Speaker 1: It's the early days of the pandemic in and doctor
Speaker 1: Daniel Cherto has a new patient, a twenty six year
Speaker 1: old male who was hospitalized with chance pain. He did
Speaker 1: not present with the typical COVID symptoms, you know, the
Speaker 1: shortness of breath, for fever and all this other stuff.
Speaker 1: It was justice comfort and he tested negative on on
Speaker 1: multiple occasions. Dan runs the Emerging Pathogen Section at the
Speaker 1: National Institutes of Health in Bethesda, Maryland, and if you're
Speaker 1: a COVID case his lab, you're not there for treatment,
Speaker 1: you're the subject of an autopsy. Dan and his team
Speaker 1: are studying this young man as part of a big
Speaker 1: emission to figure out where in the body the coronavirus goes.
Speaker 1: He thinks that by tracing the virus's path and seeing
Speaker 1: what it does, it can understand why it's causing disease
Speaker 1: and how to stop it. Think of it like he's detective,
Speaker 1: trying to collect evidence and looking for the m O
Speaker 1: of a killer before it can strike again. Primary questions
Speaker 1: that were I to address the initial questions are really
Speaker 1: the cellular distribution of the virus across the body and
Speaker 1: the brain. So, in other words, exactly where does the
Speaker 1: virus go, what cell types does it back and really,
Speaker 1: really importantly, how long does the virus stay there. Dan
Speaker 1: and his technique to work fast to get participants like
Speaker 1: his new patient. They have about twenty four hours after
Speaker 1: someone has dyed to study them certain tissues to grate
Speaker 1: quickly after death, destroying the evidence. Getting these patients in
Speaker 1: that time has become a massive logistical undertaking. They first
Speaker 1: talked to the family to get their approval. From there,
Speaker 1: they make arrangements with a funeral home to transport the
Speaker 1: remains to the NIH Clinical Center and Bethesda at least
Speaker 1: set up a call schedule where I might hear about
Speaker 1: these cases. At two o'clock in the morning, communicate with
Speaker 1: our amazing, amazing admissions department, who would facilitate our contract
Speaker 1: funel home and going out in the middle of the
Speaker 1: night bringing bodies here so that my team would be
Speaker 1: suited up. At nine o'clock in the morning on this
Speaker 1: spring day in twenty Dan and his team are in
Speaker 1: a secure along chamber wearing astronaut and spied protective gear
Speaker 1: as they examine their new patient. The man died at
Speaker 1: the hospital and tests were negative for the coronavirus, so
Speaker 1: he doesn't fit the definition of a COVID related fatality. Instead,
Speaker 1: he died of something called viral myokiditis or inflammation of
Speaker 1: the heart muscle. But dances there was a reason he
Speaker 1: still wanted to study him. And at that time you
Speaker 1: probably remembered there were a number of reports in the literature,
Speaker 1: and there were some articles coming out and of imaging
Speaker 1: of the hard and some autopsies, you know, and but
Speaker 1: case reports of viral mild cardiitis being an unusual but
Speaker 1: but present complication of COVID. As they examine his body
Speaker 1: and heart, Dan says there's good evidence COVID is the culprit.
Speaker 1: Not only that the patient offers clues about another condition
Speaker 1: link to the coronavirus. It's called multi system inflammatory syndrome.
Speaker 1: It occurs mostly in children after a saska v TO infection,
Speaker 1: but it's been reported in adults as well. Dan says
Speaker 1: it's a condition that can arise unexpectedly after a mild
Speaker 1: case of COVID. They show up later with sometimes life
Speaker 1: threatening inflammation in different oregans. So in a way he
Speaker 1: fits into that category. And so well, what's driving and
Speaker 1: that is the point of Dan's work performing these autopsies
Speaker 1: is like recreating police sketches and more and more detail.
Speaker 1: With every autopsy, the picture gets clearer of what COVID
Speaker 1: is capable of doing across our bodies and what impact
Speaker 1: it may have on them in the long run. Is
Speaker 1: there going to be, you know, some low level or
Speaker 1: subclinical injury to your heart that then may manifest differently
Speaker 1: later in life. I don't know. Is there going to
Speaker 1: be some subclinical effect on your brain that are going
Speaker 1: to cause nerve cognitive issues later in life that perhaps
Speaker 1: are not immediately noticeable or detectable. If you're going to
Speaker 1: begin to conceive of ways to prevent or treat those manifestations,
Speaker 1: either in the group that the next group that might
Speaker 1: be exposed or among the group that are suffering, you,
Speaker 1: you need to understand mechanism. You need to understand what
Speaker 1: the drivers are. But this work has a long way
Speaker 1: to go. Scientists like Dan are just starting to learn
Speaker 1: the biological means by which siskov two managers to affect
Speaker 1: virtually every organ system in the body. Those infected and
Speaker 1: experience symptoms lasting months and potentially years. The condition is
Speaker 1: called long covid, and Dan's research could help us understand
Speaker 1: how to better combat it. But science is an iterative process.
Speaker 1: New information or clues have to be checked and validated
Speaker 1: before they're accepted as proof, and right now there's a
Speaker 1: ton of information but not a lot of admissible evidence.
Speaker 1: Conflicting theories have popped up over the last year and
Speaker 1: a half, which only shows how much more fact gathering
Speaker 1: needs to be done and resources for critical research like
Speaker 1: autopsies that help us understand new diseases have been stretched
Speaker 1: in It means disease detectives have fewer tools to use
Speaker 1: in that pursuit of the killer. I'm not here to
Speaker 1: service of fear manger. I mean that's not that's not much.
Speaker 1: It's just that these are some under answered questions. I'm
Speaker 1: Jason Gale, chief biosecurity correspondent and a senior editor at
Speaker 1: Bloomberg News. From the Prognosis podcast. This is breakthrough. Pathology
Speaker 1: is one of the sort of fundamental building blocks of medicine.
Speaker 1: This is Dr Linda Isles. She's the head of Forensic
Speaker 1: Pathology Services at the Victorian Institute of Forensic Medicine. It's
Speaker 1: like a medical examiner's office, but this one in Melbourne
Speaker 1: is the largest of its kind in Australia. Linda is
Speaker 1: as heat bespectacled woman with short, salt and pepper hair.
Speaker 1: She finished medical school at the University of Tasmania more
Speaker 1: than twenty years ago and then went on to train
Speaker 1: in anatomical pathology. She estimates she probably did two hundred
Speaker 1: three d autopsies during her training, which if you compare
Speaker 1: that to kind of really old school back in the day,
Speaker 1: then that might not seem like very many. But if
Speaker 1: you compare that to anaton called pathology trainees now, then
Speaker 1: that is a very large amount. These days, pathology trainees
Speaker 1: aren't even required to do autopsies. Fundamentally, autopsies are expensive procedures.
Speaker 1: I think autopsies have been slightly undervalued by clinicians over
Speaker 1: a number of years, even decades perhaps, and as less
Speaker 1: autopsies are requested, less pathologists have experience with autopsies. This
Speaker 1: points to a big problem happening in modern medicine. Autopsies
Speaker 1: have been the bedrock of medical science since at least
Speaker 1: the fifteen hundreds, but today sophisticated imaging and other modern
Speaker 1: diagnostic tools and hospital cost cutting have turned them into
Speaker 1: a dying science. Linda says there are a few reasons
Speaker 1: why autopsies have started to go out of style. One
Speaker 1: of them is that facilities are expensive to maintain at
Speaker 1: a safe standard. So it's this spiral of decreased experience
Speaker 1: and therefore decreasing confidence and then under utilization of the
Speaker 1: facilities to some of the facilities essentially being mothballed, and
Speaker 1: then when you want to reinstat to them, then they're
Speaker 1: no longer really safe for modern practice. So it's sort
Speaker 1: of like this catch twenty two, and now we really
Speaker 1: left with the generation of pathologists that have really quite
Speaker 1: limited autopsy experience, and therefore their confidence in performing autopsies
Speaker 1: safely is significantly diminished. This lack of expertise was only
Speaker 1: exacerbated during the pandemic. In the first few months of
Speaker 1: the outbreak, health authorities warned that doctors would become infected
Speaker 1: while performing autopsies and handling virus laden tissues. That led
Speaker 1: to half of these units shutting down. In the US,
Speaker 1: the same sort of scenario played out across the world.
Speaker 1: In Germany, initially it was like, no, we will definitely
Speaker 1: not autopsy these COVID patients, and then a bunch of
Speaker 1: pathologist said no, we have to do this. Because this
Speaker 1: is a new disease process. And then they just did
Speaker 1: a complete switchero and funded the autopsy program, which is
Speaker 1: where a lot of the really valuable data has actually
Speaker 1: come out of Among the first four million fatal COVID
Speaker 1: cases worldwide, only several hundred were autopsied and the findings
Speaker 1: reported in medical journals. That delayed getting answers to some
Speaker 1: crucial questions about COVID nineteen and its effects in the body.
Speaker 1: The good news is that detailed post mortem investigations are
Speaker 1: picking up now. Linda says this could also bring greater
Speaker 1: awareness the value of autopsy research, whether it's just going
Speaker 1: to be a sort of short term thing or whether
Speaker 1: it's going to translate into something kind of more meaningful.
Speaker 1: I mean, I can only hope that it's going to
Speaker 1: be the ladder. But you know this, the idea that
Speaker 1: novel infectious diseases are a thing of the past is
Speaker 1: you know. I think this has kind of brought this
Speaker 1: certainly front and center for people. Not all doctors waited
Speaker 1: so long before returning to autopsies. Disease detectives like Dancerto
Speaker 1: accepted the risk early on in the pursuit of answers.
Speaker 1: Most of the SHOTS team he's made up of trainees,
Speaker 1: and at the start of the pandemic, he wanted to
Speaker 1: give them the chance to contribute from home if they
Speaker 1: felt more comfortable working that way. I said, we're an
Speaker 1: emerging pathoge in his lab, like there's a pandemic. If
Speaker 1: you want to work remotely, that's okay. But for those
Speaker 1: of you that want to be present on SAITE, these
Speaker 1: are the things we're going to be focusing on. Selectives
Speaker 1: stick around and with rare exception, you know, everybody's like
Speaker 1: we're on deck. Dan himself is used to working in
Speaker 1: dangerous environments. He was in Liberia during the Ebola crisis,
Speaker 1: caring for patients and later studying the virus. Before that,
Speaker 1: he worked on the nineteen eighteen Spanish flu pandemic virus.
Speaker 1: His experience provided a grounding in bio safety that's carried
Speaker 1: through to his personal life. Dan says he takes precautions
Speaker 1: like wearing a face mask when he can't physically distance
Speaker 1: to prevent getting SANSKOVI two. I'm not a risk averse person.
Speaker 1: I'm a believer in calculated and controlled risk, right, but
Speaker 1: I know that my absolute preference for myself, my family,
Speaker 1: my loved ones, my colleagues, my kids. I got an
Speaker 1: eight year old and a twelve year old, my preferences
Speaker 1: for them not to be infected. Dan says he applied
Speaker 1: one hey and I was learned from the Ebola outbreak
Speaker 1: to understanding kinvid nineteen. It started with this idea that
Speaker 1: first we gotta go find where this virus is going,
Speaker 1: what it's doing in those places, and then we got
Speaker 1: to try to link it back to what we're seeing
Speaker 1: clinically and what is coming out with volumes and volumes
Speaker 1: of evidence that we're all struggling to assimilate and trying
Speaker 1: to put those pieces together to to tell a cohesive
Speaker 1: story about the mechanisms that are contributing to severe acute illness,
Speaker 1: to some mild or asymptomatic disease and others, and in
Speaker 1: a reasonable portion of the popular sation of survivors long
Speaker 1: term symptoms that are really distressing. Dan and his group
Speaker 1: are also trying to figure out how the virus and
Speaker 1: the body interact, which is another way of saying, in
Speaker 1: all those locations that you found evidence of RUS, what
Speaker 1: was the body's response. Is there an infiltration of immune
Speaker 1: cells even in the absence of immune cells, is their
Speaker 1: evidence of damage within those tissues or organs, etcetera, etcetera.
Speaker 1: To begin to better understand that relationship between the virus
Speaker 1: and the host the host response. The more you understand
Speaker 1: that relationship, theoretically, the better equip you will be to
Speaker 1: design therapies and interventions that might mitigate aspects of the
Speaker 1: disease course. These postmoneum exams do carry risk, but the
Speaker 1: pathologists from the National Cancer Institute actually performing the autopsies
Speaker 1: have decades of experience. These are the gentlemen of physicians
Speaker 1: and their trainees that that we're here doing autopsies during
Speaker 1: the AIDS era, and these guys were in there doing
Speaker 1: autopsies on hundreds of patients with this new disease, HIV AIDS.
Speaker 1: So we have now the benefit of working with that
Speaker 1: group here now decades later, lots of experience. These aren't
Speaker 1: typical autopsies though they're done over three hours in a
Speaker 1: secure facility. That's required for work involving microbes that can
Speaker 1: cause serious and potentially lethal disease. So our group, the
Speaker 1: pathologists they design home design a grain box, which is
Speaker 1: basically plexiglass with a glove it's like a glove box.
Speaker 1: Bio Engineers on the NIH campus custom build an enclosure
Speaker 1: that fits over the head and shoulders of the deceased
Speaker 1: to contain aerosols when the brain is removed, to cut
Speaker 1: through the skulls. A little bit morbid, but there's aerosolization, right,
Speaker 1: So you don't want to overly contaminate the environment. So
Speaker 1: implementing this thing and working, and this takes some time.
Speaker 1: The seven also doctors, scientists, and technicians working inside the
Speaker 1: autopsy suite, where multiple layers of personal protective equipment, usually
Speaker 1: a plastic apron over a surgical gown, over an impermeable cover,
Speaker 1: all over surgical scrubs. Sometimes arm sleeve protectors are worn.
Speaker 1: They also donned three pairs of gloves and two pairs
Speaker 1: of shoe coverings, and instead of ninety five masks. They're
Speaker 1: breathing through controlled air purifying respirators, which provide heaper filtered
Speaker 1: air under a hood that fits over the head and shoulders.
Speaker 1: It's cumbersome, but it's not the only aspect of these
Speaker 1: COVID autopsies that makes the work painstaking. We're sampling way
Speaker 1: above in the yard. What has done in any sort
Speaker 1: of diffical We sampled almost a hundred different regions within
Speaker 1: the body across the whole body and brings a hundred
Speaker 1: different areas. And for each one of those areas, we
Speaker 1: collected and preserved adjacent pieces of tissue in different ways
Speaker 1: that are amenable to various down stream analysis that preserve
Speaker 1: the tissues in a better way. It's a ton of
Speaker 1: time and energy to analyze these samples, but time is important.
Speaker 1: The first cases of long COVID happened over a year
Speaker 1: and a half ago, and only more developing. The sooner
Speaker 1: we get results from autopsies like Dan's, the Sinner will
Speaker 1: begin to address the long term effects of COVID nineteen.
Speaker 1: Dan's are research will not only help us understand what
Speaker 1: the courses are, but how to counter them. There are
Speaker 1: many theories on white people continue to suffer from a
Speaker 1: multitude of symptoms long after a coronavirus infection. Some are
Speaker 1: easy to explain, others are a mystery. For example, it's
Speaker 1: known that if COVID gave you a severe case of pneumonia,
Speaker 1: your lungs could have scarring that might reduce lung capacity.
Speaker 1: That's an unfortunate consequence of acute respiratory distress syndrome that
Speaker 1: can also occur with the flu. If you were unlucky
Speaker 1: enough to need intensive care, that slinked to muscle weakness,
Speaker 1: memory problems, and a raft of other conditions referred to
Speaker 1: as post intensive care syndrome. And if you were really
Speaker 1: unfortunate and needed mechanical ventilation that's long been associated with
Speaker 1: post traumatic stress disorder. But these aren't the problems baffling
Speaker 1: doctors and researchers. The biggest surprise of COVID is that
Speaker 1: people who are not in the intensive care unit, people
Speaker 1: actually who are never needed to be hospitalized, are still
Speaker 1: having persistent symptoms. This is Dr Walter Kaschatz, who we
Speaker 1: heard from in our last episode. He heads the National
Speaker 1: Institute of Neurological Disorders and Stroke and Bethesda. Walter says
Speaker 1: it's this group of patients, the ones with unexplained fatigue,
Speaker 1: brain fog, weird heart palpitations, and body aches and pains,
Speaker 1: who also represent the largest pool of patients who are
Speaker 1: persistently unwell as a result of the pandemic. The long
Speaker 1: COVID have fatigue. That's the primary, very complaining factor. That's
Speaker 1: true about the post ice use cases, as well, fatigue
Speaker 1: is a major problem, but the long COVID symptom complex
Speaker 1: of fatigue, trouble with memory, travel with thinking quickly, executive function,
Speaker 1: trouble as sleep pain syndromes sometimes, and exercise and tolerance.
Speaker 1: Those are the features of this syndrome that we don't
Speaker 1: have good explanations for at this point. In some ways,
Speaker 1: the disease pattern many long COVID suffers experience resembles mono
Speaker 1: or infectious mononucleosis. It's called glandular fever where I am
Speaker 1: in Australia, and some people refer to it as the
Speaker 1: kissing disease, possibly because it's spread through saliva and often
Speaker 1: occurs in teenagers. The culprit is usually the epstein bea virus.
Speaker 1: It can cause fever, swollen glands in the neck and armpits,
Speaker 1: and a sore throat. Most cases of mono were mild
Speaker 1: and resol of in their own in one to two months,
Speaker 1: but Waltera says that's not always the case with infectious
Speaker 1: mono nucleosis. There is another syndrome which you've probably heard
Speaker 1: about well, realogic can cephalomi elitis chronic critique syndrome and
Speaker 1: symptoms are very overlapping between what long COVID folks are
Speaker 1: complaining of and what happens in NBCFS. It's just that
Speaker 1: MBCFS has a six month period. You have to had
Speaker 1: those symptoms for six months, But it looks like people
Speaker 1: are moving into that space. Waltera says. Researchers have been
Speaker 1: trying for years to figure out the causative driver of
Speaker 1: that longer term illness after infectious morning. Now with the
Speaker 1: thirty four million people with COVID, it's a tremendous challenge
Speaker 1: now that we have to take up to try to
Speaker 1: figure that out. There is now a greater chance that
Speaker 1: we're going to figure it out now because we have
Speaker 1: this opportunity to study so many people and to try
Speaker 1: and understand what differentiates those who get better quickly versus
Speaker 1: those who have these persistent symptoms. So the hope is that,
Speaker 1: you know, we can get some answers that would allow
Speaker 1: us to try different treatments to see what helps and
Speaker 1: then potentially also learns something about what causes NBCFS as well.
Speaker 1: Congress is giving the National Institutes of Health one point
Speaker 1: one five billion dollars over four years to find answers
Speaker 1: Ault along with Dr Anthony Felchi from the National Institute
Speaker 1: of Allergy and Infectious Diseases and Dr Gary Gimmons from
Speaker 1: the National Heart Institute are co directing the research. There's
Speaker 1: a clinical team, that's an autopsy team, that the electronic
Speaker 1: health record team, I know, there's a big data team,
Speaker 1: and there's probably a couple of others, So there's I
Speaker 1: think the estimate was three hundred people have been working
Speaker 1: on this project since November. The amount of money Congress
Speaker 1: has set aside to study long COVID seems a lot,
Speaker 1: but it pales compared with the trillions of dollars the
Speaker 1: pandemic has cost already and the economic toller will have
Speaker 1: decades into the future. Some estimates suggest that more than
Speaker 1: one billion people around the world have been infected with
Speaker 1: the coronavirus. We don't know yet what proportion of them
Speaker 1: will develop long COVID or the duration of their symptoms.
Speaker 1: My gut feeling is that you're probably close to a
Speaker 1: ten percent figuring out about six months out. This is
Speaker 1: Dr RV. Nath He's the clinical director at the National
Speaker 1: Institute of Neurological Disorders and Stroke. The one waterheads people
Speaker 1: do recover or a period of flame on spontaneous people.
Speaker 1: But most often if you're not better by six months,
Speaker 1: then the chances of getting better are become really less. Obviously,
Speaker 1: says the impact on individuals, families, and societies will be
Speaker 1: I mean, nobody's gonna do with the calculations for you,
Speaker 1: but it's a dream on society to get every single level.
Speaker 1: I mean, it affects women more than then. It affects
Speaker 1: people and their average ages forty that's the most productive
Speaker 1: years of your life. And so you can see that
Speaker 1: the impact worldwide impact of this is unbelievable. You couldn't
Speaker 1: translate it to money. The impact is I mean the
Speaker 1: economic toll, the psychological toll. Every aspect of society is
Speaker 1: kind of touched. It's why figuring out the cause and
Speaker 1: waste to treat and prevent long COVID are so critically important. Obviously,
Speaker 1: there could be two main driving forces behind the clinical manifestations.
Speaker 1: One is that the coronavirus manages to persist in the
Speaker 1: body somewhere somehow, and that it's lingering presence is damaging
Speaker 1: the body directly, or it's triggering an immune response that's
Speaker 1: causing the damage. Another hypothesis is that the coronavirus has
Speaker 1: sent the immune system haywire, and it's this disregulated immune
Speaker 1: response that's drive long COVID. I think they're all reasonable hypotheses,
Speaker 1: but they're not exclusive. They could be interrelated. Have He's
Speaker 1: been researching chronic fatigue for years and now he's also
Speaker 1: trying to understand it as well as other elements in
Speaker 1: long COVID patients. One of the interesting features about this
Speaker 1: illness is that if you look at it, the people
Speaker 1: who had were these long haul symptoms are often not
Speaker 1: the individuals who are hospitalized and we're sicking on and
Speaker 1: went later and stuff like that. These are individuals who actually,
Speaker 1: most often they never went to the hospital. They were
Speaker 1: at home and during that time they had relatively mild
Speaker 1: illness in the acute phase and they recovered from it. Obviously,
Speaker 1: says that the people who were sick enough to require
Speaker 1: hospitalization probably mounted a strong immune response that helped them
Speaker 1: to eventually recover and importantly get rid of the virus.
Speaker 1: But if you had a mild illness, perhaps you never
Speaker 1: mounted a strong enough immune response. You thought, oh, you know,
Speaker 1: I escaped, but in reality you've never got rid of
Speaker 1: the virus. Viruses can remain in their infectious form and
Speaker 1: a range of diseases from AIDS to chicken box to
Speaker 1: a bowler. Some sortists say that the coronavirus may cause
Speaker 1: a persistent infection in places like the gas and wind,
Speaker 1: testinal tract, and the nose, but there's no consensus among
Speaker 1: scientists that that's the case, obviously, says Another possibility is
Speaker 1: that what's persisting are viral particles. They may not be
Speaker 1: completely replicating, butter instead expressing some features of the virus.
Speaker 1: Now what the body is going to see it as
Speaker 1: a foreign object, is going to try to mount an
Speaker 1: immune response against. So you've got this conic immune activation
Speaker 1: that persists in these individuals, but it's never good enough
Speaker 1: to get rid of it because they never got river
Speaker 1: in the first place, but it's enough to start causing
Speaker 1: collateral damage. Obviously, the same pattern of immune activation and
Speaker 1: exhaustion in chronic fatigue or m ec effast patients. They
Speaker 1: look very much like these long hold COVID patients, and
Speaker 1: they had the similar problems. They usually start off with
Speaker 1: some violent infection, then they had cover from it, and
Speaker 1: then this thing persists. Whatever. The field of researchers working
Speaker 1: to unravel COVID's mysteries is growing, and it's bringing in
Speaker 1: expertise from all kinds of areas neurology, cardiology, horminology, and
Speaker 1: infectious diseases that includes HIV. Medicine Professor Steve Deetz has
Speaker 1: been researching a cure for HIV for almost thirty years
Speaker 1: at the University of California, San Francisco. When the pandemic hit,
Speaker 1: Steve took notice. We had no idea what was going
Speaker 1: to go on with Sariskoby too, but we knew it
Speaker 1: was a big deal, and we had a good sense
Speaker 1: that they're probably going to be some long term content places.
Speaker 1: Everybody was focused on short term. Steve began enrolling patients
Speaker 1: in a study aimed at identifying how saskov two affects
Speaker 1: long term health. Subset have long COVID and some don't,
Speaker 1: and we're beginning to do the biology. And one of
Speaker 1: our leading hypotheses is that the virus does persist in
Speaker 1: some people for some reason, and that that persistent virus
Speaker 1: initiates an inflammatory process. At the heart of all this
Speaker 1: has always been the concern that there is something that
Speaker 1: persists and stimulates that a normal response. Steve thinks the
Speaker 1: coronavirus might be leaving traces behind. It could be viral protein,
Speaker 1: strands of its genetic material, or even bits of antigen
Speaker 1: that the immune system responds to. We don't think it's
Speaker 1: virus replication, but I guess it could be virus that's
Speaker 1: replicating in target cells and tissues. We always thought that
Speaker 1: that was a potential reason for why this symptoms persists.
Speaker 1: Steve says Dan's research when it's published, could have significant
Speaker 1: implications for treatment. If the experts out there tell me, yes,
Speaker 1: we think that there is a persistent repository of virus protein,
Speaker 1: nucleic acid, or even virus replication, then for me it's
Speaker 1: easy to say, okay, well then thousand ways and that
Speaker 1: can cause long COVID. We need to give people an
Speaker 1: anti virus. We need to get people antibodies or therapy
Speaker 1: vaccine and see if they get better. And that's what
Speaker 1: we're planning on doing. But we need more rational. We
Speaker 1: need a paper from the NIH saying, you know, with
Speaker 1: ni H level standards, yes, indeed some people have virus.
Speaker 1: And if they tell me that these people virus also
Speaker 1: had symptoms, well, that would be helpful. Steve says. Circumstantial
Speaker 1: evidence supports the concept that there's something persistent that's causing
Speaker 1: long covids. All these ancdotes out there about people who
Speaker 1: have long COVID and get a vaccine and get better,
Speaker 1: and the only way to explain that is that there's
Speaker 1: persistent virus that's not being cleared by the immune system,
Speaker 1: and the vaccine makes the immune system better and the
Speaker 1: virus goes away and they're healthier. And if we can
Speaker 1: prove it, then me as a as a clinical trial,
Speaker 1: as can do all the clinical trials, we can look
Speaker 1: at any of these anthem virals, any of these antibodies,
Speaker 1: and these vaccines, they all should help. Well. It's a
Speaker 1: very important study and I hope it comes out soon.
Speaker 1: Deep in his lab, Dancoto and his team have amassed
Speaker 1: more than ten thousand autopsy specimens for meticulous study. Their
Speaker 1: analysis is beginning to yield some answers to the many
Speaker 1: questions around long COVID and what causes it. They know
Speaker 1: that the research tools will have in years from now
Speaker 1: will provide even greater insight, which is why a big
Speaker 1: part of their work as involved careful preservation of the
Speaker 1: samples collected from each patient. For instance, some tissues go
Speaker 1: into a solution that preserves nuclinic asset. The virus is
Speaker 1: genetic material, and then we use a highly sensitive PCR
Speaker 1: essay to query presence or absence of all orn and
Speaker 1: those tissues, and Dance group is going further to see
Speaker 1: if the virus that's collected from different areas of the
Speaker 1: body is still infectious. Can we actually get viable virus?
Speaker 1: Can we grow virus from from these different sites we've done,
Speaker 1: you know, simply put a much more extensive sampling than
Speaker 1: than others have. The data from the biospecimens are also
Speaker 1: matched with patient records, including genetic tests used to identify
Speaker 1: certain individual variations in a person's immune system. You have
Speaker 1: individuals as young as six years old, very very sad
Speaker 1: to beyond ninety years old. It's diverse, you know, across
Speaker 1: gender and raise and ethnicity. It's diverse across a really
Speaker 1: important parameter, which is when we perform the autopsy relevant
Speaker 1: to symptom on set from COVID. There have now been
Speaker 1: dozens of studies published based on autopsy findings that have
Speaker 1: added data points to a map showing where the virus
Speaker 1: is going and what it's doing across the body. Others
Speaker 1: have done a very good job of creating the outline
Speaker 1: of that map of where the virus goes, what cell types,
Speaker 1: you know, how long it sticks. We intend to put
Speaker 1: some more spots on that map, you know, to help
Speaker 1: to help kind of fill it in both as far
Speaker 1: as different locations, different cell types, period of time. You
Speaker 1: know that that researchers can then use moving forward. It's
Speaker 1: already clear to day that Sasko vie too spreads through
Speaker 1: the body wider than previously thought in patients with mild
Speaker 1: or even no symptoms. I think we're operating under the
Speaker 1: impression that for the most part, the virus is contained
Speaker 1: in the respiery track, perhaps just the upper row story track,
Speaker 1: never makes it to its lungs and then doesn't go
Speaker 1: past that right like, it doesn't get into the bloodstream,
Speaker 1: it doesn't distribute to other parts of the body, and
Speaker 1: then you clear it, you know, you're better. I'm not
Speaker 1: sure that's the case. There's not a lot of evidence
Speaker 1: in this space, and says some of the patients who
Speaker 1: died with rather than rome COVID will provide some insight
Speaker 1: into that. Those are issues that we cannot just assume.
Speaker 1: One thing and the implications of that are important because
Speaker 1: if you are mildly symptomatic or asymptomatic, but you actually
Speaker 1: do have a period of iramia or the virus tropes
Speaker 1: to different parts of your body and then you know,
Speaker 1: you feel better, but actually the virus is persisting for
Speaker 1: a certain period of time and causing injury or the
Speaker 1: body's response to clear that virus is contributing to some
Speaker 1: you know, pathogenic mechanism that is, you know, manifesting as
Speaker 1: long COVID symptoms. We gotta we gotta know that, right,
Speaker 1: We got we gotta know that because without knowing it,
Speaker 1: how are we going to address it? Right? And so
Speaker 1: so we got to begin to kind of turn these
Speaker 1: pages of the book, like peel the layers off the
Speaker 1: onion and try to answer some of these questions. Dances.
Speaker 1: A manuscript based on the young man with Manadas is
Speaker 1: under a valuation by a scientific journal. A paper on
Speaker 1: what his team found looking specifically at the eye is
Speaker 1: undergoing co author review and will be submitted shortly. His
Speaker 1: larger project, providing a map of where the virus is
Speaker 1: going in the body, is pending more data across anatomical sites.
Speaker 1: Dan says he expects this last bit of information shortly
Speaker 1: and then can finish your manuscript. But evidence pointing to
Speaker 1: the causes of long COVID are of little help to
Speaker 1: patience unless the findings in yield ways to help them.
Speaker 1: Next week on Breakthrough, doctors and physical therapists in New
Speaker 1: York are working on strategies to help long haulers manage
Speaker 1: their symptoms. Even though a cure remains a loop us
Speaker 1: thinking outside the box. It's bringing a variety of innovative
Speaker 1: and successful therapeutic options. Some of our patients who have
Speaker 1: been discharged for the longest, they're experiencing relapses. So is
Speaker 1: this something you're gonna have to manage for your entire life,
Speaker 1: or is this something that you're gonna have to manage
Speaker 1: for the next five to ten years. Or is this
Speaker 1: something that we can rehabilitate and we'll discharge you and
Speaker 1: you will never have to think about it again. So
Speaker 1: these are all open questions right now. This episode of
Speaker 1: Prognosis Breakthrough was written and reported by me Jason Gale
Speaker 1: So for four Heads is our senior producer. Carl Kevin
Speaker 1: Robinson Jr. Is our associate producer. Theme music was composed
Speaker 1: and performed by Hannes Brown Rich Shiners editor Franchise get
Speaker 1: Leavy is the head of Bloomberg Podcasts. Be sure to
Speaker 1: subscribe if you haven't already, and if you liked this episode,
Speaker 1: please leave us a review. It helps others find out
Speaker 1: about the show. Thanks for listening.