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Speaker 1: Welcome to Prognosis. I'm Laura Carlson. It's day twenties. Since

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Speaker 1: coronavirus was declared a global pandemic, cases around the world

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Speaker 1: have soared past seven hundred and forty five thousand today,

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Speaker 1: the deadly tipping point that determines when COVID nineteen kills.

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Speaker 1: But first the day's main stories. President Donald Trump extended

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Speaker 1: guidelines for Americans to practice social distancing until at least

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Speaker 1: the end of April. Last week, he had said he

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Speaker 1: hoped to see life returned to normal by Easter. Anthony Fauci,

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Speaker 1: the director of the National Institute of Allergy and Infectious Diseases,

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Speaker 1: as well as Deborah Burke's, the State Department immunologist advising

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Speaker 1: Vice President Mike Pence, were able to change the president's

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Speaker 1: lined about a swift economic restart by showing him projections

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Speaker 1: that millions of Americans may wind up infected. President Trump

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Speaker 1: said Sunday that one hundred thousand people or more may die.

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Speaker 1: Only a few weeks ago, the President repeatedly downplayed concerns

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Speaker 1: about the virus, saying it would go away and he

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Speaker 1: was not concerned at all. A former FDA commissioner proposed

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Speaker 1: a roadmap for eventually getting people back to work and

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Speaker 1: lifting restrictions on movement. Scott Gottleib is a physician and

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Speaker 1: one of the co authors of the paper released Sunday

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Speaker 1: by conservative think tank American Enterprise Institute. The paper spells

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Speaker 1: out a four phase plan for navigating the COVID nineteen pandemic.

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Speaker 1: The paper recommends continuing with aggressive social distancing measures until

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Speaker 1: there has been a sustained reduction in cases for fourteen days.

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Speaker 1: At that point, Gottleiep and his colleagues say governments could

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Speaker 1: start lifting restrictions verry gradually, but the plan requires widespread

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Speaker 1: testing that's not currently in place in the US, and

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Speaker 1: we seem far from reaching that two week period of

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Speaker 1: reduction in cases. The infection rate in the US continues

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Speaker 1: to escalate, and the number of deaths grew to more

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Speaker 1: than undred over the past two days. All around the world,

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Speaker 1: the number of places enacting strict isolation measures is going up.

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Speaker 1: The tie tourist hotspot of Poquette went on lockdown, and

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Speaker 1: Moscow's nearly thirteen million residents were ordered to stay home.

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Speaker 1: In the US, Maryland Governor Larry Hogan issued a stay

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Speaker 1: at home order saying voluntary measures weren't working, and on

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Speaker 1: Monday afternoon, Governor Ralph Northam echoed the decision. In Virginia,

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Speaker 1: Virginians were ordered to remain in their homes except for

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Speaker 1: central services and now today's main story, the deadly tipping point.

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Speaker 1: The new coronavirus has sickened hundreds of millions and will

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Speaker 1: infect many more, but only a small fraction of the

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Speaker 1: people who get the virus dye. The virus acts in

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Speaker 1: a way that scientists are still trying to figure out.

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Speaker 1: In some people who are infected, symptoms are mild, like

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Speaker 1: a common cold. Some don't have symptoms at all. In others, though,

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Speaker 1: symptoms are severe and even fatal, with the infections stopping

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Speaker 1: the lungs from functioning and causing the body to shut down.

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Speaker 1: So why are symptoms so mild in some people and

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Speaker 1: deadly in others. It turns out there's a tipping point,

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Speaker 1: a moment where the virus moves from one part of

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Speaker 1: the body to another that can determine whether the virus

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Speaker 1: is manageable or fatal. Jason Gale spoke to experts to

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Speaker 1: understand what the virus does to us once it's in

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Speaker 1: our bodies. As of nineteen, the disease caused by the

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Speaker 1: new coronavirus spreads around the world. Scientists are beginning to

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Speaker 1: understand more about how it maims and kills. A picture

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Speaker 1: is emerging of an enigmatic pathogen whose effects are mainly mild,

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Speaker 1: but which occasionally and unpredictably becomes serious. In the second

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Speaker 1: or third week in a fraction of patients. Bodily systems

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Speaker 1: start to fall apart in a cascade. But what causes

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Speaker 1: this deadly tipping point. Other diseases like SARS or severe

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Speaker 1: acute respiratory syndrome and influenza offer important clues about what's

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Speaker 1: going on inside the body when someone has COVID nineteen.

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Speaker 1: The clinical picture suggests a pattern of disease that's not

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Speaker 1: dissimilar to what we might see in influenza, with a

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Speaker 1: range of outcomes. Dr Jeffrey Taubenberger is a pathologist who

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Speaker 1: studied the infection in victims of the Spanish flu pandemic,

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Speaker 1: including one exam to more than twenty years ago from

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Speaker 1: perma frost in northwestern Alaska. Jeffrey heads the Viral Pathogenesis

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Speaker 1: and Evolution section of the National Institute of Allergy and

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Speaker 1: Infectious diseases in Bethesda, Maryland. In his spare time, he's

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Speaker 1: a musician and composes symphonies and operas, but COVID nineteen

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Speaker 1: is his current focus. The answer to what the pathogenesis

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Speaker 1: is and why certain people are having more severe disease

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Speaker 1: and others having mild disease is not fully understood. But

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Speaker 1: I think that in relation to other diseases sours twenty

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Speaker 1: years ago almost and influenza now for hundred years, we

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Speaker 1: have information where it's at least analogous. COVID nineteen causes

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Speaker 1: a little more than a cough if it stays in

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Speaker 1: the nose and throat, which it does for most people

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Speaker 1: a unlucky enough to be infected. The vast majority of

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Speaker 1: people who are exposed to a virus to which they

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Speaker 1: probably don't have protective immunity get infected, and most of

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Speaker 1: them clear their virus and get better with varying illness.

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Speaker 1: A report from China and February showed that one in

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Speaker 1: seven patients develops difficulty breathing, and six of cases are critical.

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Speaker 1: It's why hospitals worldwide are either experiencing or bracing for

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Speaker 1: scores of patients requiring mechanical ventilation. For days two weeks.

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Speaker 1: Jeffrey says infection is like a dance between the host

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Speaker 1: that's us and the pathogen, in this case, the new coronavirus.

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Speaker 1: What causes disease and how quickly it can escalate comes

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Speaker 1: down to an interplay of three factors, how nasty the

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Speaker 1: virus is, the body's immune response to it, and the

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Speaker 1: role of secondary infections. What generally happens is that you

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Speaker 1: get an infection of a virus that sets up an

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Speaker 1: infection along cells that line your respiratory tracts, starting at

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Speaker 1: your nose, maybe migrating downwards into your trachea and the bronchos,

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Speaker 1: and then maybe eventually into lungs. If your infection is

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Speaker 1: limited to the upper respiratory tract more like a call.

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Speaker 1: Even with influenza, you're mostly likely to get a cold

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Speaker 1: virus like disease mild. You sort of throat in a

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Speaker 1: cough and sniffles and sneeze, maybe fever, but you otherwise

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Speaker 1: don't get severely. Danger starts when the virus reaches the lungs.

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Speaker 1: Pathogenic viruses that induce a lot of direct sell death

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Speaker 1: along the restaur attract induce a very strong inflammatory response.

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Speaker 1: The kind of a so called pro inflammatory response that

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Speaker 1: itself is actually damaging to bystander cells. The inflammatory responses

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Speaker 1: an initial warning system, like a fire alarm. The body's

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Speaker 1: first respond is different types of white blood cells, known

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Speaker 1: as neutrophils and macrofages are sent out to destroy and

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Speaker 1: dispose of infected cells and repair damage tissue. Let's say

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Speaker 1: in an analogy, you don't necessarily know where the fire is,

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Speaker 1: but there's a fire, and so you should do something.

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Speaker 1: We should shun on sprinklers, which you call the fire department.

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Speaker 1: We should turn on the water host. So this initial

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Speaker 1: inflammatory response is that initial response. There's something wrong, we

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Speaker 1: need to do something. Normally, if this goes well, the

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Speaker 1: infection is cleared up in just a few days. The

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Speaker 1: inflammation tamps down viral replication, enabling the body to recover.

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Speaker 1: But in rare instances, this inflammatory response goes overboard and

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Speaker 1: becomes damaging. Jeffrey says, cells that may not even be

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Speaker 1: infected with the virus can be targeted and damaged by

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Speaker 1: these inflammatory cells. Your body is immediately trying to repair

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Speaker 1: the damage in the lung as soon as it's happening. Uh.

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Speaker 1: And then it's a question of does the inflammatory in

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Speaker 1: the virus win or does your reparative and immune responses win?

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Speaker 1: And most of the time evene responses win because most

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Speaker 1: people will get infective with these viruses survive, but in

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Speaker 1: some people they don't. The destruction of cells can release

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Speaker 1: toxins into the bloodstream, attracting more neutrophils to clean up

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Speaker 1: the dead material, and that can itself kind of create

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Speaker 1: kind of a perfect storm of augmenting the inflammatory response.

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Speaker 1: Further studies of fatal COVID nineteen patients have confirmed this

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Speaker 1: kind of bi standard damage along the respiratory tract. The

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Speaker 1: coronavirus targets distinctly shaped protein receptors, and these are found

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Speaker 1: on many organs and tissues, including epithelial cells. When an

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Speaker 1: infection harms the epithelium lining the trachea and bronchi, it

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Speaker 1: can result in the loss of protective mucus producing cells,

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Speaker 1: as well as the tiny hairs or cilia that sweep

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Speaker 1: dirt and respiratory secretions out of the lungs. It's part

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Speaker 1: of the interplay between the initial damage caused by the

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Speaker 1: virus and the secondary damage caused by the body's own

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Speaker 1: inflammatory response, and that combination can lead you to have

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Speaker 1: more severe disease that can set you up for the

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Speaker 1: third piece of this puzzle, which is that if you

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Speaker 1: damage especially the lower respiratory tract epithelium and all the

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Speaker 1: barriers that you have in your lungs from keeping bacteria

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Speaker 1: and other pathogens from getting down into the lung, meaning

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Speaker 1: that you've damaged the lining of the trichy bronchial trees

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Speaker 1: and that the cilia that can constantly move all this

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Speaker 1: material upward or lost, you lose mucous secretion, you have

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Speaker 1: no ability to keep stuff out of the lower respiratory track.

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Speaker 1: You can set yourself up for in an evasive secondary

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Speaker 1: bacterial infection. In the case of Spanish flu, autopsies and

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Speaker 1: experimental studies performed in the Torbenberger Lab show that almost

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Speaker 1: everyone who died from the nine eighteen pandemic succumbed to

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Speaker 1: a secondary bacterial pneumonia. Jeffrey says it's too early to

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Speaker 1: save something similar as happening with COVID nineteen. The coronavirus

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Speaker 1: has some features that set it apart from flu. One

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Speaker 1: is that it's capable of replicating not just in the

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Speaker 1: cells of the respiratory system, but also in other parts

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Speaker 1: of the body, including the gastro intestinal tract, and that's

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Speaker 1: probably why some patients experience diarrhea and why the virus

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Speaker 1: has been found in stool. But it's the damage to

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Speaker 1: the lungs that's feeling intensive care unipeds many I see

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Speaker 1: you patients require mechanical ventilation to counter low blood oxygen,

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Speaker 1: a condition doctors referred to as hypoxia in terms of

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Speaker 1: end stage disease. If the lung ist damaged knowledge from

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Speaker 1: a primary of ouril infection and or secondary of bacterial infection,

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Speaker 1: both in flu or in coronavirus, but consequence of that

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Speaker 1: is um decreased lung functions, You have decreased oxygen exchange,

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Speaker 1: and if you have less oxygen available then is needed

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Speaker 1: you start damaging other end stage organs. Of course, your kidneys,

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Speaker 1: your livering, your brain, your heart as vague get damaged

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Speaker 1: and as your kidneys stop being able to clear toxins

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Speaker 1: that in self induces more disease. You can see that

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Speaker 1: you can have this multi organ failure as an end

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Speaker 1: stage of disease, although it's really primarily related to the

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Speaker 1: loss of pulmonary function in hypoxia. During my interview, one

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Speaker 1: of Jeffrey's main collaborators join the conversation. I'm pretty sure

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Speaker 1: I don't know anything more. Dr David Morrens is a

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Speaker 1: senior scientific advisor to Tony Fauci, the director of the

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Speaker 1: National Institute of Allergy and Infectious Disease IS. David graduated

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Speaker 1: from medical school in nine three and joined the Sentence

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Speaker 1: for Disease Control and Preventions Epidemic Intelligence Service a few

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Speaker 1: years later. He's been at the institute for more than

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Speaker 1: twenty years and was wearing a navy uniform of the

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Speaker 1: United States Public Health Service. David's been studying emerging infectious diseases,

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Speaker 1: including the ways viruses cause disease, for more than forty years.

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Speaker 1: He says patterns and COVID nineteen patients are pretty familiar.

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Speaker 1: I sometimes think of it as when you get a bad,

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Speaker 1: overwhelming infection, everything starts to fall apart. In the cascade.

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Speaker 1: It's like dominoes falling over. You know, the oxygen gets

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Speaker 1: a lot of the tissue gets more damaged, the immune

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Speaker 1: responses more effective, the oxygen radicles come up, and you

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Speaker 1: pass the tipping point where everything's going downhill and at

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Speaker 1: some point you can't get it back. Both David and

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Speaker 1: Jeffrey agree that chronic conditions like hypertension, diabetes, and cancer

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Speaker 1: treatment impair the body's ability to fight the coronavirus. These

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Speaker 1: elements are more common in older people, which is one

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Speaker 1: of the reasons why age is the biggest risk factor

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Speaker 1: for dying from COVID nineteen, but that risk overall remains

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Speaker 1: relatively low. The experience doctors are gaining from managing patients

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Speaker 1: and the evidence flowing from clinical trials are informing treatment guidelines,

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Speaker 1: and that should lead to better care for patients. That's

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Speaker 1: it for the Prognosis Daily Edition. For more on the

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Speaker 1: coronavirus crisis from a hundred and twenty bureaus around the world,

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Speaker 1: visit Bloomberg dot com slash coronavirus. If you appreciate the podcast,

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Speaker 1: please take a moment to read us and leave us

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Speaker 1: a review on Apple Podcasts or Spotify to help more

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Speaker 1: listeners find our global reporting. The Prognosis Daily Edition is

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Speaker 1: hosted by me Laura Carlson. The show is produced by

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Speaker 1: Me Tob Foreheads, Jordan Gospore, and Magnus Hendriksson. Reporting by

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Speaker 1: Jason Gale, Original music by Leo Sigrid. Our editors are

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Speaker 1: Francesca Leavie and Rick Shine. Francesca Levy is Bloomberg's head

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Speaker 1: of podcasts. Thanks for listening.