Clinical and Scientific Assessment of COVID 19: March 20, 2020 by Dr. Inderpal Randhawa

Clinical and Scientific Assessment of COVID 19: March 20, 2020 by Dr. Inderpal Randhawa


(uplifting music) – My name is Dr. Inderpal Randhawa, and I’m the founder and
chief executive officer of the Translational Pulmonary and Immunology Research Center. I’m also an associate professor at both the University
of California Irvine and the University of
California Los Angeles. I maintain a number of
different board certifications in the field of adult and
pediatric pulmonology, immunological-based diseases, and the translation of disease
from children to adults. I have a specific focus
in orphan diseases, particularly rare diseases to which our centers actually build upon. I have been asked, in the last two months, to research, comment, and even participate in research studies particular to COVID-19. And in the next 30 minutes, I will be discussing some of
the summary of these findings to provide clarity to medical providers and to a degree, the general public, and others interested in this condition. So, in the last two months, really, I’d say, even
at the end of December, I started getting calls from people, you know, folks across the board, I do, obviously, international
speaking engagements as well, at universities, and people were asking me what I thought about this virus. And obviously, we didn’t know enough, but I am somebody who, has particular interest
in zoonotic viruses, some of you may or may not know this, but my father came to
this country as a PhD, and indeed, a significant
amount of his publications as a researcher were in zoonotic viruses. So, it’s also something I’ve had some particular interest in. And in the last eight weeks, what has transpired, that
is completely unprecedented, is a serious problem. And what I wanted to do is take what is peer-reviewed literature, information from CDC, WHO, and NIH, and my own particular context, and try to get that
information out to our group, as well as out to our population of individuals that we treat. So, first thing first. We first must understand that the concept of pandemics is serious, and it has occurred in very recent past. If you were around in 2009, you know what the swine flu was. You know that the swine flu
covered two functional seasons, it started in one winter,
northern hemisphere, went to a southern hemisphere, came back to a northern hemisphere. It, in the end, estimated result was it
infected 1.5 billion people. Again, 1.5 billion people got H1N1. Now, the second season was not as bad because we had proper quarantine measures and we had other measures that were taken towards drug therapies. Nonetheless, it actually
hit pediatrics pretty hard. And indeed, I mean, I
was around at that time, and I still remember that
season extremely well. However, it didn’t have the same impact that we’re dealing with now. However again, historically, we’re in a situation where
we know these things happen, we know that the risk of death, as exemplified in this
nice graphic, is there. And yet somehow, we don’t
take this very seriously. And that is what I find
particularly frustrating. The issue around coronavirus is an issue around zoonosis. Zoonotic disease requires reservoirs. And the reservoirs that are implicated in this particular situation, and what I wanna talk about
for the next few minutes, is the relationship
between this coronavirus and the coronavirus from 2002. On the left and on the
right, are two animals. On the left, is a civet, on the right is a pangolin. These are the most
heavily-trafficked animals, the pangolin, especially, is the most heavily-trafficked
animal on Earth. In Asia, in particular South East Asia, these are considered delicacies. However, they are active reservoirs for certain viruses. And so, that is the
fundamental point here. Is that if you don’t control reservoirs, you cannot control disease. And indeed, every single year, you will see uptick of avian flu because wild birds actually
serve as a reservoir, they infect a local poultry
farm in some other country, and in countries like
that, unlike the U.S., where they don’t regulate properly, you get local workers who then develop that form of avian flu, and thus, another spread begins. But unless it becomes
a significant epidemic, obviously no one seems to particularly spend enough time on that. So, if you compare SARS, again from 2002, the same virus, to what is COVID-19, we see a lot of similarities. Number one, they are
both very large viruses. They have a lot of expression molecules, they are spiked, and that spiked effect has a lot of immune system attraction, and then there’s binding receptors, which we will talk about briefly. So the host immune system of the human has a very interesting
engagement process here, where there’s an angiotensin-converting
enzyme 2 receptor, that’s the primary receptor
for those proteins. And again, these require
extensive reservoirs. So, what you see here, on the next slide, is a comparison of the SARS virus that was isolated and sequenced, to the COVID-19 virus that
was isolated and sequenced. They’re both RNA viruses, they’re both betacoronaviruses, they have very similar DNA sequence, as far as length. And they have very similar aspects towards their intermediate
and definitive hosts. The intermediate hosts are those pictures that
I showed you earlier. They are the civet and the
pangolin, respectively. But the definitive host is Rhinolophus, which is basically the horseshoe bat. And indeed, it was that
transfer in wet markets that led to what is eventually, what we see as COVID today. And it’s similarly what caused
the problem back in 2002. So, we know this information was there, we also know that the mortality rate of SARS was significant. We know that it was, individuals who were very close, physical proximity in
SARS was a big problem. If you were a caretaker
of a patient with SARS, you were likely to get that infection, it was very severe. If you lived in the same house as somebody who had SARS, you’d see the same situation. Now you can see, on this timeline, the relationship between
what happened with SARS and what’s happening here with COVID-19. And again, what you’re seeing is the difference between the infective nature of transmission. In the top timeline, you’re
seeing when this started, in late November, and by June of the following year, it was considered extinguished, which is not accurate, because
we certainly had cases, all the way up until 2013. However, if you look at the COVID virus, which really started likely in November, we’re in a situation
where it is nowhere near a point of extinction or extinguishment, and that is the big question. Why is this virus behaving in this way when it’s otherwise quite similar? If you look at the distribution, where infection took place in China? Grossly obvious differences here. The upper chart, the
upper pie chart shows you the various locations
where SARS took its toll. And the bottom is the chart of COVID-19, and you can clearly see that
one particular province, Hubei province with Wuhan, is where the vast majority
of these cases occurred. And again, this is another
very unique difference between the two epidemics
that are present. If you look at the
similarities between these, again, this has been studied now, in the last number of months, the genetic similarities, sequence-wise, between SARS and COVID-19 is over 95%. It’s literally a linear line. The proteomic similarity
is also very similar, it’s almost 95, mid-90, low 90% range. So we’re dealing with a very similar virus in the sense of its genetics, but its clinical apparatus
seems to be slightly different. If you look at it from a
basic science standpoint, we know that the receptor that’s present, and that what’s causing most of the disease in these patients is localized to the lung. The ACE2 receptor is
expressed on lung epithelia, and on various different
dynamic types of studies, they’ve tried to isolate out
this expression in the lung, and interestingly enough, the ACE2 expression that
is overly expressed, not only in the patients who get this bug, but the patients who actively maintain the inflammatory state of this bug, the expression of the ACE2 receptor is highest on the apical segment, not the basolateral segment. So pure airway disease, and the damage is quite impressive. Another example of expression. And again, this has been looked at in several different ways during the acute lung injury event that takes place, the ALI, you could see that as those
particular expression levels that are present in
patients who have SARS, and it’s that ACE2 receptor
that’s the problem. So, why is it a problem is a big question. First of all, I’m not gonna
go through this whole diagram. But you all remember, the function of the
renin-angiotensin-aldosterone system. And the function that is there is largely around utilizing an angiotensin-converting enzyme, which is present on the surface
of the pulmonary lining, and that angiotensin-converting enzyme has two parts to it, or two receptors that are functional. Those functional receptors
are typically upregulated in states where angiotensin II levels are either trying to be manipulated by, say, for example, an
ACE inhibitor or an ARB. Interestingly enough, patients who also have type 2 diabetes, if you look at adult literature, that people who just have
type 2 diabetes by themselves, seem to have upregulation of ACE in the lining of the lung. So, there’s a question about why, maybe there’s more patients who have, who are in this situation, who seem to get this infection are potentially at risk, if they have this type of hypertension affecting their renin-angiotensin access. But we still have much more to know. So, in the largest studies to date, again, there’s only a few studies that cross 40,000 patients, these are all studies that are from China, and primarily from Wuhan. Keep in mind that the largest pockets, where patients were hospitalized, and you can actually study
what happened to them all the way through the ICU, were in Shanghai and in Wuhan. And in the Wuhan cohort, these are patients who
basically had active infection and tested positive, 91% developed fever. And these were not low-grade fevers, these were significant
fevers that persisted. They also developed cough after the fever. There’s a argument if it’s
a dry cough or a wet cough. If you look at most literature, it’s somewhere in between. It is definitely a loose
cough that’s the problem. And it does follow fever manifestation. Next is fatigue. And the fatigue lasts a
significant amount of time, even for recovery, the estimation of the fatigue is sometimes pushing out
all the way to six weeks, at least on the literature
that’s so far been published. Dyspnea is present in
about 30% of patients who test positive, at least
in this largest cohort. If you look at comorbidities, again there’s been a
lot of talk about this. And there’s been, you know, a handful of publications
from different countries. And while there is
definitely a higher risk if you’re an older
person with hypertension, it is certainly extremely not
correlative as a risk factor. Similar with type 2 diabetes, which is the primary group
that was represented here, and similar with patients who
have cardiovascular disease, particularly prior stroke. Interestingly, patients who have asthma and patients who have COPD were
very, very low on the list. And I think there’s some interesting possibilities around that. But that is the data
that’s been consistent now for the last number of weeks. If you looked at the
largest cohort of patients, again this was done in Shanghai, where they were able to actually measure their entire inpatient stay, all the way to the ICU, almost 250 patients with
a mean age of 51 years. Interestingly enough, fever was a marked
characteristic for these patients who ended up staying in the hospital. Mean duration of 10 days. And indeed, the patients
who tended to be sickest had the longest fever patterns. No information about how diurnal or patterns of day-to-day
fevers that occurred, but you saw consistent fevers, some as long as 30 days, especially when they went to the ICU. This is not accounting
for other superinfections and things of that nature. Also very interesting is
that CT image findings were present by day seven in
about 65% of the patients. So, relatively early in the
case of this viral pneumonia, or viral disease, you’re seeing CT findings. And the median duration
once they were admitted to a negative RT-PCR test, which is the same test that’s used here in the U.S., is 11 days. 86% were discharged after two weeks. And again, the vast majority of patients did not need major ventilatory support. They did need oxygen, but they did not need
intubation, ventilation, or even non-invasive
ventilation significantly. There are very few cases on autopsy. This is one that was in three patients who succumbed to COVID-19. And I think my main takeaway message here is that it’s pretty clear, we know for example, that only about 10% of patients with COVID-19 are viremic. In fact, it’s a little
bit less than that number. So, it’s not getting in the bloodstream, at least in a measurable fashion, where is it sitting? And it seems very clear that this virus, when it starts to invade, it causes significant necrosis. You’re gonna see, wherever
there’s expression, particularly of this ACE2 receptor, so that’s bronchial epithelium, all the way into
interstitial-based cell types, you’re gonna see significant
exudative disease and necrosis. If the patient can survive that, you’re gonna see secondary fibrosis and that will likely stain. And in these three autopsies at least, what they found was, you can detect coronavirus
particles on EM, on electron microscopy that’s present, but you could not find it in other organs. You couldn’t find it in the kidneys, you could not find it in the heart. So again, I think this is, at least, very early information but it’s gonna tell us, you know, a pathway of what to do next. CT scan became a big
player in this condition because of only one reason, and that it’s rapid progression. As we all know, most pneumonias, you know, are typically present
at the time of diagnosis. Recovery from a pneumonia
from a radiologic standpoint always lags behind clinical improvement. Not in this case. If you look at, at just one example, there’s actually many of these in the peer-reviewed literature, this is a younger patient, who had progressive COVID, and you can see the number of days that are taking place here, and the progression of this pneumonia in the number of days. And it’s remarkable. It’s localized, it’s
really sublobular disease, and it is significantly causing hypoxemia in these patients. This patient, however,
never required intubation, and at day 11, the repeat scan
looked significantly better. And this is a tool that
has been widely deployed in most other countries. And again, interestingly enough, you’re seeing similarities between this and the same SARS virus
from 2002 and 2003. What other findings do we know about? We also know that laboratory findings are starting to be reported. So for example, this is
SARS data on the right. With SARS, we clearly knew
that we saw lymphopenia. We saw thrombocytopenia, we saw elevation in LDH, and elevation in CK, in creatine kinase. In this particular virus, we’re seeing significant
amount of CRP elevation, there was just a publication
that came out today, or I believe late yesterday in Journal of Pediatrics, that looked at some of the lab markers, and they also validate
some of these findings. So again, we’re seeing
a lot of similar aspects to this condition, these lab findings to what we saw in SARS many, many years ago. The treatment of SARS, and indeed, the treatment of COVID, at least in the current setup in China and in East Asia has been deployed in all the modalities
that are listed here. Protease inhibitors,
lopinavir and ritonavir, direct HIV-1 protease
inhibitors have an effect. Not sure exactly how effective it is, but only case studies exist. Interestingly enough,
in the last decade plus, you’ve seen 23 clinical trials of the use of antiinflammatory chloroquine in the treatment of SARS-type
or SARS viruses themselves. Ribavirin was widely used, especially in the first
round of SARS in Hong Kong, and the results are well-published. So again, that’s even been
deployed in a few cases. Interferon alpha and beta, but primarily alpha deployment, has been there to
upregulate immune response and evacuation of viral particles. IVIG has a little bit of data. And I wanna say one last
point about steroids. This is one of those few
conditions in lung disease, whether you believe this is ARDS or whether you believe this is some other form
of acute infection, that more steroids have
been thrown at this than anything similar. Now that includes SARS, it includes MERS, and it now includes this. We don’t know what the
right answer is on this. But the vast majority of
patients who were treated, at least in the SARS category with systemic steroids as noted, and actually had a appropriate
wean on the excess, did have the best outcome
of progressive lung disease. So, again, there’s no
guidelines per se on this, but it’s something we wanna be particularly cognizant and aware of. What active treatments
are being developed? Right now, the only
U.S.-based clinical trial is with remdesivir, which is a nucleotide analog. It has a wide spectrum of activity against various viruses. And again, unfortunately, these clinical trials are
very small and very selective, based on the number of patients who are particularly ill. They’re restricting it to the very ill. We’re seeing a handful of drugs, particularly drugs that are
actually somewhat similar to drugs that are in oseltamivir, Japanese-based drugs, that are actually producing
some pretty good results. Why is that? Because these viruses,
these RNA-based viruses are not very robust when you start stressing
their nucleotide support. And so it’s gonna be interesting to see how quickly they can start to deploy a series of viruses to get
these patients better, faster. I am particularly optimistic
about vaccine development. I know, you know, they’re not necessarily
talking about that, but the fact is, you already have about a dozen companies, over the last number of years, who are very successful at the development of
virus-like particles, VLPs are kind of the new
generation of vaccine development. You’re using E. coli, yeast, plant cells, with expression of
specific modified proteins that are listed there on the right. And the beauty again, of this virus, is you have a number of
different protein targets that an immune system can hit. And you can get results
relatively quickly. That’s how they’re able
to start a clinical trial on vaccines last week, so quickly. Because the production of this vaccine can be extremely rapid, end goal being that you can
either create an immune response or you can create
cross-neutralizing antibodies. And either way, that’s a significant win. Other pipeline targets right now are endoribonuclease,
Nsp15 expression protein. Which, in many ways, if they can find a targe
monoclonal antibody, this is very specific to coronavirus. You can actually see some, almost the typical model of a synergist, treatment for this type of target. Interfering RNAs, small interference RNA has actually been
well-studied in RNA viruses. Seems to have a benefit of there, that one may be a little bit out there. And also of interest is the fact that the use of steroids have been well-studied
against RNA viruses, particularly SARS and its variants. And indeed, even the use of antivirals compared to steroid suppression seems to change the way the
virus can actually replicate. More to be determined on that, but maybe perhaps, this
is one of the reasons why, asthmatics and other COPD patients, who tend to be on these drugs don’t exhibit similar types of symptoms. So what happens to these patients? If we have to look back at SARS, there’s only one good long-term study. The long-term study was for 15 years, and it looked at 80 healthcare providers who were in a large hospital who took care of these patients. Two of those patients died up front, after contracting SARS. 78 of them were able to survive and they were followed up for 15 years. It’s very interesting. The vast majority of these patients had significant declines
in their lung function, and indeed, they required a
significant amount of steroids for the first two years
post-SARS diagnosis. So, these patients, a portion of them, about 1/3 of them had
persistently abnormal CT scans, even past two to three years. Their lung function differed
between the two groups. But the overall response was, 10 years plus later, their lung function largely recovered. Both in small airways and large airways, as well as in full lung capacity, and total lung capacity
and diffusion capacity. So, I think we have some
very interesting data here on these processes and steps. But the end question’s the same. If you go to the CDC guidelines, which are from now, the current recommendations on
how we handle these patients and what we do with them
is absolutely unclear. Now, I don’t think it’s
anybody’s particular fault. This is all being run and
organized at the same time. And information’s not
getting out to physicians and it’s not getting out to patients. I think it’s important to recognize that we are trying to deal with an epidemiologic problem currently. Where the rate of infection is been, certainly unforeseen in
the last few decades. And the question then becomes, how is this going to be
tracked and managed over time when we don’t have appropriate testing? Even despite more cases in recovery now than confirmed cases, do we really understand what the transmission
and spread looks like? In addition to that, if you look at the rate of infection versus the rate of fatality, we see incredible discrepancies. Why is that certain
countries like South Korea can have very significant
numbers of infection and yet have a very low death rate? That’s a big question. Why is it that Iran, for example, is having the opposite? Is it really just a
healthcare system issue or is there something else that’s present? Or is it the behavior of the virus? These are the questions that
we are trying to understand. So, the infection rate
is the big question. And the infection rate right now is currently hovering
around an R naught of three. If this continues at its current rate, it’s clearly significantly above SARS, significantly above that of the swine flu, and if this continues unchecked, then you would have the entire U.S. population
infected by September. And because of this potential, everyone is talking about these curves. And one of the fundamental
problems with these curves is the area under the
curve is largely the same. The number of cases will be the same, you’re simply trying to avoid the overuse of the
healthcare system capacity. And that is the frustration
that is part of this as well. Because if you look at the
Chinese data, in particular, and you look at their response, the number of patients who required significant healthcare support was unique. It was there. But they also had a great system in place. If you actually study how they did this, since 2002, when they actually had this first epidemic of SARS, since that time, they have
data tracking systems in place, fever clinics in place. So when this initial outbreak took place, hundreds of fever clinics opened up. Patients would be, have a digital thermometer, check their temperature, they had their lungs examined, and they’d be immediately isolated. Mass transportation stopped
to high risk areas in total. Social distancing was way more, I’d say effective than what we see here. They did not even allow the
patients to leave their, the individuals to leave their apartments, and food was distributed to them in a safe and clean fashion. They had a relatively, I’d say, a quick access to PCR-based testing, and they had 30-second
rapid CT scan availability, which was widely deployed in hospitals that were solely built for COVID. In addition, what they did
that was extremely important is they confirmed negative
cases past 28 days. Because they had the
technology to identify, they could identify who’s positive, and make sure that same identification was negative on those individuals. This was an intensive effort
based on prior experience, and despite that, you saw
3,000 plus deaths now, and that is absolutely amazing. The U.S. response has been very simple. Can’t determine case incidence, we have an increased, significantly increased
number of non-primary cases, meaning patients who are getting positive and they never had a travel history, no one around them’s had a
travel history, and so forth. So we know the spread of this
is becoming quite rampant. And in more local distances, the degree of viremia, we know is low. That’s certainly been
consistent across the board. So how this is being passed is clearly through respiratory droplets. We’re only focused on the
most sick patients right now, which means that the only
patients who are getting tested are typically the very sick. And that leaves us limited data. And the turnaround time on PCR right now is six days plus, because it’s all being
run through public health. And the CDC can’t handle that bandwidth. And in the end, we have fragmented, changing response on a daily basis, and that creates a lot
of frustration for folks. So, if you, the fundamental question
comes down to this, you know, are we in a situation where it’s beyond containment? Well, I think everyone will argue, to some degree, we’re
probably at this situation, but we don’t know because
we don’t have the data. So, if we are going to actually assess this issue of containment, we have to take a series of steps, and these types of studies are
already being administered. And these types of processes
are already being adopted. And the first point is testing. There will be a massive
expansion of testing in the next week. There’s no doubt about that. I have direct contact with
the largest private labs in the work that I do. And this is a definitive
move in that direction. So, if you can test a million
asymptomatic carriers, you can get a sense of what this actual
transmission looks like. It’s gonna require a centralized database, and we already have the
tech companies engaged on that level. And obviously the CDC’s gonna have to take a different seat in this position, because they could not
build this fast enough. One of the other biggest problems is the duplicate number of inclusions. Currently in the CDC, they’re not using a singular database that identifies every
single person as unique. So you can have the potential
of duplicate test results. And that’s why the
integration of private labs is likely gonna be the
solution to this problem. If this data is out there, then you can have proper
hospital resource allocation, staff resources can be organized, and then you’re gonna start
to see targeted quarantines as we saw in H1N1. We’re gonna target
specific groups of people who are considered highest risk. And the availability to
testing will give us the data around retesting for clearance and being put back in the population. Beyond that, the next phase
has to do with research. Research studies right now, the NIH is kind of in the lead. You have a number of CTSA organizations, including UCI, who’s in
charge of some of this work, but again, it’s very, I’d say, cursory at this stage. Rapid publications, you already have about
1,500 publications on COVID, primarily from China and Korea. And unfortunately, we
are not in a position to translate that
knowledge into direct care and is being done on a individual basis, which is not ideal. If we can start to
organize this type of data and this type of research in a coordinated effort, very similar to what we do
with ARDSNet, as an example, you will start to see the next phase, which is gonna be better
triage for outcomes, more clear plans of action for providers, and hopefully some best
clinical management algorithms that are developed. And lastly, the drugs themselves. So, I actually am in a position where we are working directly with the NIH through our laboratory and our R&D lab to pull about 100 patient’s blood from all over the U.S., because we have those
patients at our center. And running their immunity, essentially, their IgG, IgM. Direct to COVID-19, and get a sense of what this
actual immunity looks like, memory-wise, versus acute infection. And more and more
organizations are able to do so need to work together on this. And to get a sense of what
influence prior immunity has against typical coronaviruses, and to get a better sense of what’s going on in the
pediatric-aged group itself. There’s nobody else
currently working on this. It’s gonna take a lotta work to get Kaiser moving on this. But in the end, this is where you’re gonna see movement
towards vaccines, safety, and so on, and so forth. My last couple slides are focused on, I think what are the main points. And I think if there’s
two numbers to study in the next two to three weeks, to see where this goes, the first is gonna be fatal
events among the elderly. Those fatal events are
starting to be discernative. If that number continues to go up, I think the therapeutic side and the tracking and targeting
of a specific population will become the greater precedence. The second aspect is the doubling rates. And as you can see, the United States is here. And somewhere around 15,000, somewhere around 15,000 confirmed cases, you will see this, well, you will or will
not see this flattening. You see it with China at the top, you see it with South Korea. And why is this happening
around this level of cases? We don’t know. Is is the quarantine? Is it the social distancing? Is it the behavior of the virus? Is it other factors? But this is the pattern and
the trend that we’re seeing and I think this is what a lot of the epidemiology
folks are hoping for and given the current rate of
doubling that is occurring, we should have that data
back in the next week or so. So, if you take all this together, I try to put all the data together, all the information together. And I tried to come up with a timeline, some sort of summary of what we’re seeing. Right now, we’re defined by quarantine. Increased testing is gonna
define the next number of weeks. Localization of high risk
patients is definitely on the, it is clearly on the table. Major organizations, including the AAFP, are really pushing hard for this. Especially for seniors. Limitation of social activity and heavy resource analysis will define the next couple of weeks. I think by April, the economic strain and quarantine fatigue are gonna really start to
push the issue of saying, how many people are
actively infected with this? The concept of herd immunity is presence, only if you’re gonna really hit 40 to 50% of the general
population that’s been infected. So we’ll have to see if those
numbers actually add up. And if that changes policies that exist. But by next month, we should have some degree
of screening algorithms and testing algorithms in place. And I don’t know that a decline in transmission will be seen, but certainly that would be the hope. By May, I think, that is when, if you follow the Chinese and the Korean approach as it stands, epidemiologically, there
will be a staged reduction in some of the limitations. It’s only staged, and the first groups that
go back are healthcare. So healthcare offices, hospitals, these considered
non-essential type activities, physical exams will be opened up first. In addition to that, the
restrictions around PP and E, the personal protective equipment, will be modified. And that will hopefully
occur around this time, allowing better and increased access to hospitals and clinics. And secondly, being in a position where we can actually allow a focused and a targeted approach towards
the highest risk patients to pick them up early,
diagnose them early, and hit an actual decline in transmission. June and July, I think are gonna see a lot of more of the
self-quarantine model, which clearly existed in H1N1. That was a heavy
self-quarantine-based disease, that had some good results. I think the amount of published data, especially amongst high risk groups will be much more present. I’d long to see some lifted
restrictions in those groups. And the end goal is the same, we need to see less than
100 new cases a day, that is the clear, at the current rate that we’re at, this would be the goal
to see an active decline. You’re gonna see a considerable
restriction in air travel all the way through the summer. I don’t think that’s gonna be lifted, if you look at the current
data amongst other countries. That’s gonna be likely there to stay. And even currently, right now in China, despite eight to nine weeks later, children are still at home. They’re not being sent back
to school in the major areas. In certain cities, you’re seeing slow
movement back towards that. So this is gonna take quite some time. And finally, hopefully, by August, if these scenarios play out, you will see that the actual
drug therapeutics, drug safety, and particularly consensus
statements around therapy will start to come out, and I’m, again, very hopeful that you’ll see some
early data on vaccines, even as early as that point in time. I think there’s two points, or several points that
play as factors here. Number one, India’s rate of transmission is very important to look at. Mainly because they have very few cases, they have a large number
of physicians and hospitals and they have the ability to test. If that large population has
not actually seen a spike, you know, clearly it’s not
because of social distancing, because that is not their key strength. It means that something has changed about the behavior of the virus. And remember that this
is an enveloped virus. Enveloped viruses do not
like significant temperature and humidity dynamics. That is the case. Coronaviruses are second leading cause of common cold, behind rhinovirus, these enveloped viruses have
very, very keen seasons, and really almost latitudes
that they operate in. I encourage you to look into that, and Nature has a number
of good publications. Another issue is southern hemisphere. If this actually circles
into the southern hemisphere, where we’ve not seen a
significant number of cases, this could replicate what happened in H1N1 and it could replicate what happened a little bit
with SARS in ’02 to ’03. So, I think there are clear
future opportunities in this. You know, we know that this
is a reservoir-based disease. These markets still exist. We’ll see what happens. Clearly there needs to be
organization around that. Global data tracking is really key. You know, the WHO has taken, I think, a reasonable charge on this by getting other governments engaged. Mass public knowledge towards
this is really not present. The hygiene effect, you know, at least globally, is not equivocal. Cooperation amongst the epidemiologists, the first responders,
the hospitals systems, and government is exactly why we’re stuck in this current situation. There’s not clean cooperation, it creates a lot of messaging issues and even a level of distrust. And I think it’s also extremely important that when quarantine measures
actually are deployed, you have to have the ability to track. China actually made everybody in their local areas download apps, so they could actually track where those patients were located. That’s a separate issue from, maybe perhaps from a privacy aspect. But these are the kinds of things that allowed them to do this right. And I’d say, last main point is that, this is not the last time
this is gonna happen. You know, there has to
be active education. There has to be drills. There has to be simulations. These things, I think,
are extremely important. And I just have a couple more slides. I’m gonna share these with everybody. If you compile the data that exists, we can identify high risk patients, we can come up with a
series of decision points on how to manage these patients. And these are things that, again, these are just recommendations, so these are things that you could use to decide if this is
what you wanna follow. But I think it’s particularly important for high risk individuals to know that they should be
engaged with their physician, that they need to know what medications that they have available
to them right away, and they have appropriate
lung support medications, you know, should they actually get sick. And then the process of
actually testing them is gonna be based largely on symptoms. You know, the screening of
every single person with COVID is not gonna be a sustainable model, as we’ve seen in other countries. And in the end, if you’re
considered a high risk person, the two tests that are initial are gonna be a chest X-ray and the actual COVID-19 swab, and it’s the patients
who are dually positive, who are gonna get immediate CT scanning, and then that’s gonna pretty much put them in the hospital setting and that’s certainly what we’ve seen so far in most of the U.S.-based cases. Not all of ’em, but most of them. And I think we have to be careful about the concept of quarantining at home for patients who are COVID positive. We don’t have any clear
guidelines on that. So the CDC is still working
on their recommendations. Lastly, is pediatrics. The low risk patient groups. There were three publications
out in the last week. One just came out yesterday with JPeds. And again, it’s very clear that, you know, 90% of these patients, who even got sick with this, well, let me, I’ll say one point, you’re looking at a 70 to
one ratio in these studies. 70 adults who are symptomatic
to one symptomatic child, at least in China. Who are testing positive. So, it’s a clear
predilection towards adults. In the kids who happen to get this, 90% of them are considered
either very mild, mild, or moderate. Even the patients who
are considered severe are the ones who are considered hypoxemic. And that’s a very small percentage. The one subgroup that
seems to be more at risk is perhaps infants, but again, we need much more data. Korean literature does not back up that one study with JPeds. And so, more is to be determined. We have not seen that same issue in a lot of Western-based, at least collections of data so far. So I think there has to be, again, a set of strategies to determine what makes the most sense
on testing these patients. This should really go out to
the primary care doctors first. And then eventually, this will obviously hit the world of specialists and so forth. So, that’s a conclusion of my time. Thank you. (uplifting music)

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