The terrifying track of how one ‘super-spreader’ was responsible for nearly half of MERS cases in South Korea

South Korean elementary school students wear masks as a precaution against the Middle East Respiratory Syndrome (MERS) virus as they go to school in Seoul in 2015. (Ahn Young-joon/AP) The outbreak of Middle East Respiratory Syndrome (MERS) in the huge megalopolis of Seoul from May to July last year was among the most chilling examples of how fast infectious diseases can spread in our modern world. From a single businessman who acquired the virus abroad, the disease jumped rapidly from person to person until 36 were dead, 186 infected and thousands were quarantined -- leaving huge swaths of the South Korean capital region, where 25 million people live, paralyzed with fear. Schools closed, department store sales tanked, and tourist visas were canceled. The economic toll was so severe that the country's central bank had to cut interest rates. First identified in Saudi Arabia in 2012, MERS has since made its way around the world and infected people in 27 countries. The illness is severe, with patients developing fever, cough and respiratory distress. The death rate is believed to be more than 30 percent. Both men first were seen at Pyeongtaek St. Mary's Hospital, a regional facility that had opened months earlier, for what appeared at the time to be pneumonia. They were treated on the same floor, according to health investigators. Both recovered enough to be released. When their conditions worsened, Patient 1 and Patient 14 separately sought help at one of Seoul's premier health centers -- the Samsung Medical Center, a massive university-affiliated hospital with 1,982 beds and a staff of 9,000. Patient 14's story at Samsung began when he arrived in the emergency department and was treated for breathing problems. He was given a mask, the authors note, but "frequently could not hold it because of severe respiratory symptoms." At the time, doctors did not suspect he had been exposed to MERS, so he was not isolated. But two days later, he was contacted by Korean health authorities about his potential contact with Patient 1. (The Lancet) The potential damage was estimated to be vast. A total of 1,576 people -- 675 patients, 683 visitors and 218 health-care workers -- were identified as contacts. And testing confirmed doctors' worst fears. The attack rate of the virus, calculated by dividing the number of people infected by the number exposed, was extremely high and caused an "epidemic curve" of cases.

South Korean elementary school students wear masks as a precaution against the Middle East Respiratory Syndrome (MERS) virus as they go to school in Seoul in 2015. (Ahn Young-joon/AP)
The outbreak of Middle East Respiratory Syndrome (MERS) in the huge megalopolis of Seoul from May to July last year was among the most chilling examples of how fast infectious diseases can spread in our modern world. From a single businessman who acquired the virus abroad, the disease jumped rapidly from person to person until 36 were dead, 186 infected and thousands were quarantined -- leaving huge swaths of the South Korean capital region, where 25 million people live, paralyzed with fear.
Schools closed, department store sales tanked, and tourist visas were canceled. The economic toll was so severe that the country's central bank had to cut interest rates.
Now, doctors involved in the care of the first patients have gone back and documented in exacting detail the geography of MERS as it spread in one hospital. In a paper published Friday in the journal the Lancet, Sun Young Cho and colleagues reconstructed the transmission of the virus through a series of maps, tables and diagrams that would have made Michael Crichton shudder.
First identified in Saudi Arabia in 2012, MERS has since made its way around the world and infected people in 27 countries. The illness is severe, with patients developing fever, cough and respiratory distress. The death rate is believed to be more than 30 percent.
One of the most revealing details in the analysis is its finding that the traveler, dubbed Patient 1, wasn't the "super-spreader" as previously thought. Patient 1, who was 68, transmitted the virus to another man early in his illness and before he knew he had MERS. It was this other man, 35-year-old Patient 14, who exposed so many others.
Both men first were seen at Pyeongtaek St. Mary's Hospital, a regional facility that had opened months earlier, for what appeared at the time to be pneumonia. They were treated on the same floor, according to health investigators. Both recovered enough to be released.
When their conditions worsened, Patient 1 and Patient 14 separately sought help at one of Seoul's premier health centers -- the Samsung Medical Center, a massive university-affiliated hospital with 1,982 beds and a staff of 9,000.
Patient 14's story at Samsung began when he arrived in the emergency department and was treated for breathing problems. He was given a mask, the authors note, but "frequently could not hold it because of severe respiratory symptoms." At the time, doctors did not suspect he had been exposed to MERS, so he was not isolated. But two days later, he was contacted by Korean health authorities about his potential contact with Patient 1.
After Patient 14's infection was confirmed, Samsung officials combed through electronic medical records and security video footage to map where he had been. The investigation showed the man was treated in three "zones" of the emergency department, went to the radiology suite four times, walked around both within and outside the ER and went to the bathroom several times. In the map below, Patient 14 was in zones II, III and IV, the registration area, radiology suite and presumably the hallways.
(The Lancet)
The potential damage was estimated to be vast. A total of 1,576 people -- 675 patients, 683 visitors and 218 health-care workers -- were identified as contacts. And testing confirmed doctors' worst fears. The attack rate of the virus, calculated by dividing the number of people infected by the number exposed, was extremely high and caused an "epidemic curve" of cases.
For the purposes of analysis, the researchers divided the patients into three risk groups. Those in Group A, considered close contacts, had been in the same zone of the emergency room as Patient 14. (Close contact with an infectious patient is traditionally defined as within six feet or within the same room or area for a prolonged period.) Group B consisted of people who were treated in different zones but had overlapped with Patient 14 in the registration area or radiology suite. Group C included patients who were treated in different zones and did not otherwise directly overlap with Patient 14 in space or time in any specific location.
The overall attack rate for patients and visitors was only 2 percent in Group C (15 of 1,003) and 5 percent in Group B (six of 116). But for Group A it was incredibly high at 20 percent (47 of 239). The rate of infection for health-care workers was also just 2 percent (five of 218).
A timeline of infections is shown below. Those in Group A are in shown as dark grey-blue squares.
(The Lancet)
The analysis turned up other worrisome details about the virulence of the virus: Several patients in the emergency department got MERS although Patient 14's bed was not adjacent to theirs. In one case, it was about 20 feet away. And numerous visitors accompanying loved ones in the emergency department were also infected. As for the incubation period, it averaged seven days, but patients in closest proximity to Patient 14 appeared to get the virus faster -- within five days -- while those farther away did not develop symptoms for 11 days on average.
In total, Patient 14 was linked to 82 MERS cases, or nearly 45 percent of the 186 cases seen in South Korea during the outbreak.
(The Lancet)
By contrast, researchers found that Patient 1 had been in contact with 285 other patients and 193 health-care workers while at the medical center. No transmissions occurred on the day that he was in the general ward before being isolated. (Patient 1 infected 28 others at his previous hospital.)
The researchers could not explain the difference but suggested it could have been due to "a number of factors such as time from onset of disease, symptoms, duration of contact, pattern of movement and the spread of the virus itself."
They found that individuals who overlapped with Patient 14 in the radiology suite or registration area had higher attack rates (5 percent) than the other patients (1 percent), "suggesting that transmission might occur by even brief exposures to recently contaminated objects or encounters with individuals carrying a super-spreader."
The role of super-spreaders was also critically important during the 2002-2004 SARS outbreak in Hong Kong and the bordering Chinese province of Guangdong.
In an accompanying commentary, David S. Hui, a professsor of emerging infectious diseases at the Chinese University of Hong Kong, wrote that the retrospective analysis highlights shortcomings in hospital systems worldwide. He noted the failure of St. Mary's to implement strict isolation of patients and quarantine of contacts as well as both facilities' poor communication and knowledge of patient movement between hospitals. More generally, he highlighted emergency department overcrowding, inadequate ventilation and limited availability of isolation rooms as issues needing to be addressed to prevent future outbreaks.
"Failure in infection control and prevention in health-care facilities has resulted in large numbers of secondary cases of [MERS] infection involving health-care workers, existing patients and visitors in Saudi Arabia and several other countries in the past few years," Hui said.
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COVID-19 variants appear to transmit faster and are fueling outbreaks from the U.K. to South Africa. The U.K. variant of the COVID-19 virus, which contains 17 mutations, appears to be a more highly transmissible form of the virus and is showing up in at least 19 countries around the world.  The South Africa variant is being seen in 4 other countries. Both variants seem to be more contagious but there is no evidence that they cause more severe illness. Documents that discuss long-covid or the flu are irrelevant.

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Doctors keep discovering new ways the coronavirus attacks the body

Deborah Coughlin was neither short of breath nor coughing. In those first days after she became infected by the novel coronavirus, her fever never spiked above 100 degrees. It was vomiting and diarrhea that brought her to a Hartford, Conn., emergency room on May 1.
“You would have thought it was a stomach virus,” said her daughter, Catherina Coleman. “She was talking and walking and completely coherent.”
But even as Coughlin, 67, chatted with her daughters on her cellphone, the oxygen level in her blood dropped so low that most patients would be near death. She is on a ventilator and in critical condition at St. Francis Hospital, one more patient with a strange constellation of symptoms that physicians are racing to recognize, explain and treat.
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Today, there is widespread recognition that the novel coronavirus is far more unpredictable than a simple respiratory virus. Often it attacks the lungs, but it can also strike anywhere from the brain to the toes. Many doctors are focused on treating the inflammatory reactions it triggers and its capacity to cause blood clots, even as they struggle to help patients breathe.
They have little solid research to guide them as they learn on the fly about a new disease with more than 78,000 U.S. deaths attributed to it. The World Health Organization’s database already lists more than 14,600 papers on covid-19. Even the world’s premier public health agencies, including the Centers for Disease Control and Prevention, have constantly altered their advice to keep pace with new developments.
“We don’t know why there are so many disease presentations,” said Angela Rasmussen, a virologist at the Center for Infection and Immunity at Columbia University’s Mailman School of Public Health. “Bottom line, this is just so new that there’s a lot we don’t know.”
More than four months of clinical experience across Asia, Europe and North America has shown the pathogen does much more than invade the lungs. “No one was expecting a disease that would not fit the pattern of pneumonia and respiratory illness,” said David Reich, a cardiac anesthesiologist and president of Mount Sinai Hospital in New York City.
It attacks the heart
It can begin with a few symptoms or none at all, then days later, squeeze the air out of the lungs without warning. It picks on the elderly, people weakened by previous disease, and, disproportionately, the obese. It harms men more than women, but there are also signs it complicates pregnancies.
It mostly spares the young. Until it doesn’t: Last week, doctors warned of a rare inflammatory reaction with cardiac complications among children that may be connected to the virus. On Friday, New York Gov. Andrew M. Cuomo (D) announced 73 children had fallen severely ill in the state and a 5-year-old boy in New York City had become the first child to die of the syndrome. Two more children had succumbed as of Saturday.
That news has shaken many doctors, who felt they were finally grasping the full dimensions of the disease in adults. “We were all thinking this is a disease that kills old people, not kids,” Reich said.
Mount Sinai has treated five children with the condition. Reich said each started with gastrointestinal symptoms, which turned into inflammatory complications that caused very low blood pressure and expanded their blood vessels. This led to heart failure in the case of the first child who died.
“The pattern of disease was different than anything else with covid,” he said.
Of the millions, perhaps billions, of coronaviruses, six were previously known to infect humans.
Four cause colds that spread easily each winter, barely noticed. Another was responsible for the outbreak of severe acute respiratory syndrome that killed 774 people in 2003. Yet another sparked the outbreak of Middle East respiratory syndrome in 2012, which kills 34 percent of the people who contract it. But few do.
SARS-CoV-2, the bad seed of the coronavirus family, is the seventh. It has managed to combine the infectiousness of its cold-causing cousins with some of the lethality of SARS and MERS. It can spread before people show symptoms of disease, making it difficult to control, especially without widespread and accurate testing. At the moment, social distancing is the only effective countermeasure.
It has infected 4 million people around the globe, killing more than 280,000, according to the Johns Hopkins University Coronavirus Resource Center. In the United States, 1.3 million have been infected and more than 78,000 have died.
Had SARS or MERS spread as widely as this virus, Rasmussen said, they might have shown the same capacity to attack beyond the lungs. But they were snuffed out quickly, leaving only a small sample of disease and death.
Trying to define a pathogen in the midst of an ever-spreading epidemic is fraught with difficulties. Experts say it will be years until it is understood how the disease damages organs and how medications, genetics, diets, lifestyles and distancing impact its course.
“This is a virus that literally did not exist in humans six months ago,” said Geoffrey Barnes, an assistant professor at the University of Michigan who works in cardiovascular medicine. “We had to rapidly learn how this virus impacts the human body and identify ways to treat it literally in a time-scale of weeks. With many other diseases, we have had decades.”
In the initial days of the outbreak, most efforts focused on the lungs. SARS-CoV-2 infects both the upper and lower respiratory tracts, eventually working its way deep into the lungs, filling tiny air sacs with cells and fluid that choke off the flow of oxygen.
But many scientists have come to believe that much of the disease’s devastation comes from two intertwined causes.
The first is the harm the virus wreaks on blood vessels, leading to clots that can range from microscopic to sizable. Patients have suffered strokes and pulmonary emboli as clots break loose and travel to the brain and lungs. A study in the Lancet, a British medical journal, showed this may be because the virus directly targets the endothelial cells that line blood vessels.
The second is an exaggerated response from the body’s own immune system, a storm of killer “cytokines” that attack the body’s own cells along with the virus as it seeks to defend the body from an invader.
Research and therapies are focused on these phenomena. Blood thinners are being more widely used in some hospitals. A review of records for 2,733 patients, published Wednesday in the Journal of the American College of Cardiology, indicates they may help the most seriously ill.
“Things change in science all the time. Theories are made and thrown out. Hypotheses are tweaked. It doesn’t mean we don’t know what we are doing. It means we are learning,” said Deepak Bhatt, executive director of interventional cardiology at Brigham and Women’s Hospital in Boston.
Inflammation of those endothelial cells lining blood vessels may help explain why the virus harms so many parts of the body, said Mandeep Mehra, a professor of medicine at Harvard Medical School and one of the authors of the Lancet study on how covid-19 attacks blood vessels.
That means defeating covid-19 will require more than antiviral therapy, he said.
“What this virus does is it starts as a viral infection and becomes a more global disturbance to the immune system and blood vessels — and what kills is exactly that,” Mehra said. “Our hypothesis is that covid-19 begins as a respiratory virus and kills as a cardiovascular virus.”
The thinking of kidney specialists has evolved along similar lines. Initially, they attributed widespread and severe kidney disease to the damage caused by ventilators and certain medications given to intensive-care patients, said Daniel Batlle, a professor of medicine at Northwestern University Feinberg School of Medicine.
Then they noticed damage to the waste-filtering kidney cells of patients even before they needed intensive care. And studies out of Wuhan found the pathogen in the kidneys themselves, leading to speculation the virus is harming the organ.
“There was nothing unique at first,” Batlle said. But the new information “shows this is beyond the regular bread-and-butter acute kidney injury that we normally see.”
Like other coronaviruses, SARS-Cov-2 infiltrates the body by attaching to a receptor, ACE2, found on some cells. But the makeup of the spikes that protrude from this virus is somewhat different, allowing the virus to bind more tightly. As a result, fewer virus particles are required to infect the host. This also may help explain why this virus is so much more infectious than SARS, Rasmussen said.
Other factors can’t be ruled out in transmission, she said, including the amount of virus people shed and how strictly they observe social distancing rules.
Once inside a cell, the virus replicates, causing chaos. ACE2 receptors, which help regulate blood pressure, are plentiful in the lungs, kidneys and intestines — organs hit hard by the pathogen in many patients. That also may be why high blood pressure has emerged as one of the most common preexisting conditions in people who become severely ill with covid-19.
The receptors differ from person to person, leading to speculation that genetics may explain some of the variability in symptoms and how sick some people become.
Those cells “are almost everywhere, so it makes sense that the virus would cause damage throughout the body,” said Mitchell Elkind, a professor of neurology at Columbia University’s College of Physicians and Surgeons and president-elect of the American Heart Association.
Inflammation spurs clotting as white blood cells fight off infection. They interact with platelets and activate them in a way that increases the likelihood of clotting, Elkind said.
Such reactions have been seen in severe infections, such as sepsis. But for covid-19, he said, “we are seeing this in a large number of people in a very short time, so it really stands out.”
“The virus can attack a lot of different parts of the body, and we don’t understand why it causes some problems for some people, different problems for others — and no problems at all for a large proportion,” Elkind said.
Coughlin, in critical condition at a hospital in Connecticut, deteriorated quickly after she reached the emergency room. Her fever shot up to 105, and pneumonia developed in her lungs.
On Wednesday, she called her six daughters on FaceTime, telling them doctors advised she go on a ventilator.
“If something happens to me, and I don’t make it, I’m at peace with it,” she told them.
The conversation broke daughter Coleman’s heart.
“I am deciding to help her go on a ventilator, and she may never come off,” she said. “That could have been my last phone conversation with her.”
Illustrations from iStock. Edited by
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What you need to know about coronavirus

What you need to know about coronavirus

Planning to travel? Here’s what to know. Mapping the spread of coronavirus Read more about the illness here. Read more about how long social distancing might last here. Coronavirus: Covid-19: Community transmission: Asymptomatic transmission: Outbreak: Epidemic: Pandemic: “ Containment: Mitigation: Isolation: Quarantine: Zoonotic:

What began with a handful of mysterious illnesses in a central China city has traveled the world. First detected on the last day of 2019, the novel coronavirus has killed more than 705,000 people with infections surpassing 18 million worldwide. It has triggered nationwide lockdowns, stock market upheaval and dangerous conspiracy theories.
Most cases are mild, but health officials say much is still unknown about the virus that causes the disease covid-19.
The Washington Post has spoken to scores of doctors, officials and experts to answer as many of your questions as we can about the newest global health emergency. Here’s what we know so far.
Sign up for our Coronavirus Updates newsletter to track the outbreak. All stories linked within the newsletter are free to access.
These days, “coronavirus” is often prefaced with the word “novel,” because that’s precisely what it is: a new strain in a family of viruses we’ve all seen before — and, in some form, had. According to the WHO, coronaviruses are a large family of viruses that range from the common cold to much more serious diseases. These diseases can infect both humans and animals. The strain that began spreading in Wuhan, the capital of China’s Hubei province, is related to two other coronaviruses that have caused major outbreaks in recent years: severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS).
Symptoms of a coronavirus infection range in severity from respiratory problems to cases of pneumonia, kidney failure and a buildup of fluid in the lungs. They may appear 2 to 14 days after exposure to the virus.
In April, the CDC added new symptoms of the disease to its list, shedding more light on how the virus infects patients. The symptoms now include: a cough, shortness of breath, fever, chills, repeated shaking with chills, muscle pain, headache, sore throat and a loss of taste or smell.
Covid-19 spreads more easily than SARS and is similar to other coronaviruses that cause cold-like symptoms, experts have said. It appears to be highly transmissible, and since cases are mild, the disease may be more widespread than current testing numbers suggest.
Read more about coronaviruses, their symptoms and how they are spread here.
Why outbreaks like coronavirus spread exponentially, and how to “flatten the curve”
Public health officials say the novel coronavirus is less deadly than SARS, which killed about 10 percent of people who were infected during the outbreak that began in 2002. But epidemiologists are still trying to determine exactly how deadly covid-19 is.
Similar to other respiratory illnesses, older people and those with illnesses such as diabetes and high blood pressure are at increased risk. Data show that the virus is killing more men than women in the U.S.
But, as with other diseases, there can be tremendous individual variation in how people respond. There will be people with known risk factors who recover as well as people who develop severe cases for reasons we don’t understand.
There’s also no evidence that children are more prone to contracting covid-19, according to the CDC, and that was also the case with the disease′s cousins, SARS and MERS.
Read more about the deadliness of coronavirus here.
The coronavirus primarily spreads from person to person and not easily from a contaminated surface. In updated guidance issued in late-May, the CDC said the virus spreads “easily and sustainably” between people. The agency added that contaminated objects, surfaces and infected animals do not appear to be significant modes of transmission.
The virus travels through the droplets a person produces when talking or coughing, the CDC website says. An individual does not need to feel sick or show symptoms to spread it.
Read more about how the coronavirus spreads here.
Planning to travel? Here’s what to know.
There are some basic precautions you can take, which are the same as what you should be doing every day to stave off other respiratory diseases. You’ve seen the guidance before: Wash your hands regularly. Cover your nose and mouth when you sneeze. And when you’re sick, stay home from work or school and drink lots of fluids.
The CDC recommends washing with soap and water for at least 20 seconds after using the bathroom, before eating and after blowing your nose or sneezing. It also advises not to touch your eyes, nose and mouth and to clean objects and surfaces you touch often.
Read more about preparing for coronavirus here.
Mapping the spread of coronavirus
Symptoms are primarily respiratory. Coughing and shortness of breath are common, according to the CDC. Fever is also possible. The severity of the symptoms depends highly on the patient’s age and immune system.
For the elderly and those with underlying heart disease, diabetes or other conditions, coronavirus can cause pneumonia and lead to organ failure and death. But for most people, cases have been mild, requiring little to no medical intervention.
Read more about one man’s experience with coronavirus here.
Kawasaki disease is an inflammatory disease affecting children. In May, doctors identified a syndrome similar to Kawasaki that appeared to be triggered by covid-19. When the puzzling connection first emerged, public health warnings focused on young patients, who have suffered symptoms that look more like traditional Kawasaki, which is characterized by inflammation of the blood vessels.
But in the weeks that followed, some doctors said they began to see the illness in young adults and teens, who have more of an “overwhelming” response involving the heart and multiple organs.
The syndrome appears to be rare, but the Centers for Disease Control and Prevention — which recently dubbed the condition MIS-C or multisystem inflammatory syndrome in children — has expressed alarm about the rapid decline of patients with the illness. The health agency and major medical groups have urged parents to seek an urgent evaluation if they suspect their child may have the condition.
Read more about the illness here.
It is a good idea to call your primary-care doctor if you have both a fever and a cough, experts said. And if you have shortness of breath, unremitting fever, weakness or lethargy, it’s definitely time to get in touch with a health-care professional, they say. Those could be signs of pneumonia, which is common in severe cases of coronavirus.
The Centers for Disease Control and Prevention also recommends that you seek medical help if you recently traveled to a coronavirus-infected area or had close contact with a known infected person and have a fever, a cough or trouble breathing.
Read more about seeking medical help and getting tested here.
If you have mild symptoms, you probably won’t be. If you are sick enough to be hospitalized, you’ll likely get tested. If you are in the middle group, it’s unclear.
And even as more tests are being manufactured and shipped around the country, many public health labs receiving them don’t have enough staff or equipment to meet the testing need. Some medical centers are  offering their own tests, and some primary care doctors are exploring how to administer the tests in their offices, but many are reluctant because it carries risks for their staff and other patients.
Other hospitals and localities are setting up testing locations away from emergency rooms, clinics and doctors’ offices to minimize the risk of health care workers and other patients being infected. And, in declaring a national emergency, Trump said the administration will work with retailers like Walmart and Target to develop drive-through testing clinics across the country.
Read more about how testing in the U.S. is working here.
The most honest answer, according to experts, is: “It depends.” It’s not going to be over anytime soon — a matter of months rather than weeks. And a few key factors will determine just how many months.
First, it depends on when U.S. cases finally reach their peak — a time that’s impossible to predict because of how limited testing remains in America. And even after the peak, we may need drastic actions to keep the virus at bay. It also depends on how the virus behaves, and whether it’ll be affected by the change of seasons like the flu.
But, ultimately, how well America is able to flatten and bend its epidemiological curve of infections depends largely on how willing people will be to sacrifice individual conveniences and on their desire to save the lives of others.
“I don’t know if people are ready now for how long they’re probably going to have to keep up this social distancing," said Natalie Dean, a biostatistician at the University of Florida. "But as they see the hospital situation get more extreme, I think that attitude will change.”
Read more about how long social distancing might last here.
This depends on where you live. Almost all states issued a sweeping directive, but in some places, cities and counties enacted their own measures. In all, 315 million Americans were affected. Most orders allowed residents to leave their homes to shop for groceries and other essentials, to exercise outdoors, to go to the doctor and to pick up prescriptions. But each jurisdiction had its own list of do’s and don’ts.
Georgia, Tennessee and Florida were among the first states to begin lifting restrictions — a move that experts and math models say will almost certainly lead to more infections and deaths. Other places, like New York City and California, have taken a more cautious approach. The Post is keeping track of how states reopen.
Read more about the stay-at-home order in your state here.
President Trump announced new guidance in April that people in the U.S. wear face coverings in public to slow the spread of the coronavirus, a reversal of the administration’s earlier recommendations.
The guidance makes clear that wearing face coverings or cloth masks is an additional public health measure to prevent the spread of the virus, not a substitute for social distancing. Social distancing of at least six feet is still recommended even when wearing a mask. Guidance and internal memos from CDC emphasize that a cloth facial mask is intended not so much to protect the wearer but to help prevent people who do not know they are infected from spreading of the virus to others.
The new CDC guidance was prompted by increasing evidence that infected people without symptoms can spread the coronavirus. Simple cloth masks that cover the mouth and nose can prevent virus transmission from such individuals when they are out buying groceries, where people may come into closer contact, for example.
This coronavirus could follow a seasonal pattern, peaking in the winter months. It could infect lots of people now and then recede in the Northern Hemisphere before returning in the fall.
“This virus can do anything it wants,” said Allison McGeer, an infectious-disease epidemiologist at the University of Toronto. “That pattern of how it’s going to spread is completely unknown, but it is critical to what the burden is going to be to all of us. … It could be just like another coronavirus, a bunch of colds. It could be like a regular flu season. It’s possible it could be different and worse.”
Coronavirus:
Covid-19:
Community transmission:
Asymptomatic transmission:
Outbreak:
Epidemic:
Pandemic:
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Containment:
Mitigation:
Isolation:
Quarantine:
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Read more about these terms here.


The code: How genetic science helped expose a secret coronavirus outbreak

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POSTVILLE, Iowa — It wasn’t until their colleagues began to disappear that workers at Agri Star Meat and Poultry realized there was a killer in their midst.
First came the rumors that rabbis at the kosher plant had been quarantined. Then a man who worked in the poultry department fell ill. They heard whispers about friends of friends who had been stricken with scorching fevers and unbearable chills — characteristic symptoms of the novel coronavirus.
Where was the contagion coming from?
No one would say. Not Agri Star’s wealthy owner, who didn’t shut down production lines after cases were confirmed among workers. Not the Iowa Occupational Safety and Health Administration, which closed a complaint containing multiple allegations against the plant without an inspection. Not Iowa Gov. Kim Reynolds (R), whose administration threatened to prosecute officials who released covid data and did not conduct testing at the plant until seven weeks after the first infections.
The mystery terrified Magdalena Toj García, a 36-year-old worker in the beef department who worried about bringing the virus home to her three young daughters. It infuriated John Ellingson, a council member in a nearby town desperate to know if his constituents were at risk.
But it intrigued Paraic Kenny, a tumor geneticist turned disease detective, who knew that the killer had left behind vital clues.
The coronavirus mutates as it moves through its victims. Infectious particles swabbed from a patient’s nose carry small but distinctive differences in its genome that can be used, like a molecular bar code, to track where the virus came from and how it had been transmitted. By reading the virus’s RNA, Kenny could unveil how cases were connected to one another, exposing the secret spread of the disease.
The truth of what happened at Agri Star — and across America — is written in that code.
Small, stealthy and skilled at exploiting human vulnerabilities, the novel coronavirus seems tailor-made to wreak havoc on humanity. Its surface spikes fit as neatly as keys into the receptors that unlock our cells. It turns our organs into factories for its own reproduction, putting our molecular machinery to work building its proteins and transcribing its genome. In 24 hours it can fill a human’s respiratory tract with a trillion copies of itself.
And, with the cunning that comes from millennia of evolution, the virus exploits all of our most human habits. Traveling invisibly on the breath of its victims, it spreads most efficiently wherever we gather to work, to eat, to pray.
“It’s an amazing evolutionary machine dedicated to making more copies of itself,” Kenny said. “And it’s sadly very good at doing just that.”
A native of Ireland who still speaks in a soft brogue, he’d come to the Midwest by way of the Bronx after deciding he wanted to raise his son someplace more like home. For five years he has served as director of the Kabara Cancer Research Institute at the Gundersen Health System in La Crosse, Wis., practicing what he called “small town science.” He sequenced patients’ tumor genomes to determine what therapies would work for them and read journal articles to keep up with breakthroughs happening elsewhere.
But suddenly, this March, Gundersen’s rural health system was facing a disease no doctor had seen before. All nonessential labs, including Kenny’s, were shutting down.
“We were looking at this, you know, wondering: Is there something we can do with the expertise and equipment that we have?” Kenny said.
That’s when he turned to an emerging field called genomic epidemiology.
The coronavirus is far simpler than a living cell — little more than a protein capsule protecting a packet of genetic material.
The nearly 30,000 nucleotide “letters” of that genome convey all the information the virus needs to survive.
But every so often, perhaps every two weeks, the virus makes a mistake as it replicates, introducing a mutation to the code.
Once a mutation occurs, it will remain in the genome of the virus and all its future offspring — a clue that can reveal how the virus has spread.
These single-letter switches rarely change the way the virus behaves. But much the way shared features help a person recognize members of the same family, researchers use the mutations to group samples into virus “sub-strains.” Their findings can help decipher which infections are related to one another, exposing links invisible to traditional contact tracers.
Kenny wasn’t sure what he would find in the SARS-CoV-2 genome. But it would be information — objective evidence in a pandemic rife with obfuscation and uncertainty. He figured he had to try.
He converted his suddenly empty lab into a coronavirus sequencing facility. He ordered the chemicals and kits needed to study viral genomes, sought approval from Gundersen’s institutional review board to sequence samples taken from patients at the system’s hospital and clinics.
The first vials of virus arrived in early April, carried by courier in a cooler packed with ice. Sequencing them was a multistep operation that took the better part of 48 hours, but the data was more useful the faster it came in. To keep the process going, Kenny would drive to his darkened laboratory at odd hours of the night, carefully pipetting samples onto sequencing chips while the world around him slept.
When he at last had results in hand, Kenny uploaded each genome to a global database, then sorted the sequences into their spots on the coronavirus family tree. This allowed him to identify distinct sub-strains introduced to the region from outbreaks around the world.
Two sub-strains, found in La Crosse and Postville, shared a distinctive mutation, marking them as part of the same major lineage.
By the time the viruses arrived in the Midwest, they had acquired additional key mutations that Kenny could use to track each sub-strain.
Each virus variant acts as a spark; if it lands on poor kindling — say, someone who practices social distancing and is able to quarantine as soon as she realizes she is sick — it will soon die out. Most of the sub-strains Kenny sequenced, including the La Crosse variant, showed up only a few times in his data, suggesting these sparks were quickly extinguished.
But the Postville sub-strain — characterized by three distinctive mutations that have not been found in combination anywhere else in the world — appeared over and over again, picking up additional mutations along the way.
Kenny found 27 cases, mostly from Postville and the surrounding area.
“I thought, ‘Wow. This is a crazy, out-of-control situation,’ ” Kenny said. “The fact that they all . . . clustered together on this tree really indicated there was a single introduction to that region that really took hold and expanded.”
The scientist began to scour the documents that accompanied his virus samples. Though the tiny vials of virus had no names attached to them, they came with fairly detailed medical records. The patients ranged in age from 7 to 80. Their symptoms spanned from mild coughs and headaches to breathlessness and raging fever.
But most compelling was this: The majority of initial patients infected with this sub-strain worked at Agri Star or lived with someone who did.
Something had gone terribly wrong in Postville, Kenny realized. Something that provided fuel for a single virus spark to erupt into an inferno.
Magdalena Toj Garcia had worked at Agri Star for more than a decade. She went in six days a week to carve up carcasses and clean up spills, arriving before dawn and leaving long after dark. When she learned about the virus in March, she wanted one thing: a mask.
“No,” a supervisor told her. “We are only going to give them to the sick.”
“But that is precisely why I need a mask,” Toj insisted. “So I will not get sick.”
The answer was still no.
“That is a lie,” Agri Star owner Hershey Friedman said when asked about this incident. He said that all workers were required to wear masks in the facility.
Agri Star’s head of health, safety and human resources, Diane Guerrero, later clarified that in March the plant was following guidance from the Centers for Disease Control and Prevention that only sick people wear masks. The plant switched to universal mask use when the agency recommended it on April 3.
Both Friedman and Guerrero said the company undertook extensive efforts to protect its 575 workers. The plant plastered public health notices around the facility, doubled the number of hand sanitizer dispensers and installed barriers between workstations. A cadre of workers called “the Covid Crusaders” cleaned surfaces. Starting in early April, they began taking every employee’s temperature and asking them about their health before they entered.
If plant employees became infected, Friedman told The Post, it wasn’t while at work. “There was zero covid-19 in our facility,” he said.
Toj, and several of her colleagues who were diagnosed with the coronavirus, told a different story.
Agri Star confirmed Postville’s first coronavirus cases in mid-March, fracturing the uneasy peace among its diverse residents: the Orthodox Jews who help run the plant, the immigrants from Somalia, Mexico and Central America who make up much of its workforce, the White descendants of the German and Scandinavian farmers who founded the town generations ago.
Twelve years earlier, the plant had been the target of one of the largest Immigration and Customs Enforcement raids in history. The town rebounded after Friedman, a Canadian business magnate, bought the plant out of bankruptcy in 2009. But the effects of the raid are still felt in the way people mostly keep to their ethnic enclaves. Conversations about the coronavirus are held in hushed tones — when they are held at all.
“The problem was here, but people didn’t want to talk about it,” said one ranch worker, whose wife — an Agri Star employee — was hospitalized with covid-19 for more than a week.
Agri Star acknowledged three early cases connected to the plant in a brief statement in The Yeshiva World, an Orthodox Jewish online news publication. But Toj and her colleagues, many of whom speak little English, didn’t read the article. Though Guerrero said the company told supervisors to notify anyone who worked near someone who tested positive, six workers who got sick told The Post that no one from the plant warned them about their potential exposure or asked who else they might have infected. Workers said they were forced to triangulate their risk based on snatches of rumor and snippets of fact.
“They’re going to get us sick,” Toj would often say, “and they don’t even know it.”
The closest health clinic to Postville had so few covid-19 tests that many residents were sent to Gundersen’s main hospital in La Crosse, where Kenny worked, more than an hour away.
Agri Star should conduct its own testing, Toj told her husband, Rudy Pérez. If workers at least knew where the sickness was, they could protect themselves.
The company said it asked the state to test its workers on April 20, more than a month after it confirmed the first infections connected to the plant.
Before then, plant executives told employees to stay home if they had symptoms, Pérez said. That wasn’t much of an option for Agri Star’s low-wage employees, who, like about a quarter of all U.S. workers, have no paid sick leave. The emergency coronavirus legislation passed this March includes a requirement for paid sick leave, but it does not apply to businesses like Agri Star with more than 500 employees — even when workers are instructed to quarantine.
Toj took matters into her own hands, purchasing six face masks for herself and her husband. The couple would bathe as soon as they got home from work and drank mug after mug of hot tea with lemon, which they hoped would ward off disease.
On a Friday morning in early April, a plant supervisor instructed Toj, Pérez and several others to scrub down the offices, bathrooms and dining area used by the plant’s rabbis, who were not coming into work. It wasn’t until they finished that their supervisor asked if they had used protective equipment, Toj said.
One worker said she had been given a mask that day, but it became so soaked with blood from her work in the slaughterhouse that she had to take it off to breathe. Toj said she had been given no protection at all.
The company’s policy, Guerrero said, is to hand out gear to employees based on their daily assignment. As long as they describe where they’re headed, “everybody is issued the proper equipment,” she said. “Whether they choose to wear it or not is a concern.”
In the days after the cleaning, Toj recalled, “I really started feeling bad, bad, bad.” Though Guerrero said the plant required employees to report symptoms, Toj tried to push through her illness, worried that missing a shift could get her fired. But the virus was settling in her cells, fogging her head and flooding her with fatigue.
Finally, Toj felt her chest tighten until she couldn’t breathe. She rushed outside the plant, gasping for air.
“I’m scared,” she told her husband. “I am going to the hospital. I need to know if I have it.”
The diagnoses came for both of them two days later: positive.
Toj called a friend who had cleaned the rabbi’s rooms alongside her. Her friend had also been diagnosed with the virus; her husband was feverish and presumed positive. At least two other members of the cleaning crew tested positive, Toj said, and all the others showed symptoms.
Both women are convinced they contracted the virus at Agri Star. “We didn’t go anywhere else — from our house to work, from our house to work,” said Toj’s friend, who spoke on the condition anonymity out of fear for her job.
Toj sent her daughters to live with her mother while she and her husband fought off the virus. For three weeks, they were bedridden. And the bills kept piling up: rent, groceries, $300 for Toj’s chest x-ray. She looked over her scant belongings, trying to think of what to sell. She ran through a mental list of friends who might support them and called her boss at Agri Star to ask for financial assistance. Help never came.
The company says it has no record of Toj’s request.
Seventeen miles north of Postville, in the county seat of Waukon, city councilman John Ellingson could barely step out of his house in April without being bombarded with anxious questions.
“John, what do you know?” constituents would ask, at the grocery store or passing his table at the S&D Café on Main Street. “What’s going on?”
Like him, they had been tracking the unusually high case counts for their rural area; the county’s positivity rate was almost as high as Manhattan’s. Yet in a place as spread out as Allamakee, those cases could be next door, or about an hour away. It wasn’t enough to know that the virus was in the county, Ellingson said — people needed to know where.
But when the Republican councilman asked the state health department for a breakdown of infections in each of the county’s 18 townships, the state refused.
Officials claimed that would violate medical privacy law, even though many other states stratify case counts by Zip code. The state wouldn’t even tell Ellingson how many cases were in his own town. When he persisted, the department stopped returning his calls.
The numbers reported at the governor’s news conferences “were damn near worthless,” Ellingson said. “It was more a political show than it was informative to the citizens.”
And his constituents?
“They were pissed,” Ellingson said, “knowing the government had information and they weren’t giving it.”
In seeking what seemed like a simple answer to an obvious question, Ellingson ran into what scientists say is one of the biggest barriers to controlling the pandemic: a dire shortage of facts. There are few national standards for collecting and reporting case counts and hospitalizations. A review of outbreak data led by former CDC director Tom Frieden found that no state discloses even half of what health experts consider “15 essential indicators” for managing the disease.
As the government shifted its coronavirus reporting system, numbers have vanished from CDC Web pages. News organizations have had to sue for information about racial disparities in deaths. In many Florida counties, officials won’t tell parents whether there are coronavirus cases at their children’s schools.
Iowa is no exception. The state has refused to release its pandemic plan, which guides its response to the coronavirus, saying the document is “confidential." The health department’s covid-19 dashboard doesn’t list hospitalizations among health care workers or outbreaks in congregate facilities such as homeless shelters and prisons.
In July, state auditor Rob Sand said Iowa’s system for reporting test results was rife with “illegal and unbusinesslike practices, inefficiencies, and apparently pointless risks.” He criticized Iowa’s use of medical privacy laws to justify its secrecy.
“If you live in this town, you’re literally making decisions that affect your health,” Sand said. “And you have people like the state of Iowa and people like meatpacking companies that are falsely describing what the law allows them to do in order to shield the fact that they simply don’t want to share that information.”
By the time Ellingson launched his quest for data, Iowa officials had already received warnings about Agri Star. Weeks earlier, an anonymous worker had called the Iowa Occupational Safety and Health Administration (IOSHA), reporting that employees had been exposed to rabbis who had tested positive for the virus, one of whom was “deathly ill.” A few days later, a lawyer for Iowa Legal Aid told IOSHA that two Agri Star workers said the plant was unsafe. According to the April 3 complaint, released under a public records request from The Post, employees were working closely together and were not given protective equipment.
“Several employees are required to come to work ill,” the complaint said. “Management is telling workers that covid-19 is a lie and it has been made up by the government.”
IOSHA never visited the plant to investigate these claims; on-site inspections in Iowa have been curtailed during the pandemic. Instead, the agency asked Agri Star for a written response.
“Not everyone understands the value of our operations being open, but we can assure you we have taken precautions to ensure our employees are safe,” Guerrero wrote in an April 14 letter.
She denied all the allegations in the complaint and offered a long list of the measures she said the company had adopted: handwashing trainings, homemade masks. The complaint was closed.
Those early months of the pandemic were a scramble, Guerrero recalled. She’d never handled a health crisis like this — no one had — and the government provided little help. The Department of Labor and the CDC didn’t release guidance for meatpacking facilities until April 26. The Iowa health department rarely communicated with her about tracking new cases or tracing their contacts, leaving Guerrero to cobble together a spreadsheet of sick workers on her own. When she walked outside the plant, she said, it seemed as though the rest of the town wasn’t taking any precautions at all.
“Nobody was really able to guide us on how we should maneuver through this,” she said.
It wasn’t until May 5, more than seven weeks after the first Postville cases were diagnosed and 15 days after Agri Star requested help, that a state testing strike force finally came to the plant. Over 450 workers were tested for current and past infections.
Iowa did not make the results of that event public, and Guerrero said the state provided no interpretation when it sent the company its lab report.
The state’s policy, articulated by Department of Public Health deputy director Sarah Reisetter at a May 27 news conference, is to only disclose outbreaks in workplaces like meatpacking plants if 10 percent of employees test positive, and then only if specifically asked by a member of the media. (A nursing home is considered to have an outbreak once three people test positive.) The state declined The Post’s requests for Agri Star’s case data.
“We didn’t really provide any information about them at all,” Polly Carver-Kimm, a former spokeswoman for the Iowa health department, said of towns like Postville.
She said secrecy was the state’s unwritten rule. The governor’s communications director wouldn’t let her talk to the press without his approval, Carver-Kimm said. She believes she was retaliated against for doing her job: talking with reporters and releasing vital information about covid-19.
After 13 years on the job, Carver-Kimm resigned in July. This month she filed a wrongful termination lawsuit against Iowa, saying she was pressured to leave after pushing to make more covid-19 data available to the public.
Pat Garrett, communications director for Reynolds, declined to answer a detailed list of questions about the state’s response. He instead issued a brief statement, saying, “The state of Iowa worked to get testing to all meat processing facilities in Iowa. We regularly reported outbreaks at meat packing facilities if 10 percent of their workforce tested positive.”
After more than a month of effort, Ellingson finally got a hold of case numbers broken down by Zip code as of May 12: Postville had 87 of Allamakee’s 97 covid-19 infections.
Waukon had three.
The councilman posted the numbers on Facebook and told constituents he planned to update them every few days. But then he found out the county workers who had shared the data had been told they could be fined, fired, even imprisoned for violating medical privacy laws.
Ellingson stopped clamoring for data. The number of cases in Postville has not been released since.
Toj and Pérez spent three weeks battling the coronavirus. Their oldest daughter also apparently came down with the disease: The 14-year-old lost her sense of taste for several days.
Even more frightening was when Toj’s mother fell sick. She spent six days in the hospital, breathing oxygen through a tube. She recovered, Toj said, because God was protecting her. This whole time, God was the only one protecting them all.
Toj walked back into the plant for the first time in late April and encountered a changed Agri Star. All around the building, posters proclaimed the importance of hand washing. New workstations had been marked out on the floor to help people maintain social distance. Every employee was given a homemade mask.
“Now we need masks?” Toj asked, infuriated. “Six feet of distance — for what? Everybody is already infected because there were lots of people who got sick and they didn’t even notice."
But Kenny did. He kept a vast chart of the region’s coronavirus outbreak pinned to a cork board in his office in La Crosse. Tiny colored dots represented cases for which he had a genome. Thin lines connected them according to the mutations they shared.
Looking at the Postville cluster — more than two dozen yellow dots linked by three distinctive mutations — it was clear to him what happened. The sub-strain started with a single case. But in the crowded conditions of the meat processing plant, it exploded.
“A single viral introduction led to unrestrained spread within the facility,” Kenny wrote in a study on the website MedRxiv, where scientists post “preprint” research that has not yet been published in a peer-reviewed journal. His research, he said, showed “the collateral damage resulting from widespread dissemination of this disease from a meat-packing epicenter across a large midwestern region.”
Multiple lines of evidence put Agri Star at the epicenter of this outbreak, Kenny said. The fact that patients from across Postville’s diverse communities were infected with the same sub-strain — despite living, shopping and worshiping in different places — suggests they contracted the illness in the one setting they shared: the plant.
Also key was that Kenny found a husband and wife with “clearly genetically distinct” variants of the Postville sub-strain. Usually couples infect each other, so they carry identical versions of the virus. But these two had acquired their infections separately — most likely at the plant, where they both worked.
“I think one needs to jump through a lot of mental hoops to avoid the conclusion that the plant itself was a significant nexus for spread,” Kenny said.
Since Kenny’s results have not undergone peer review, The Post asked seven independent researchers to assess his findings. All agreed that Kenny had found evidence of a cluster of closely related cases, though some cautioned that broader and more representative sampling would strengthen his conclusions.
They also made a key point: While Kenny had clearly found a chain of genetically linked viruses in people who worked at or were connected to Agri Star, an analysis like his cannot definitively show how the virus got into the plant or exactly how individuals became infected. Those details may never be known.
Yet an explosion of genetically linked cases is exactly what scientists would expect from the conditions that workers described, said Bronwyn MacInnis, a virologist at the Broad Institute in Boston.
MacInnis, who has worked on genomic epidemiology investigations during outbreaks of Zika, malaria and now the coronavirus, noted that the vast majority of covid-19 cases are thought to be driven by “super-spreader” situations, where large groups gather in enclosed areas. Kenny’s data, she said, “show that was the case in this setting.”
Hoping he could help the government response, Kenny took his results to a coalition of local health departments, including Allamakee County officials. In other countries, genomic epidemiology has helped identify chains of transmission so officials could stop the coronavirus from spreading.
But few U.S. health departments have taken full advantage of the cutting-edge tool. As far as Kenny knows, no one from Allamakee County or the state of Iowa ever acted on his genetic evidence.
And the virus kept on spreading. Kenny identified the Postville sub-strain in patients from 15 cities across three states. A case was detected by researchers in Ecuador this July. According to Kenny, at least one person infected with the sub-strain has died.
Both Agri Star and Iowa knew many plant employees became sick, The Washington Post has found. The strike force testing of 463 workers in May found 12 active cases of covid-19 and at least 106 people with antibodies, which are evidence of past infection. Agri Star received lab results for a further 49 positive antibody tests, which Iowa did not report among the county’s case totals.
“That’s a lot of people who were positive for antibodies,” said Gigi Gronvall, an immunologist at Johns Hopkins University who is an expert on serology tests. The figures suggest “they had an outbreak and it went on for some time.”
It’s unclear why the state did not report the full number of positive antibody tests. But at least 20 percent and as many as 29 percent of Agri Star workers contracted the coronavirus between mid-March and early May. These numbers, which Guerrero confirmed, clearly exceed the CDC’s recommended definition for an outbreak — two or more linked cases of a disease — and likely meet Iowa’s 10 percent threshold.
Health experts and worker advocates have criticized Iowa’s metric, which was adapted from an older policy for monitoring flu outbreaks in schools.
Covid-19 is far more contagious and virulent than the flu, said Jan Flora, a sociology professor at Iowa State University. “To use the same threshold means that the state and the meatpacking plant will always be attempting to close the barn door after the horse has escaped.”
In denying The Post’s request for Agri Star’s case numbers, the Iowa Department of Public Health said it only released information about workplaces in cases of “active viral infection." In other words, because the state took so long to test workers, the peak of the outbreak had already passed — so Iowa never had to acknowledge that the outbreak occurred at all.
Cases in Allamakee County are creeping back up. With 27 new daily cases per 100,000 residents, Iowa has one of the highest infection rates in the country.
It also has some of the nation’s loosest coronavirus restrictions. Reynolds has rebuffed a White House task force recommendation to issue a statewide mask mandate. Bars remain open in all but six counties, and public schools are required to hold at least half of their classes in person. Since the state does not report school outbreaks, an Ames couple have taken it upon themselves to track cases in the state’s education system; as of Sept. 24 they have found 473 infected students and 246 infected staff.
Many people in Postville think the danger is over, because no one in power has said otherwise. Masks are rare on the small town’s streets. Toj and Pérez have returned to their storefront church, where they shake hands, share hymnals and sing with their faces uncovered.
“It’s sad,” Kenny said. What he’d found in the genome was not just the transmission history of the coronavirus in his region. It was a record of humanity’s failures — of mistakes made and warnings missed and information withheld during those early months of the pandemic. In exposing what went wrong, it offered a guide to getting things right.
“But we don’t learn from our mistakes,” Kenny said. “And we certainly don’t learn from science.”
Alice Crites and Nate Jones in Washington contributed to this report. Milli Legrain provided translations.


Losing sense of smell may be a hidden symptom of coronavirus, doctors warn

While every case is different, the telltale symptoms of the novel coronavirus have been widely agreed upon — a high fever, persistent cough or shortness of breath. In the most severe instances, those afflicted have reported confusion or difficulty breathing, and sometimes, anxiety is the most prevailing symptom of all.
But a team of British ear, nose and throat doctors on Friday raised the possibility of a new indicator of the coronavirus, one they say has been observed globally, even in patients who are otherwise asymptomatic: anosmia, a condition that causes the loss of sense of smell. In a statement, they warned that adults experiencing recent anosmia could be unknown carriers of covid-19, and urged them to consider self-isolation.
“All of this evidence is accumulating very rapidly, but there’s nothing yet robustly in print,” Claire Hopkins, president of the British Rhinological Society, said in an interview. “Since then, I’ve had colleagues from around the world saying: ‘That’s exactly what we’re seeing.’ They’ve been trying [to raise awareness], but it hasn’t been picked up.”
Experts at the World Health Organization say they have not yet confirmed the loss of smell or taste as a symptom of the coronavirus but haven’t ruled it out.
Hopkins, who published the statement along with Nirmal Kumar, the president of ENT UK, a body that represents ear, nose and throat specialists in Britain, said she was driven by recent discussions on rhinological discussion boards related to the coronavirus pandemic. There, she observed ENTs reporting a surge of reported anosmia across their patients, and even among themselves.
In their statement, Hopkins and Kumar cited reports from South Korea, China, Iran and Italy, where, they wrote, “significant numbers of patients with proven covid-19 infection have developed anosmia/hyposmia,” the latter of which signals a reduced ability to detect smells. In Germany, they wrote, more than two-thirds of confirmed coronavirus cases included anosmia. And in South Korea, a country that has seen ample covid-19 testing, “30 percent of patients testing positive have had anosmia as their major presenting symptom in otherwise mild cases.”
“This week, I saw nine patients that lost their sense of smell, which is unheard of in my practice,” Hopkins said. “They were almost all under 40, and they were all told not to self-isolate."
Anosmia and hyposmia are historically linked to early symptoms of upper-respiratory infections — including previous strains of coronavirus — because the virus damages olfactory bulbs that are involved in the sense of smell. But Hopkins raised concern at the number of covid-19 patients who were otherwise asymptomatic. She pointed to guidance in the United States and Britain, which generally instructs people to self-isolate if they are experiencing more-obvious coronavirus symptoms.
Hopkins said she hopes that flagging another potential symptom will resonate with those who haven’t taken social distancing and self-isolation seriously enough — the ones who fail to realize they may unknowingly carry the virus.
“The lack of awareness allows these people to carry on,” she added. “This potentially gives us an opportunity to capture some of those people who are silent spreaders of disease. The patients I’m seeing haven’t had a cough or fever at all."
Citing the ENT UK statement, the American Academy of Otolaryngology on Sunday wrote that in the absence of allergies, sinusitis or rhinitis, the loss of smell or taste should “warrant serious consideration for self-isolation and testing."
“Anosmia, in particular, has been seen in patients ultimately testing positive for the coronavirus with no other symptoms,” the academy wrote. “We propose that these symptoms be added to the list of screening tools for possible covid-19 infection.”
Reports of anosmia appearing as a possible symptom of coronavirus have reverberated online in recent days. In response to a news article on the topic, Daniel Goldman — the former lead investigative counsel for the House Intelligence Committee Democrats who said last week that he and his wife had tested positive for covid-19 — wrote on Twitter that “this has been the case with both my wife and me.”
Rudy Gobert, the Utah Jazz center whose positive novel coronavirus test prompted the National Basketball Association to shut down entirely, said Sunday that he, too, had lost his sense of smell.
Thomas Hummel, an ear, nose and throat expert at the University of Dresden in Germany, said Monday that he wasn’t surprised by the reported linkages between covid-19 and anosmia. While he understands the need for urgent measures to “flatten the curve,” he warned that many people are functionally anosmic — including about 5 percent of all Germans — and reiterated that it will take more data to prove a true correlation.
He said the warning, without further research, could cause panic even among those who have long suffered from anosmia, further straining outpatient clinics. (For those experiencing short-term anosmia, both Hummel and Hopkins agree that the sense of smell typically returns as the body recovers).
“On one end, it would be nice to have a good study. On the other hand, it’s about not spreading the virus,” he said. “Many people out there have anosmia. They don’t have a good sense of smell. And if you alert all these people that if you have anosmia you need to stay home, there would be many false positives. That’s the other side of the coin.”
WHO experts expressed a similar sentiment, announcing Monday that they have not yet confirmed the loss of smell or taste as a symptom of the coronavirus.
“We don’t have the answer to that yet, although there’s quite a bit of interest in this online,” Maria Van Kerkhove, head of the WHO’s emerging diseases and zoonosis unit, said at a daily news briefing Monday.
Van Kerkhove said a number of countries were collecting data on the symptoms of early infections, and that the WHO is working to learn if they have identified the loss of smell or taste as a symptom.
“We have a good handle on what the major ones are: Those are fevers. This is dry cough, and this is shortage of breath,” said Van Kerkhove, adding that aches and pains and headaches were also found. Some patients, though “very few” overall, had reported gastrointestinal problems, runny noses or sneezing.
But still, Hopkins said the tendency to focus on the major symptoms could further perpetuate the spread of the virus.
“While there is a chance the apparent increase in incidence could merely reflect the attention covid-19 has attracted in the media, and that such cases may be caused by typical rhinovirus and coronavirus strains, it could potentially be used as a screening tool to help identify otherwise asymptomatic patients, who could then be better instructed on self-isolation,” Hopkins and Kumar wrote.
Adam Taylor and Cindy Boren contributed to this report.


This coronavirus mutation has taken over the world. Scientists are trying to understand why.

When the first coronavirus cases in Chicago appeared in January, they bore the same genetic signatures as a germ that emerged in China weeks before.
But as Egon Ozer, an infectious-disease specialist at the Northwestern University Feinberg School of Medicine, examined the genetic structure of virus samples from local patients, he noticed something different.
A change in the virus was appearing again and again. This mutation, associated with outbreaks in Europe and New York, eventually took over the city. By May, it was found in 95 percent of all the genomes Ozer sequenced.
At a glance, the mutation seemed trivial. About 1,300 amino acids serve as building blocks for a protein on the surface of the virus. In the mutant virus, the genetic instructions for just one of those amino acids — number 614 — switched in the new variant from a “D” (shorthand for aspartic acid) to a “G” (short for glycine).
But the location was significant, because the switch occurred in the part of the genome that codes for the all-important “spike protein” — the protruding structure that gives the coronavirus its crownlike profile and allows it to enter human cells the way a burglar picks a lock.
And its ubiquity is undeniable. Of the approximately 50,000 genomes of the new virus that researchers worldwide have uploaded to a shared database, about 70 percent carry the mutation, officially designated D614G but known more familiarly to scientists as “G.”
“G” hasn’t just dominated the outbreak in Chicago — it has taken over the world. Now scientists are racing to figure out what it means.
At least five laboratory experiments suggest that the mutation makes the virus more infectious, although only one of those studies has been peer-reviewed. That study, led by scientists at Los Alamos National Laboratory and published Thursday in the journal Cell, also asserts that patients with the G variant actually have more virus in their bodies, making them more likely to spread it to others.
The mutation doesn’t appear to make people sicker, but a growing number of scientists worry that it has made the virus more contagious.
“The epidemiological study and our data together really explain why the [G variant’s] spread in Europe and the U.S. was really fast,” said Hyeryun Choe, a virologist at Scripps Research and lead author of an unpublished study on the G variant’s enhanced infectiousness in laboratory cell cultures. “This is not just accidental.”
But there may be other explanations for the G variant’s dominance: biases in where genetic data are being collected, quirks of timing that gave the mutated virus an early foothold in susceptible populations.
“The bottom line is, we haven’t seen anything definitive yet,” said Jeremy Luban, a virologist at the University of Massachusetts Medical School.
The scramble to unravel this mutation mystery embodies the challenges of science during the coronavirus pandemic. With millions of people infected and thousands dying every day around the world, researchers must strike a high-stakes balance between getting information out quickly and making sure that it’s right.
SARS-CoV-2, the novel coronavirus that causes the disease covid-19, can be thought of as an extremely destructive burglar. Unable to live or reproduce on its own, it breaks into human cells and co-opts their biological machinery to make thousands of copies of itself. That leaves a trail of damaged tissue and triggers an immune system response that for some people can be disastrous.
This replication process is messy. Even though it has a “proofreading” mechanism for copying its genome, the coronavirus frequently makes mistakes, or mutations. The vast majority of mutations have no effect on the behavior of the virus.
But since the virus’s genome was first sequenced in January, scientists have been on the lookout for changes that are meaningful. And few genetic mutations could be more significant than ones that affect the spike protein — the virus’s most powerful tool.
This protein attaches to a receptor on respiratory cells called ACE2, which opens the cell and lets the virus slip inside. The more effective the spike protein, the more easily the virus can break into the bodies of its hosts. Even when the original variant of the virus emerged in Wuhan, China, it was obvious that the spike protein on SARS-CoV-2 was already quite effective.
But it could have been even better, said Choe, who has studied spike proteins and the way they bind to the ACE2 receptor since the severe acute respiratory syndrome outbreak in 2003.
The spike protein for SARS-CoV-2 has two parts that don’t always hold together well. In the version of the virus that arose in China, Choe said, the outer part — which the virus needs to attach to a human receptor — frequently broke off. Equipped with this faulty lock pick, the virus had a harder time invading host cells.
“I think this mutation happened to compensate,” Choe said.
Studying both versions of the gene using a proxy virus in a petri dish of human cells, Choe and her colleagues found that viruses with the G variant had more spike proteins, and the outer parts of those proteins were less likely to break off. This made the virus approximately 10 times more infectious in the lab experiment.
The mutation does not seem to lead to worse outcomes in patients. Nor did it alter the virus’s response to antibodies from patients who had the D variant, Choe said, suggesting that vaccines being developed based on the original version of the virus will be effective against the new strain.
Choe has uploaded a manuscript describing this study to the website bioRxiv, where scientists can post “preprint” research that has not yet been peer reviewed. She has also submitted the paper to an academic journal, which has not yet published it.
The distinctive infectiousness of the G strain is so strong that scientists have been drawn to the mutation even when they weren’t looking for it.
Neville Sanjana, a geneticist at the New York Genome Center and New York University, was trying to figure out which genes enable SARS-CoV-2 to infiltrate human cells. But in experiments based on a gene sequence taken from an early case of the virus in Wuhan, he struggled to get that form of the virus to infect cells. Then the team switched to a model virus based on the G variant.
“We were shocked,” Sanjana said. “Voilà! It was just this huge increase in viral transduction.” They repeated the experiment in many types of cells, and every time the variant was many times more infectious.
Their findings, published as a preprint on bioRxiv, generally matched what Choe and other laboratory scientists were seeing.
But the New York team offers a different explanation as to why the variant is so infectious. Whereas Choe’s study proposes that the mutation made the spike protein more stable, Sanjana said experiments in the past two weeks, not yet made public, suggest that the improvement is actually in the infection process. He hypothesized that the G variant is more efficient at beginning the process of invading the human cell and taking over its reproductive machinery.
Luban, who has also been experimenting with the D614G mutation, has been drawn to a third possibility: His experiments suggest that the mutation allows the spike protein to change shape as it attaches to the ACE2 receptor, improving its ability to fuse to the host cell.
Different approaches to making their model virus might explain these discrepancies, Luban said. “But it’s quite clear that something is going on.”
Although these experiments are compelling, they’re not conclusive, said Kristian Andersen, a Scripps virologist not involved in any of the studies. The scientists need to figure out why they’ve identified different mechanisms for the same effect. All the studies still have to pass peer review, and they have to be reproduced using the real version of the virus.
Even then, Andersen said, it will be too soon to say that the G variant transmits faster among people.
Cell culture experiments have been wrong before, noted Anderson Brito, a computational biologist at Yale University. Early experiments with hydroxychloroquine, a malaria drug, hinted that it was effective at fighting the coronavirus in a petri dish. The drug was touted by President Trump, and the Food and Drug Administration authorized it for emergency use in hospitalized covid-19 patients. But that authorization was withdrawn this month after evidence showed that the drug was “unlikely to be effective” against the virus and posed potential safety risks.
So far, the biggest study of transmission has come from Bette Korber, a computational biologist at Los Alamos National Laboratory who helped build one of the world’s biggest viral genome databases for tracking HIV. In their paper published this week, Korber’s team argues that the G variant “may have a fitness advantage” that explains its overwhelming dominance.
Using two statistical approaches, the researchers analyzed some 30,000 sequences from across the world; they found that most places where the original virus was dominant before March were eventually taken over by the mutated version. This switch often took place in a matter of weeks. This was especially apparent in the United States: Ninety-six percent of early sequences here belonged to the D variant, but by the end of March, more than two thirds of sequences carried the G amino acid instead.
Korber’s collaborators in the U.K. also found evidence that people with the G variant had more viral particles in their bodies. Although this higher viral load didn’t seem to make people sicker, it might explain the G variant’s rapid spread, the scientists wrote. People with more virus to shed are more likely to infect others.
Meanwhile, the paper describes two laboratory experiments confirming what Sanjana, Choe and others have found: the G variant was 3 to 6 times more infectious.
A preliminary version of the Los Alamos paper, which did not include these laboratory findings, drew intense scrutiny when it was released as a pre-print in the spring. Though the additional data and the credibility of peer review make the case for increased transmissibility even stronger, many scientists -- including Korber -- say more research is needed.
“There are so many biases in the data set here that you can’t control for and you might not know exist,” Andersen said. In a time when as many as 90 percent of U.S. infections are still undetected and countries with limited public health infrastructure are struggling to keep up with surging cases, a shortage of data means “we can’t answer all the questions we want to answer.”
Pardis Sabeti, a computational biologist at Harvard University and the Broad Institute, noted that the vast majority of sequenced genomes come from Europe, where the G variant first emerged, and the United States, where infections thought to have been introduced by travelers from Europe spread undetected for weeks before the country shut down. This could at least partly explain why it appears so dominant.
The mutation’s success might also be a “founder effect,” she said. Arriving in a place like Northern Italy — where the vast majority of sequenced infections are caused by the G variant — it found easy purchase in an older and largely unprepared population, which then unwittingly spread it far and wide.
Scientists may be able to rule out these alternative explanations with more rigorous statistical analyses or a controlled experiment in an animal population. And as studies on the D614G mutation accumulate, researchers are starting to be convinced of its significance.
“I think that slowly we’re beginning to come to a consensus,” said Judd Hultquist, a virologist at Northwestern University.
Solving the mystery of the D614G mutation won’t make much of a difference in the short term, Andersen said. “We were unable to deal with D,” he said. “If G transmits even better, we’re going to be unable to deal with that one.”
But it’s still essential to understand how the genome influences the behavior of the virus, scientists say. Identifying emerging mutations allows researchers to track their spread. Knowing what genes affect how the virus transmits enables public health officials to tailor their efforts to contain it. Once therapeutics and vaccines are distributed on a large scale, having a baseline understanding of the genome will help pinpoint when drug resistance starts to evolve.
“Understanding how transmissions are happening won’t be a magic bullet, but it will help us respond better,” Sabeti said. “This is a race against time.”
Correction: An initial version of this article gave an incorrect affiliation for Jeremy Luban. He is a virologist at the University of Massachusetts Medical School.


U.K. coronavirus mutation prompts more travel bans and major disruptions at ports

LONDON —
The British government scrambled Monday to dampen the impact of travel entry bans from more than 40 countries prompted by fear of a new coronavirus mutation believed to have originated in England.
Health officials said they do not believe the mutation is more deadly or vaccine resistant, but evidence that it spreads much more easily has alarmed governments in Europe and around the world.
Scientists advising the British government estimated that the new variant was 50 percent more transmissible.
As country after country shut their borders to people traveling from Britain, the greatest travel disruption emerged along both sides of the English Channel, after France imposed a far more comprehensive ban than the border closures during the first wave of the virus in spring.
The short passage from Britain to France across the channel is one of the most important transport corridors in Europe. On Monday, hundreds of trucks backed up for miles, prompting concern that food and other time-sensitive cargo might end up rotting on the roadside.
British supermarket chain Sainsbury’s warned: “If nothing changes, we will start to see gaps over the coming days on lettuce, some salad leaves, cauliflowers, broccoli and citrus fruit — all of which are imported from the continent at this time of year.”
The hashtag #lettuce trended on Twitter in Britain, as panicked shoppers tried to stock up on supplies for Christmas and beyond.
In a news conference at Downing Street on Monday evening, Prime Minister Boris Johnson played down the impact of border closures and batted away questions about the need for a national lockdown, while emphasizing progress on vaccines. More than 500,000 people in Britain have gotten an initial Pfizer-BioNTech shot.
Johnson said he understood the fears of other countries about the new virus strain, but was talking to French President Emmanuel Macron — who is self-isolating after coming down with covid-19 last week — about getting the ports moving again.
Meanwhile, Johnson reported, the line of trucks idling at the Dover port had been reduced from 500 to 170. And he said France’s travel ban affected only 20 percent of the trade going in and out of Britain — freight carried by trucks with drivers, who travel by ferry or tunnel.
“Which means the vast majority of food, medicines and other supplies are coming and going as normal,” Johnson said, adding that British supermarket supply chains are “strong and robust.”
British scientists advising the government said Monday that this coronavirus mutation first arose in England in September, but it wasn’t until December that researchers saw how quickly it began to dominate. Today, 80 percent of newly diagnosed cases in London, for example, were likely caused by the new mutation.
A review of the latest data underscored “high confidence” that the new strain has a transmission advantage over earlier versions of the coronavirus seen in Britain, said Peter Horby, professor of emerging infectious diseases at the University of Oxford.
The scientists said that in nasal and throat swabs taken from patients, there appeared to be more virus particles present, compared to earlier versions.
Researchers on Monday also flagged early evidence that children appeared to be more susceptible to the new strain, although they cautioned it did not make the children more likely to have symptoms or become sick.
The new strain may make children “as equally susceptible as adults,” said Wendy Barclay, head of the infectious-disease department at Imperial College London.
Adam Finn, a professor of pediatrics at the University of Bristol, said Monday that the new strain was being tested to see if it might be more resistant to vaccines. “It is a matter of immediate interest,” he said, adding that predictions are it will “have either no effect or a minor effect” on the efficacy of vaccines.
In the interim, scientists said Britain’s vaccine rollout should continue as quickly as possible.
The World Health Organization sought to temper panic. Chief scientist Soumya Swaminathan said the coronavirus is mutating at a much slower rate than the seasonal flu. “And so far, even though we’ve seen a number of changes and a number of mutations, none has made a significant impact on either the susceptibility of the virus to any of the currently used therapeutics, drugs or the vaccines under development, and one hopes that that will continue to be the case,” she said.
Tobias Kurth, director of the Institute of Public Health at Berlin’s Charité University Hospital, said the decision by numerous countries to “pull the emergency brakes” and suspend travel with Britain is “understandable.”
But Kurth cautioned that the mutation is “certainly already in continental Europe, and likely in Germany.”
“We won’t be able to stop it,” even though travel restrictions may slow the spread of the mutation, he said.
French Health Minister Olivier Véran acknowledged Monday morning that the new variant may already be in France. Italy, the Netherlands and Denmark said they have identified the mutation among recently discovered coronavirus cases in their countries.
Mutations of the virus that share traits with the British variant have also been detected in South Africa and are responsible for an increases in infection there.
In Britain, officials on Monday announced 33,364 new coronavirus cases and 215 deaths.
With cases soaring, some stoked by the new variant, Johnson ordered London and parts of the southeast England into Tier 4 lockdown over the weekend, telling 18 million people to “stay at home” and only venture out to shop for food and medicine, attend medical appointments or do outdoor exercise.
The travel bans compounded the upheaval. They come less than two weeks before Britain is set to cut its last membership ties with the European Union. The two sides have yet to agree on a post-Brexit trade deal, and the disruptions on Monday provided a preview of what could happen if Britain crashes out of the bloc without one.
Johnson tried to suggest that anticipation of a possible no-deal Brexit offered an advantage when faced with pandemic-related border closures. “The government has been preparing for a long time for exactly this kind of event,” he said.
British Transport Minister Grant Shapps said the government was providing portable toilets for stranded lorry drivers and rerouting trucks at Britain’s southern port, where tens of thousands of trucks normally converge every day to board ferries or travel through the Eurotunnel to France. Authorities made contingency plans to deliver medicines by military helicopter if necessary.
Earlier Monday, French Transport Minister Jean-Baptiste Djebbari had tweeted that in the coming hours, in coordination with other European nations, the country would “put in place a robust sanitary protocol to allow traffic flows from the United Kingdom to resume.” But no announcement had been made by evening.
Even though the European travel restrictions do not ban trucks from entering the United Kingdom, industry representatives cautioned that few companies would be willing to take the risk of then becoming stranded there, meaning trade was impacted in both directions.
“No driver wants to deliver to the U.K. now, so the U.K. is going to see its freight supply dry up,” said Vanessa Ibarlucea, a spokeswoman for the French road haulage federation, according to Reuters.
Beyond the ports, many passengers were left stranded, as more countries canceled flights to and from the United Kingdom.
Beth Gabriel Ware, a British citizen who lives in Turkey, found herself stuck at her parents’ home in Kent after the Turkish government banned flights from Britain on Sunday. She had surprised her family with a visit after they had been apart for 10 months.
“I will be sleeping on the couch for the foreseeable future,” said Ware, 23.
Hind Mrabet, 21, who planned to move from Britain to Paris for school at the end of this week, now does not know when she will be able to cross into France.
“They seem to be making last-minute decisions that leave people in panic,” she said of the British government.
william.booth@washpost.com
rick.noack@washpost.com