be more precise), the outbreak grew. And if it was considerably greater than 1.0, then kaboom: an epidemic. The rate in Ceylon, he deduced from available data, had probably been about 10. That’s very high, as disease parameters go. Plenty high enough to yield a severe epidemic. But it was the lower side of the range for circumstances such as those in Ceylon. On the upper side, MacDonald imagined this: that a single infected person, left untreated and remaining infectious for eighty days, exposed to ten mosquitoes each day, if those mosquitoes enjoyed reasonable longevity and reasonable opportunities to bite, could infect 540 other people. Basic reproduction rate: 540.

I wonder what it's like for COVID

Wagner-Juaregg solved that problem after noting that Treponema pallidum didn’t survive in a test tube at temperatures much above 98.6 degrees Fahrenheit. Raise the blood temperature of the infected person a few degrees, he realized, and you might cook the bacterium to death. So he began inoculating patients with Plasmodium vivax. He would allow them to cycle through three or four spikes of fever, delivering potent if not terminal setbacks to the Treponema, and then dose them with quinine, bringing the plasmodium under control. “The effect was remarkable;15 the downward progression of late-stage syphilis was stopped,”

Killing syphilis with malaria

Ciuca evidently felt that Plasmodium knowlesi might be a better weapon against neurosyphilis than other kinds of the parasite. He inoculated several hundred patients and, in 1937, reported fairly good success. His program of treatments continued until, almost twenty years later, a problem arose. Repeatedly passaging P. knowlesi through a series of human hosts (injecting infected blood, allowing the merozoites to multiply, and then extracting infected blood) had made Ciuca’s strain increasingly virulent—too virulent for comfort. After 170 such passages, he and his colleagues became concerned with its growing ferocity and stopped using it. That was a first cautionary signal, but still just a laboratory effect. (Passaging was necessary for replenishing a supply of the parasite, since it couldn’t be cultured in a dish or a tube; but passaging it directly through humans liberated the parasite from whatever different evolutionary pressures had been entailed in completing its life cycle within mosquitoes. It became like the protist equivalent of a designated hitter—very capable of batting, and freed from the responsibility to play outfield.) Other evidence would eventually show that P. knowlesi could be dangerous enough to humans in its wild form.

Poison turned medicine turned poison again

PCR amplification of DNA fragments, followed by sequencing (reading out the genetic spelling) of those fragments, plumbs far deeper than microscopy. It allows a researcher to see below the level of cellular structure to the letter-by-letter genetic code.

Why PCR testing is better

In the RNA molecule, which serves for translating DNA into proteins (and has other roles, as we’ll see), a different piece called uracil substitutes for thymine, and the Scrabble pieces are therefore A, C, G, and U.

RNA has Uracine instead of Thymine

Her husband pulled down a box and opened it. “This is our collection of blood spots,” he said with quiet pride. Borneo is off the beaten path and, I suppose, not many science journalists visit. Inside the box was a neat file of plastic envelopes, each one containing a piece of porous paper no bigger than a business card; on each card was a rusty black spot. Near the center of the dark spot, on the card I inspected closely, was a perfectly round little hole. The punched dot, missing there, had already surrendered its secrets to science. DNA confetti.

Loved this XD

Plasmodium knowlesi malaria, they wrote, is not a new emergent infection of humans. It has been getting into people for some while but it was overlooked. Three kinds of Asian primate serve as its reservoir hosts: the long-tailed macaque, the pig-tailed macaque, and the banded leaf monkey. Other monkeys, still unidentified, might be harboring the parasite too. Transmission from monkey to monkey (and from monkey to human) occurs by way of mosquitoes belonging to one group of closely related species, Anopheles leucosphyrus and its cousins, including Anopheles latens in Borneo. Anopheles latens is a forest-dwelling mosquito accustomed to biting macaques, but it will bite humans too, if presented with the necessity and the opportunity. As humans have increasingly entered the Bornean forests—killing and displacing macaques, cutting timber, setting fires, creating massive oil-palm plantations and small family farm plots, presenting themselves as an alternative host—both the necessity and the opportunity have increased. (Borneo has been deforested at a high rate within recent decades, to the point that its forest coverage is now less than 50 percent; meanwhile the island’s human population has grown to about 16 million.

Greed shall bring us down

the level of human jeopardy depends on other factors besides the geographical ranges of the mosquitoes and the monkeys. It depends on whether those mosquitoes come out of the forest to bite humans, and whether people go into the forest to be bitten. It depends on whether sizable expanses of forest are left standing within that region and, if not, how the mosquitoes react. As deforestation proceeds, do the forest mosquitoes go extinct, or do they adapt? It depends on whether the parasite becomes so well established within human populations that monkey hosts are no longer necessary. It depends on whether the parasite colonizes a new vector, achieving transmission via some other kind of mosquito—members of a species more willing to seek out humans in their longhouses, their villages, their cities. In other words, it depends on chance and ecology and evolution.

Two aspects of what made SARS so threatening were its degree of infectiousness—especially within contexts of medical care—and its lethality, which was much higher than in familiar forms of pneumonia. Another ominous trait was that the new bug, whatever it might be, seemed so very good at riding airplanes.

Novel coronavirus: "Hold my beer"

Snake on the menu wasn’t unusual in Guangdong. It’s a province of ravenous, unsqueamish carnivores, where the list of animals considered delectable could be mistaken for the inventory of a pet store or a zoo.

Symptoms included headache, high fever, chills, body aches, severe and persistent coughing, coughing up bloody phlegm, and progressive destruction of the lungs, which tended to stiffen and fill with fluid, causing oxygen deprivation that in some cases led to organ failure and death.

SARS symptoms

While R0 (that important variable introduced to disease mathematics by George MacDonald) represents the average number of secondary infections caused by each primary infection at the start of an outbreak, a superspreader is someone who dramatically exceeds the average. The presence of a superspreader in the mix, therefore, is a crucial factor in practical terms that might be overlooked by the usual math. “Population estimates of R0 can obscure5 considerable individual variation in infectiousness,” according to J. O. Lloyd-Smith and several colleagues, writing in the journal Nature, “as highlighted during the global emergence of severe acute respiratory syndrome (SARS) by numerous ‘superspreading events’ in which certain individuals infected unusually large numbers of secondary cases.” Typhoid Mary was a legendary superspreader. The significance of the concept, Lloyd-Smith and his coauthors noted, is that if superspreaders exist and can be identified during a disease outbreak, then control measures should be targeted at isolating those individuals, rather than applied more broadly and diffusely across an entire population. Conversely, if you quarantine forty-nine infectious patients but miss one, and that one is a superspreader, your control efforts have failed and you face an epidemic.

On superspreaders

Back in Singapore, health officials and government authorities cooperated to stanch further transmission. They enacted firm measures that reached far beyond the hospitals—such as enforced quarantine of possible cases, jail time and fines for quarantine breakers, closure of a large public market, school closures, daily temperature checks for cab drivers—and the outbreak was brought to an end. Singapore is an atypical city, firmly governed and orderly (that’s putting it politely), therefore especially capable of dealing with an atypical pneumonia, even one so menacing as this. On May 20, 2003, eleven people were taken to court and fined $300 each for spitting.

the culturing work had established that an unknown coronavirus was present in SARS patients—some of them, anyway—but that didn’t necessarily mean it had caused the disease. To establish causality, Peiris’s team tested blood serum from SARS patients (because it would contain antibodies) against the newfound virus in culture. This was like splashing holy water at a witch. The antibodies recognized the virus and reacted strongly. Less than a month later, based on that evidence plus other confirming tests, Malik Peiris and his colleagues published a paper cautiously announcing this new coronavirus as “a possible cause”9 of SARS.

Just the presence of the virus doesn't prove causality

SARS-CoV has no ominous ring. In older days, the new agent would have received a more vivid, geographical moniker such as Foshan virus or Guangzhou virus, and people would have run around saying: Watch out, he’s got Guangzhou! But by 2003 everyone recognized that such labeling would be invidious, unwelcome, and bad for tourism.

Smart

IN A CROWDED country with 1.3 billion hungry citizens, it should be no surprise that people eat snake. It should be no surprise that there are Cantonese recipes for dog. Stir-fried cat, in such a context, seems sadly inevitable rather than shocking. But the civet cat (Paguma larvata) is not really a cat. More accurately known as the masked palm civet, it’s a member of the viverrid family, which includes the mongooses. The culinary trade in such unusual wild animals, especially within the Pearl River Delta, has less to do with limited resources, dire necessity, and ancient traditions than with booming commerce and relatively recent fashions in conspicuous consumption. Close observers of Chinese culture call it the Era of Wild Flavor. One of those observers is Karl Taro Greenfeld, who served as editor of Time Asia in Hong Kong during 2003, oversaw the magazine’s coverage of SARS, and soon afterward wrote a book about it, China Syndrome. Before his editing role, Greenfeld had covered “the new Asia” as a journalist for some years, giving him opportunity to see what people were putting in their stomachs. According to him: Southern Chinese have always noshed more widely11 through the animal kingdom than virtually any other peoples on earth. During the Era of Wild Flavor, the range, scope, and amount of wild animal cuisine consumed would increase to include virtually every species on land, sea, or air.

The Era of Wild Flavor

Li’s focused specifically on bats. The team trapped animals from the wild, drew blood, took fecal and throat swabs, and then analyzed duplicate samples of the material independently at labs in China and Australia, creating a double-check on themselves that strengthened the certitude of their results. What they found was a coronavirus that, unlike Leo Poon’s, closely resembled SARS-CoV as seen in human patients. They called it SARS-like coronavirus. Their sampling showed that this SARS-like virus was especially prevalent in several bats belonging to the genus Rhinolophus, known commonly as horseshoe bats. Horseshoe bats are delicate little creatures with large ears and flanged, opened-out noses that, homely but practical, seem to play a role in directing their ultrasonic squeaks. They roost mainly in caves, of which southern China has an abundance; they emerge at night to feed on moths and other insects. The genus is diverse, encompassing about seventy species. Li’s study showed bats of three species in particular carrying SARS-like virus: the big-eared horseshoe bat, the least horseshoe bat, and Pearson’s horseshoe bat. If you ever notice these animals on the menu of a restaurant in southern China, you might want to choose the noodles instead.

SARS-CoV2?