Speaker 1: Welcome to Prognosis. I'm Laura Carlson. It's day twenties. Since
Speaker 1: coronavirus was declared a global pandemic, cases around the world
Speaker 1: have soared past seven hundred and forty five thousand today,
Speaker 1: the deadly tipping point that determines when COVID nineteen kills.
Speaker 1: But first the day's main stories. President Donald Trump extended
Speaker 1: guidelines for Americans to practice social distancing until at least
Speaker 1: the end of April. Last week, he had said he
Speaker 1: hoped to see life returned to normal by Easter. Anthony Fauci,
Speaker 1: the director of the National Institute of Allergy and Infectious Diseases,
Speaker 1: as well as Deborah Burke's, the State Department immunologist advising
Speaker 1: Vice President Mike Pence, were able to change the president's
Speaker 1: lined about a swift economic restart by showing him projections
Speaker 1: that millions of Americans may wind up infected. President Trump
Speaker 1: said Sunday that one hundred thousand people or more may die.
Speaker 1: Only a few weeks ago, the President repeatedly downplayed concerns
Speaker 1: about the virus, saying it would go away and he
Speaker 1: was not concerned at all. A former FDA commissioner proposed
Speaker 1: a roadmap for eventually getting people back to work and
Speaker 1: lifting restrictions on movement. Scott Gottleib is a physician and
Speaker 1: one of the co authors of the paper released Sunday
Speaker 1: by conservative think tank American Enterprise Institute. The paper spells
Speaker 1: out a four phase plan for navigating the COVID nineteen pandemic.
Speaker 1: The paper recommends continuing with aggressive social distancing measures until
Speaker 1: there has been a sustained reduction in cases for fourteen days.
Speaker 1: At that point, Gottleiep and his colleagues say governments could
Speaker 1: start lifting restrictions verry gradually, but the plan requires widespread
Speaker 1: testing that's not currently in place in the US, and
Speaker 1: we seem far from reaching that two week period of
Speaker 1: reduction in cases. The infection rate in the US continues
Speaker 1: to escalate, and the number of deaths grew to more
Speaker 1: than undred over the past two days. All around the world,
Speaker 1: the number of places enacting strict isolation measures is going up.
Speaker 1: The tie tourist hotspot of Poquette went on lockdown, and
Speaker 1: Moscow's nearly thirteen million residents were ordered to stay home.
Speaker 1: In the US, Maryland Governor Larry Hogan issued a stay
Speaker 1: at home order saying voluntary measures weren't working, and on
Speaker 1: Monday afternoon, Governor Ralph Northam echoed the decision. In Virginia,
Speaker 1: Virginians were ordered to remain in their homes except for
Speaker 1: central services and now today's main story, the deadly tipping point.
Speaker 1: The new coronavirus has sickened hundreds of millions and will
Speaker 1: infect many more, but only a small fraction of the
Speaker 1: people who get the virus dye. The virus acts in
Speaker 1: a way that scientists are still trying to figure out.
Speaker 1: In some people who are infected, symptoms are mild, like
Speaker 1: a common cold. Some don't have symptoms at all. In others, though,
Speaker 1: symptoms are severe and even fatal, with the infections stopping
Speaker 1: the lungs from functioning and causing the body to shut down.
Speaker 1: So why are symptoms so mild in some people and
Speaker 1: deadly in others. It turns out there's a tipping point,
Speaker 1: a moment where the virus moves from one part of
Speaker 1: the body to another that can determine whether the virus
Speaker 1: is manageable or fatal. Jason Gale spoke to experts to
Speaker 1: understand what the virus does to us once it's in
Speaker 1: our bodies. As of nineteen, the disease caused by the
Speaker 1: new coronavirus spreads around the world. Scientists are beginning to
Speaker 1: understand more about how it maims and kills. A picture
Speaker 1: is emerging of an enigmatic pathogen whose effects are mainly mild,
Speaker 1: but which occasionally and unpredictably becomes serious. In the second
Speaker 1: or third week in a fraction of patients. Bodily systems
Speaker 1: start to fall apart in a cascade. But what causes
Speaker 1: this deadly tipping point. Other diseases like SARS or severe
Speaker 1: acute respiratory syndrome and influenza offer important clues about what's
Speaker 1: going on inside the body when someone has COVID nineteen.
Speaker 1: The clinical picture suggests a pattern of disease that's not
Speaker 1: dissimilar to what we might see in influenza, with a
Speaker 1: range of outcomes. Dr Jeffrey Taubenberger is a pathologist who
Speaker 1: studied the infection in victims of the Spanish flu pandemic,
Speaker 1: including one exam to more than twenty years ago from
Speaker 1: perma frost in northwestern Alaska. Jeffrey heads the Viral Pathogenesis
Speaker 1: and Evolution section of the National Institute of Allergy and
Speaker 1: Infectious diseases in Bethesda, Maryland. In his spare time, he's
Speaker 1: a musician and composes symphonies and operas, but COVID nineteen
Speaker 1: is his current focus. The answer to what the pathogenesis
Speaker 1: is and why certain people are having more severe disease
Speaker 1: and others having mild disease is not fully understood. But
Speaker 1: I think that in relation to other diseases sours twenty
Speaker 1: years ago almost and influenza now for hundred years, we
Speaker 1: have information where it's at least analogous. COVID nineteen causes
Speaker 1: a little more than a cough if it stays in
Speaker 1: the nose and throat, which it does for most people
Speaker 1: a unlucky enough to be infected. The vast majority of
Speaker 1: people who are exposed to a virus to which they
Speaker 1: probably don't have protective immunity get infected, and most of
Speaker 1: them clear their virus and get better with varying illness.
Speaker 1: A report from China and February showed that one in
Speaker 1: seven patients develops difficulty breathing, and six of cases are critical.
Speaker 1: It's why hospitals worldwide are either experiencing or bracing for
Speaker 1: scores of patients requiring mechanical ventilation. For days two weeks.
Speaker 1: Jeffrey says infection is like a dance between the host
Speaker 1: that's us and the pathogen, in this case, the new coronavirus.
Speaker 1: What causes disease and how quickly it can escalate comes
Speaker 1: down to an interplay of three factors, how nasty the
Speaker 1: virus is, the body's immune response to it, and the
Speaker 1: role of secondary infections. What generally happens is that you
Speaker 1: get an infection of a virus that sets up an
Speaker 1: infection along cells that line your respiratory tracts, starting at
Speaker 1: your nose, maybe migrating downwards into your trachea and the bronchos,
Speaker 1: and then maybe eventually into lungs. If your infection is
Speaker 1: limited to the upper respiratory tract more like a call.
Speaker 1: Even with influenza, you're mostly likely to get a cold
Speaker 1: virus like disease mild. You sort of throat in a
Speaker 1: cough and sniffles and sneeze, maybe fever, but you otherwise
Speaker 1: don't get severely. Danger starts when the virus reaches the lungs.
Speaker 1: Pathogenic viruses that induce a lot of direct sell death
Speaker 1: along the restaur attract induce a very strong inflammatory response.
Speaker 1: The kind of a so called pro inflammatory response that
Speaker 1: itself is actually damaging to bystander cells. The inflammatory responses
Speaker 1: an initial warning system, like a fire alarm. The body's
Speaker 1: first respond is different types of white blood cells, known
Speaker 1: as neutrophils and macrofages are sent out to destroy and
Speaker 1: dispose of infected cells and repair damage tissue. Let's say
Speaker 1: in an analogy, you don't necessarily know where the fire is,
Speaker 1: but there's a fire, and so you should do something.
Speaker 1: We should shun on sprinklers, which you call the fire department.
Speaker 1: We should turn on the water host. So this initial
Speaker 1: inflammatory response is that initial response. There's something wrong, we
Speaker 1: need to do something. Normally, if this goes well, the
Speaker 1: infection is cleared up in just a few days. The
Speaker 1: inflammation tamps down viral replication, enabling the body to recover.
Speaker 1: But in rare instances, this inflammatory response goes overboard and
Speaker 1: becomes damaging. Jeffrey says, cells that may not even be
Speaker 1: infected with the virus can be targeted and damaged by
Speaker 1: these inflammatory cells. Your body is immediately trying to repair
Speaker 1: the damage in the lung as soon as it's happening. Uh.
Speaker 1: And then it's a question of does the inflammatory in
Speaker 1: the virus win or does your reparative and immune responses win?
Speaker 1: And most of the time evene responses win because most
Speaker 1: people will get infective with these viruses survive, but in
Speaker 1: some people they don't. The destruction of cells can release
Speaker 1: toxins into the bloodstream, attracting more neutrophils to clean up
Speaker 1: the dead material, and that can itself kind of create
Speaker 1: kind of a perfect storm of augmenting the inflammatory response.
Speaker 1: Further studies of fatal COVID nineteen patients have confirmed this
Speaker 1: kind of bi standard damage along the respiratory tract. The
Speaker 1: coronavirus targets distinctly shaped protein receptors, and these are found
Speaker 1: on many organs and tissues, including epithelial cells. When an
Speaker 1: infection harms the epithelium lining the trachea and bronchi, it
Speaker 1: can result in the loss of protective mucus producing cells,
Speaker 1: as well as the tiny hairs or cilia that sweep
Speaker 1: dirt and respiratory secretions out of the lungs. It's part
Speaker 1: of the interplay between the initial damage caused by the
Speaker 1: virus and the secondary damage caused by the body's own
Speaker 1: inflammatory response, and that combination can lead you to have
Speaker 1: more severe disease that can set you up for the
Speaker 1: third piece of this puzzle, which is that if you
Speaker 1: damage especially the lower respiratory tract epithelium and all the
Speaker 1: barriers that you have in your lungs from keeping bacteria
Speaker 1: and other pathogens from getting down into the lung, meaning
Speaker 1: that you've damaged the lining of the trichy bronchial trees
Speaker 1: and that the cilia that can constantly move all this
Speaker 1: material upward or lost, you lose mucous secretion, you have
Speaker 1: no ability to keep stuff out of the lower respiratory track.
Speaker 1: You can set yourself up for in an evasive secondary
Speaker 1: bacterial infection. In the case of Spanish flu, autopsies and
Speaker 1: experimental studies performed in the Torbenberger Lab show that almost
Speaker 1: everyone who died from the nine eighteen pandemic succumbed to
Speaker 1: a secondary bacterial pneumonia. Jeffrey says it's too early to
Speaker 1: save something similar as happening with COVID nineteen. The coronavirus
Speaker 1: has some features that set it apart from flu. One
Speaker 1: is that it's capable of replicating not just in the
Speaker 1: cells of the respiratory system, but also in other parts
Speaker 1: of the body, including the gastro intestinal tract, and that's
Speaker 1: probably why some patients experience diarrhea and why the virus
Speaker 1: has been found in stool. But it's the damage to
Speaker 1: the lungs that's feeling intensive care unipeds many I see
Speaker 1: you patients require mechanical ventilation to counter low blood oxygen,
Speaker 1: a condition doctors referred to as hypoxia in terms of
Speaker 1: end stage disease. If the lung ist damaged knowledge from
Speaker 1: a primary of ouril infection and or secondary of bacterial infection,
Speaker 1: both in flu or in coronavirus, but consequence of that
Speaker 1: is um decreased lung functions, You have decreased oxygen exchange,
Speaker 1: and if you have less oxygen available then is needed
Speaker 1: you start damaging other end stage organs. Of course, your kidneys,
Speaker 1: your livering, your brain, your heart as vague get damaged
Speaker 1: and as your kidneys stop being able to clear toxins
Speaker 1: that in self induces more disease. You can see that
Speaker 1: you can have this multi organ failure as an end
Speaker 1: stage of disease, although it's really primarily related to the
Speaker 1: loss of pulmonary function in hypoxia. During my interview, one
Speaker 1: of Jeffrey's main collaborators join the conversation. I'm pretty sure
Speaker 1: I don't know anything more. Dr David Morrens is a
Speaker 1: senior scientific advisor to Tony Fauci, the director of the
Speaker 1: National Institute of Allergy and Infectious Disease IS. David graduated
Speaker 1: from medical school in nine three and joined the Sentence
Speaker 1: for Disease Control and Preventions Epidemic Intelligence Service a few
Speaker 1: years later. He's been at the institute for more than
Speaker 1: twenty years and was wearing a navy uniform of the
Speaker 1: United States Public Health Service. David's been studying emerging infectious diseases,
Speaker 1: including the ways viruses cause disease, for more than forty years.
Speaker 1: He says patterns and COVID nineteen patients are pretty familiar.
Speaker 1: I sometimes think of it as when you get a bad,
Speaker 1: overwhelming infection, everything starts to fall apart. In the cascade.
Speaker 1: It's like dominoes falling over. You know, the oxygen gets
Speaker 1: a lot of the tissue gets more damaged, the immune
Speaker 1: responses more effective, the oxygen radicles come up, and you
Speaker 1: pass the tipping point where everything's going downhill and at
Speaker 1: some point you can't get it back. Both David and
Speaker 1: Jeffrey agree that chronic conditions like hypertension, diabetes, and cancer
Speaker 1: treatment impair the body's ability to fight the coronavirus. These
Speaker 1: elements are more common in older people, which is one
Speaker 1: of the reasons why age is the biggest risk factor
Speaker 1: for dying from COVID nineteen, but that risk overall remains
Speaker 1: relatively low. The experience doctors are gaining from managing patients
Speaker 1: and the evidence flowing from clinical trials are informing treatment guidelines,
Speaker 1: and that should lead to better care for patients. That's
Speaker 1: it for the Prognosis Daily Edition. For more on the
Speaker 1: coronavirus crisis from a hundred and twenty bureaus around the world,
Speaker 1: visit Bloomberg dot com slash coronavirus. If you appreciate the podcast,
Speaker 1: please take a moment to read us and leave us
Speaker 1: a review on Apple Podcasts or Spotify to help more
Speaker 1: listeners find our global reporting. The Prognosis Daily Edition is
Speaker 1: hosted by me Laura Carlson. The show is produced by
Speaker 1: Me Tob Foreheads, Jordan Gospore, and Magnus Hendriksson. Reporting by
Speaker 1: Jason Gale, Original music by Leo Sigrid. Our editors are
Speaker 1: Francesca Leavie and Rick Shine. Francesca Levy is Bloomberg's head
Speaker 1: of podcasts. Thanks for listening.