This is How the Virus Kills

hoped to see life returned to normal by Easter. Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, as well as Deborah Burke's, the State Department immunologist advising Vice President Mike Pence, were able to change the president's lined about a swift economic restart by showing him projections that millions of Americans may wind up infected. President Trump said Sunday that one hundred thousand people or more may die.

Only a few weeks ago, the President repeatedly downplayed concerns about the virus, saying it would go away and he was not concerned at all. A former FDA commissioner proposed a roadmap for eventually getting people back to work and lifting restrictions on movement. Scott Gottleib is a physician and one of the co authors of the paper released Sunday by conservative think tank American Enterprise Institute. The paper spells out a four phase plan for navigating the COVID nineteen pandemic.

The paper recommends continuing with aggressive social distancing measures until there has been a sustained reduction in cases for fourteen days. At that point, Gottleiep and his colleagues say governments could start lifting restrictions verry gradually, but the plan requires widespread testing that's not currently in place in the US, and we seem far from reaching that two week period of

reduction in cases. The infection rate in the US continues to escalate, and the number of deaths grew to more than undred over the past two days. All around the world, the number of places enacting strict isolation measures is going up. The tie tourist hotspot of Poquette went on lockdown, and Moscow's nearly thirteen million residents were ordered to stay home. In the US, Maryland Governor Larry Hogan issued a stay at home order saying voluntary measures weren't working, and on

Monday afternoon, Governor Ralph Northam echoed the decision. In Virginia, Virginians were ordered to remain in their homes except for central services and now today's main story, the deadly tipping point. The new coronavirus has sickened hundreds of millions and will infect many more, but only a small fraction of the people who get the virus dye. The virus acts in a way that scientists are still trying to figure out. In some people who are infected, symptoms are mild, like

a common cold. Some don't have symptoms at all. In others, though, symptoms are severe and even fatal, with the infections stopping the lungs from functioning and causing the body to shut down. So why are symptoms so mild in some people and deadly in others. It turns out there's a tipping point, a moment where the virus moves from one part of the body to another that can determine whether the virus

is manageable or fatal. Jason Gale spoke to experts to understand what the virus does to us once it's in our bodies. As of nineteen, the disease caused by the new coronavirus spreads around the world. Scientists are beginning to understand more about how it maims and kills. A picture is emerging of an enigmatic pathogen whose effects are mainly mild, but which occasionally and unpredictably becomes serious. In the second or third week in a fraction of patients. Bodily systems

start to fall apart in a cascade. But what causes this deadly tipping point. Other diseases like SARS or severe acute respiratory syndrome and influenza offer important clues about what's going on inside the body when someone has COVID nineteen. The clinical picture suggests a pattern of disease that's not dissimilar to what we might see in influenza, with a

range of outcomes. Dr Jeffrey Taubenberger is a pathologist who studied the infection in victims of the Spanish flu pandemic, including one exam to more than twenty years ago from perma frost in northwestern Alaska. Jeffrey heads the Viral Pathogenesis and Evolution section of the National Institute of Allergy and Infectious diseases in Bethesda, Maryland. In his spare time, he's a musician and composes symphonies and operas, but COVID nineteen

is his current focus. The answer to what the pathogenesis is and why certain people are having more severe disease and others having mild disease is not fully understood. But I think that in relation to other diseases sours twenty years ago almost and influenza now for hundred years, we have information where it's at least analogous. COVID nineteen causes a little more than a cough if it stays in the nose and throat, which it does for most people

a unlucky enough to be infected. The vast majority of people who are exposed to a virus to which they probably don't have protective immunity get infected, and most of them clear their virus and get better with varying illness. A report from China and February showed that one in seven patients develops difficulty breathing, and six of cases are critical. It's why hospitals worldwide are either experiencing or bracing for scores of patients requiring mechanical ventilation. For days two weeks.

Jeffrey says infection is like a dance between the host that's us and the pathogen, in this case, the new coronavirus. What causes disease and how quickly it can escalate comes down to an interplay of three factors, how nasty the virus is, the body's immune response to it, and the

role of secondary infections. What generally happens is that you get an infection of a virus that sets up an infection along cells that line your respiratory tracts, starting at your nose, maybe migrating downwards into your trachea and the bronchos, and then maybe eventually into lungs. If your infection is limited to the upper respiratory tract more like a call. Even with influenza, you're mostly likely to get a cold

virus like disease mild. You sort of throat in a cough and sniffles and sneeze, maybe fever, but you otherwise don't get severely. Danger starts when the virus reaches the lungs. Pathogenic viruses that induce a lot of direct sell death along the restaur attract induce a very strong inflammatory response. The kind of a so called pro inflammatory response that itself is actually damaging to bystander cells. The inflammatory responses

an initial warning system, like a fire alarm. The body's first respond is different types of white blood cells, known as neutrophils and macrofages are sent out to destroy and dispose of infected cells and repair damage tissue. Let's say in an analogy, you don't necessarily know where the fire is, but there's a fire, and so you should do something. We should shun on sprinklers, which you call the fire department. We should turn on the water host. So this initial

inflammatory response is that initial response. There's something wrong, we need to do something. Normally, if this goes well, the infection is cleared up in just a few days. The inflammation tamps down viral replication, enabling the body to recover. But in rare instances, this inflammatory response goes overboard and becomes damaging. Jeffrey says, cells that may not even be infected with the virus can be targeted and damaged by

these inflammatory cells. Your body is immediately trying to repair the damage in the lung as soon as it's happening. Uh. And then it's a question of does the inflammatory in the virus win or does your reparative and immune responses win? And most of the time evene responses win because most people will get infective with these viruses survive, but in

some people they don't. The destruction of cells can release toxins into the bloodstream, attracting more neutrophils to clean up the dead material, and that can itself kind of create kind of a perfect storm of augmenting the inflammatory response. Further studies of fatal COVID nineteen patients have confirmed this kind of bi standard damage along the respiratory tract. The coronavirus targets distinctly shaped protein receptors, and these are found

on many organs and tissues, including epithelial cells. When an infection harms the epithelium lining the trachea and bronchi, it can result in the loss of protective mucus producing cells, as well as the tiny hairs or cilia that sweep

dirt and respiratory secretions out of the lungs. It's part of the interplay between the initial damage caused by the virus and the secondary damage caused by the body's own inflammatory response, and that combination can lead you to have more severe disease that can set you up for the third piece of this puzzle, which is that if you damage especially the lower respiratory tract epithelium and all the barriers that you have in your lungs from keeping bacteria

and other pathogens from getting down into the lung, meaning that you've damaged the lining of the trichy bronchial trees and that the cilia that can constantly move all this material upward or lost, you lose mucous secretion, you have no ability to keep stuff out of the lower respiratory track. You can set yourself up for in an evasive secondary

bacterial infection. In the case of Spanish flu, autopsies and experimental studies performed in the Torbenberger Lab show that almost everyone who died from the nine eighteen pandemic succumbed to a secondary bacterial pneumonia. Jeffrey says it's too early to save something similar as happening with COVID nineteen. The coronavirus

has some features that set it apart from flu. One is that it's capable of replicating not just in the cells of the respiratory system, but also in other parts of the body, including the gastro intestinal tract, and that's probably why some patients experience diarrhea and why the virus

has been found in stool. But it's the damage to the lungs that's feeling intensive care unipeds many I see you patients require mechanical ventilation to counter low blood oxygen, a condition doctors referred to as hypoxia in terms of

end stage disease. If the lung ist damaged knowledge from a primary of ouril infection and or secondary of bacterial infection, both in flu or in coronavirus, but consequence of that is um decreased lung functions, You have decreased oxygen exchange, and if you have less oxygen available then is needed you start damaging other end stage organs. Of course, your kidneys, your livering, your brain, your heart as vague get damaged and as your kidneys stop being able to clear toxins

that in self induces more disease. You can see that you can have this multi organ failure as an end stage of disease, although it's really primarily related to the loss of pulmonary function in hypoxia. During my interview, one of Jeffrey's main collaborators join the conversation. I'm pretty sure I don't know anything more. Dr David Morrens is a senior scientific advisor to Tony Fauci, the director of the

National Institute of Allergy and Infectious Disease IS. David graduated from medical school in nine three and joined the Sentence for Disease Control and Preventions Epidemic Intelligence Service a few years later. He's been at the institute for more than twenty years and was wearing a navy uniform of the United States Public Health Service. David's been studying emerging infectious diseases, including the ways viruses cause disease, for more than forty years.

He says patterns and COVID nineteen patients are pretty familiar. I sometimes think of it as when you get a bad, overwhelming infection, everything starts to fall apart. In the cascade. It's like dominoes falling over. You know, the oxygen gets a lot of the tissue gets more damaged, the immune responses more effective, the oxygen radicles come up, and you pass the tipping point where everything's going downhill and at

some point you can't get it back. Both David and Jeffrey agree that chronic conditions like hypertension, diabetes, and cancer treatment impair the body's ability to fight the coronavirus. These elements are more common in older people, which is one of the reasons why age is the biggest risk factor for dying from COVID nineteen, but that risk overall remains

relatively low. The experience doctors are gaining from managing patients and the evidence flowing from clinical trials are informing treatment guidelines, and that should lead to better care for patients. That's it for the Prognosis Daily Edition. For more on the coronavirus crisis from a hundred and twenty bureaus around the world,

visit Bloomberg dot com slash coronavirus. If you appreciate the podcast, please take a moment to read us and leave us a review on Apple Podcasts or Spotify to help more listeners find our global reporting. The Prognosis Daily Edition is hosted by me Laura Carlson. The show is produced by Me Tob Foreheads, Jordan Gospore, and Magnus Hendriksson. Reporting by Jason Gale, Original music by Leo Sigrid. Our editors are Francesca Leavie and Rick Shine. Francesca Levy is Bloomberg's head

of podcasts. Thanks for listening.