COVID Webinar Series: Transcript of session with Buck CEO, Eric Verdin, MD

Buck Institute President and CEO Eric Verdin, MD, led off a series of Buck webinars focused on the COVID-19 pandemic.  His session is available for viewing online.  This is a transcript of the Q & A:

MODERATOR: I know you have some folks on your team that crunch numbers as it relates to the pandemic.  It’s April 15th; where are we right now?

ERIC VERDIN:  So we are quite early. And I know that this is already not what our audience wants to hear, but we’re quite early. And three different models have emerged from looking at the world. One model is what happens if we let this virus roam free, and this is what we see happening in Spain, and in Italy, and, unfortunately, in New York City. That’s the model that shows the consequence, of what happens if we act late.

The second model is what has happened in some Asian countries. Singapore and South Korea are, actually, good examples, where very active and aggressive public health measures have largely controlled the infection so far. And, finally, the third model is the model of California, where we have acted early but in a different manner, with a lockdown, which, obviously, brings its own set of economic consequences. So I think, right now, it’s clear what works, it’s clear what are the consequences of each of these actions, and I think we’re going to have to really decide which way we move into the future.

MODERATOR:  It looks like California did the right thing early on, and we are in better shape than expected, right?

ERIC VERDIN: Yes, the lockdown clearly works, especially when applied early.  There is clear evidence that the numbers in California, and especially in the Bay Area, are really flat, with a very low level of mortality and what appears to be a low penetrance of the virus.

MODERATOR: Why are older adults more at risk for this disease?

ERIC VERDIN:  Well, it’s not only older adults, even though of course, your age is a direct predictor. The older you are, the more you are at risk, not so much for the infection, but for the bad complications and the fatalities associated with the infection. 

But, again, it’s not only in older people. It turns out that obesity is also a really high risk factor for complications. And so are a number of the chronic conditions that we have known for a long time to be associated with aging. And these are heart disease, heart attacks, stroke, cancer survivors, type 2 diabetes, and chronic obstructive pulmonary disease. So this whole group of conditions we know is associated with aging, but some people can actually get them earlier. It turns out that the people who develop these complications early are also at increased risk for COVID-19.

MODERATOR:  What happens to the immune system as we age?

ERIC VERDIN:  So that’s what we think is central to why older individuals and those who have these chronic diseases become more affected.  First I’ll speak a little bit about immunology. There are two broad arms in the immune system. The first arm is the immediate response that organisms have against any invading pathogens, bacteria or viruses. It’s called the innate immune response. It’s the first line of defense. It is non-specific, it’s not targeted towards one virus or the other. It just protects us globally. But that protection, obviously, is not complete, and viruses and bacteria can evade this initial response. So that response, early and non-specific, is actually what becomes dysregulated during aging, and becomes hyperactive. And this is a phenomenon that people have called chronic inflammation or inflammaging. And, interestingly, this is actually a driving factor for these chronic disease of aging. It’s not only about aging, itself, but heart attacks, type 2 diabetes, are all driven, in significant part, by this chronic inflammation. So that response is hyper-activated.

The second part of the immune system is the adaptive immune response, which is really important, and will become particularly important when we develop a vaccine. The adaptive response is highly specific and targeted against the virus.

And so, obviously, right now, since no one is immune to this virus, we are all relying on this initial innate defense, which you might think is actually a good thing. If it’s hyperactive we should be more protected. It’s a good thing, initially, but it becomes a problem later in the infection, because we think this is what actually causes the death, is this overactive immune response.

MODERATOR:  Older adults are still able to mount this hyperactive immune response?

ERIC VERDIN:  Yes, and it seems that what differentiates the people who actually are doing well and not doing well after infection with this coronavirus are those that mount an appropriate immune response and those who mount a disproportionate response. Actually, the response itself becomes the problem. There is a phenomenon that people have called the cytokine storm, which is made of these cytokines, and these cytokines are chemical mediators that the immune system uses to signal the emergency, and to induce a response. So that response is disproportionate in older individuals, and we think this is one of the problems.

MODERATOR:  Researchers around the world are focused on developing a vaccine. I have read that vaccines often fail in older adults because our immune systems are weak. Is that going to be an issue for any vaccine that might developed?

ERIC VERDIN:  That’s a very good question. So I just told you about the innate immune response, the early non-specific response. Vaccines are dependent on this second part of the immune response, which is called adaptive, which is highly selective. And we know from previous experience with other viruses, in particular, the flu, that as you become older that adaptive immune response becomes deficient. And that could also be a significant problem in terms of vaccination. And we know, for example, in terms of the flu, that in people above 70 years old, only 20- to 30% of people respond in an appropriate manner.

And so here comes the concept of herd immunity. The way vaccines work, typically, is not so much by protecting everybody against the virus, but it also limits the spread of the virus. And so the way the flu vaccine works, in general, and especially for older individuals, is by restricting the circulation of the virus in the population. And so even though there is a concern that an older individual may not respond to a SARS-CoV-2 vaccine, they should be protected by herd immunity when we get there.

MODERATOR:  That would mean that older adults probably would need to take precautions longer than other folks, while everybody catches up to being immune from this disease.

ERIC VERDIN:  Absolutely.  So a lot has been said, and a lot of hope is being placed in terms of what this vaccine is going to do for us. I think, you know, we should be cautious in our optimism. The good news is that coronaviruses are immunogen, they evoke an immune response,  they are  not like HIV. So it is very likely we will be able to develop a vaccine. The question is how soon. And the second question is how soon will we be able to deploy it on the scale needed to protect everyone? And so until that day, and even after that, it will be highly recommended to all those at risk to keep some degree of social distancing. I know this is not what anybody wants to hear, but this is the reality of what we’re going to have to deal with in the coming year, year-and-a-half.

MODERATOR: I want to go to a question that somebody posed online. It talks about the publication that came out of UCSF being led by Dr. Nevan Krogan, who’s going to be with us in early May. He identified a catalog of human proteins that interact with the virus that causes COVID-19. Prohibiting these interactions could result in novel drugs that would stall viral replication. Do you favor any of the identified interactions? Can you talk about what’s most promising and what you’re working on?

ERIC VERDIN:  Yeah. So this is an exciting development. So Nevan Krogan and Melanie Ott are both adjunct faculty here at the Buck, and both work at UCSF and at the Gladstone Institute. Nevan, as you said, identified a large number of cellular proteins that the virus latches onto.  So think about the virus as a parasite. It comes into the cell and it needs to replicate itself to make new virus. And the way it does this, because these are relatively simple genetic organisms, is by sort of co-opting and really taking over the machinery of the cell to make more virus. And so this is done, typically, by having the viral proteins latch on to cellular proteins and redirecting their activities.

And so Nevan and his colleagues were able to do this and to identify a large number of cellular proteins. And it turns out, quite interestingly, that many of these cellular proteins are proteins that we know at the Buck are involved in the aging process. And so this led to the identification of 69 potential drugs that we know interfere with these processes that are currently being tested at the Pasteur Institute and at Mount Sinai in New York. And I just got off a call this morning with Nevan, who mentioned that they got their first batch of results, and some of the drugs actually make the virus grow faster, and some others make it grow slower. So, hopefully, out of this panoply of new drugs and new interactions, we’re going to learn more precisely how the virus works and identify its Achilles heel in places that might allow us to suppress its ability to replicate.

MODERATOR:  Some of those promising drugs involve compounds that have been shown to be involved in the aging process, correct?

ERIC VERDIN:  Absolutely. And this is quite exciting. This is where I think the history of the Buck in conducting research on aging is really incredibly important to this effort. Some of your listeners might be familiar with rapamycin. This is a drug that is currently being explored as a drug against the aging process. It targets a cellular protein called TOR. It delays aging. And this was identified as one of the promising potential drugs. Now, there’s some worries about rapamycin because it is also in high doses an immunosuppressive. There’s early evidence that at low doses it might actually have a very beneficial effect on the immune system.

Another drug that some of your viewers might know about is Metformin, or Glucophage. This is an antidiabetic drug that is emerging as having quite powerful anti-aging effects. That also emerged in the analysis that Nevan led.

So we are busy at work trying to really understand how these proteins and these pathways and these drugs interfere with the virus processes.  And then we can discover how can we exploit these characteristics for novel therapies.

I should say one word of caution. Hydroxychloroquine, and actually chloroquine, emerged out of that screen, as well, and has been shown to be working on the virus in an individual system, in the laboratory system. But there is a long way to go from these early basic research discoveries to actually doing something in a patient. We need to prove that these treatments are not only effective but also safe. And so I certainly do not want to paint a picture that we are just about to discover the drugs for COVID-19. I think it’s going to take quite a while, but we have no other choice than to go down this route.

MODERATOR:  Just to cut folks short who might be making a note about Metformin or rapamycin, you’re not recommending that anybody goes out and tries to get these drugs and to start taking them as a preventive for COVID-19.

ERIC VERDIN:  Absolutely not. On the other hand, if you are on these drugs, continue taking them. But I would certainly not recommend starting them. We don’t know how these drugs exert their effect in the long-term. There is no known beneficial effect on COVID-19, but there are interesting links that make us think that the research on aging that the Buck has been focusing on is highly relevant to this virus and to this epidemic.

MODERATOR:  Why do males appear to be at extra risk for COVID-19?

ERIC VERDIN:  The short answer is we do not know. There are a number of hypotheses. This is a risk for complications; it’s not the infection. Males and females appear to be infected at the same rates. It turns out that males appear to be more at risk for complications.

Now, there was a lot of discussion, initially, a hypothesis was that this might be related to smoking. We know smokers have an altered immune function in the lungs. And we know that in many parts of the world, males tend to be more smokers. However, that data has been questioned.

There are other hypotheses that are linked, in general, to male behavior and response to epidemics. They tend to listen less to public health recommendations. Males tend to wash their hands less frequently. There’s a whole series of arguments that have been made that might explain why males might actually be getting a larger inoculum or exposure to the virus. There seems to be an increased risk of complication if you are exposed to large amounts of virus. And we see this best exemplified in healthcare workers who tend to be getting sick at higher rates, at more significant rates than other people.

MODERATOR:  Why does COVID-19 seem to affect the lungs so much?

ERIC VERDIN:  That’s a very good question. The short answer, again, is we don’t fully know. The virus is an aerosolized virus, so it is transmitted via aerosols. That means its portal of entry is by breathing, so it might be as simple as this. In addition we know that the receptor for the virus, at least one of the receptors that has been identified, is highly expressed in cells in the lung. So it might be a combination of the two factors. But, obviously, we know the virus is not restricted to the lung. There are symptoms of infection in other organs. We just know that the lung, in most cases, is the primary portal of entry.

MODERATOR:   What can people do right now to give themselves the best shot at either not getting COVID-19, or if they get it, that they’re going to come out of it okay?

ERIC VERDIN:  Everyone is hoping for a magic bullet. And so, right now, it is actually amazing, and disturbing, to see the proliferation of advice on supplements and a number of modifications that people are recommending.

I think it’s important to go back to the basics, and we know from our work, and the work of many, that the good elements of a good immune response are rooted in good general health. And so the first thing, I encourage everyone to pay attention to is what we know actually will create health. And that is adequate sleep. Lack of sleep actually has a profound effect on the immune system. Even one bad night can affect your immune system, so get adequate sleep.  Eat nutritional foods, such as vegetables and fruits. So sleep, nutrition, moderate physical activity, which actually might be challenging for many of our listeners. However, in many parts of the country, one is still able to go for a walk, and I’ve argued to try to make this part of your routine. There are profound effects from physical activity and exercise. So those would be my major areas—good nutrition, good sleep, and regular physical activity. These are things that we know make you healthy anyway, but they will make your immune system actually more resistant.

The last one that I think we should probably pay particular attention to these days is stress. Even though many of us are comfortable at home, these are highly stressful times, and they are stressful for a significant fraction of the population who have lost their jobs, who are staying at home with screaming kids. And so there is a lot on people’s mind to be confined in the space, along with the uncertainties that we’re all living through. ‘When is this going to be finished?’ Most of us have at least a relative or a friend who has been infected, or we’ve watched Chris Cuomo on CNN. So all of this exerts a toll on our psyche and generates a significant level of stress even if you’re not conscious of it. And so this means we should think about stress alleviation techniques that we know work and have also a profound effect on the immune system. And I don’t have a precise prescription, but meditation, yoga, exercise, calm time -- anything that you can do that seems to actually relieve your level of stress level should be an important aspect of staying as healthy and as strong to resist this virus.

MODERATOR:  What’s your take on those, on melatonin and vitamin D?

ERIC VERDIN:  There’s also vitamin C.  It’s a difficult question to answer. I’ll speak a little more about vitamin C because I think that’s one that has created more noise.

The vitamin C story started with Linus Pauling, who was a Nobel Prize winner, who became convinced in his later days that vitamin C had amazing abilities as an antioxidant, and actually used to take enormous amounts of vitamin C, and also wrote books claiming that vitamin C would prevent the common cold and similar problems. Because of his visibility and his notoriety there was a lot of work actually on vitamin C, a large number of clinical trials have been conducted. And the conclusion at the end was that vitamin C does, indeed, confer some limited amount of protection against the common cold and against the flu. It was thought that it translated to about 8% less duration of symptoms. So if you have normally a cold that lasts 10 days, it would last nine days. There was no effect on mortality. No effect on complications.

Now, because of this there are urban myths and rumors that vitamin C is a miracle antiviral. I think it is clearly not. Nonetheless, clinical trials are underway, especially in China, with high doses of intravenous vitamin C. And as for any other modification that involves a significant dose, I think we need to wait for the results. I would say that most virologists cannot see any reason why vitamin C should have such a profound effect, but the clinical trials have to be done. It could become something significant.

Now, the same arguments can be made about melatonin, vitamin D, and other supplements including quercetin and zinc. At minor doses, they will almost certainly not hurt you. If you’re considering taking them at high doses, I urge caution because at high doses, some of these supplements can have untoward effects. And so you want to make sure that you’re helping yourself, not actually making it worse. And for any of these supplements that emerge as potentially promising, I can guarantee you that clinical trials will be conducted. And, personally, I would resist taking them at high doses until the evidence is there, because we know the potential for harm is truly there, as well.

MODERATOR: Is there any danger that if you take immune boosters you might be tipping the balance towards the cytokine storm? The goal is to have a balanced immune system, right?  

ERIC VERDIN:  That’s an important point. Another area in which we are working involves the NAD boosters, some of the ones you might be familiar with are NR and NMN. These are boosters that increase your level of NAD. Well, at this point there clearly is an interaction between the virus and the NAD pathways. What we don’t know is in which direction. Is it better to have more NAD or less NAD? And so, again, we don’t know. The work has to be done. If you’re taking a small dose of NAD boosters at this point, I would say there’s no reason to stop it, but I would not argue to increase the dose either.

We know, for example, in the aging field that many of the interactions that we see between a drug and its effects are not linear. It’s not because you’re taking more of something that you’re actually going to get a bigger effect. Sometimes there’s a sweet spot where you have to be in order to see the beneficial effect.

MODERATOR:  So there’s been some press recently about an antiviral drug called Remdesivir? What about that drug is a potential treatment for those who already have COVID-19?

ERIC VERDIN:  So Remdesivir is a true drug that is going through the FDA approval process, which is the way that all of our drugs are actually demonstrated to be effective, which is not the case for supplements. So I think we have to make the clear distinction between these true drugs versus the supplements which live in an unregulated world. Remdesivir was generated to fight another virus, Ebola. You might recall a few years back there was a huge epidemic of Ebola in Africa, and the drug was generated for this. It turned out to be not effective for Ebola, which has similarities with coronaviruses. It turns out that Remdesivir actually works on a key coronavirus protein, the polymerase, which is the enzyme that the virus uses to replicate its own RNA. And so very strong effects in the laboratory setting, which has led to the idea of testing it in clinical trial, and this is where it is now. We don’t have any results, but I think these results should come in the near future.

MODERATOR:  What is antibody testing, and what do you think about it?

ERIC VERDIN: So I’ll step back and tell you a little bit of when we talk about testing right now for the virus, what are we testing for? So when you go now to one of the detection centers because you have symptoms, you are being tested for the presence of the virus, itself. And so we can now, using a technique called PCR, identify the presence of the RNA from the virus. This is what the current detection tests are. Now, obviously, this only looks at people who are actively infected, productively infected. What we are very interested in having as a tool, especially if we consider moving to the next stage of the pandemic where we begin to lift the lockdown and try to go back to a more normal way of living, is to identify the subset of us that has been infected already. And so the way we can do this is by looking for these antibodies. The antibodies come from the adaptive immune system; it is an educated immune response that is specific for the virus. So when we get infected by a virus, we generate these antibodies. They have the ability to latch onto the virus and to neutralize it. We can detect them in the blood of people who have been infected, usually within three to four weeks after they recover. Typically, for most viruses these antibodies indicate immunity which means that you are actually protected from a super infection. So the reason we all want to identify who has been infected is you can imagine that these people will be the first ones to be able to go back to work because they are protected from COVID-19.

This test would also give us an idea of how close are we to herd immunity. Obviously, we know depending on different viruses, it takes a different fraction of the population to have immunity to actually confer herd immunity to the rest of the population. And so those numbers vary between 50- and 70%, depending on the virus. Obviously, we’re not there now. Although I should say that I read a study yesterday from New York City, in which they tested every pregnant woman at the New York Presbyterian Hospital. Every woman that came in to deliver a baby in the last few weeks was tested for the presence of coronavirus and the presence of antibodies. They found two things: 15% of these women actually had antibodies, which means we have quite a lot more penetration of the virus, at least in New York City, than we had suspected. And perhaps more remarkably, out of these 15% of women, 88% were asymptomatic and had no recollection of having been infected. So this really, again, indicates that the virus might actually be much more distributed in the population that we had assumed. It’s both bad news and good news. It’s good news because we know that the virus only affects a very small fraction of the population in a really bad manner. The bad news is there are probably a lot more infected people than we had suspected, and that means we will need to identify all of the asymptomatic shedders, carriers, to be able to go back to a normal situation.

MODERATOR:  There’s some talk about people who are super spreaders. Who are they?

ERIC VERDIN:  So we’ve seen this with most viruses. This is not something that’s unique to this particular coronavirus. The word says it. There are a number of people who are just generating a larger amount of virus and spreading it in a more efficient manner. And the key questions are why is this, and how do we identify them, because, obviously, they are the ones who are really contributing to the spreading of the epidemic.

MODERATOR: Somebody wants to know if the Buck is working on a vaccine. I can say no, we’re not working on a vaccine. Why don’t you talk about what it takes as far as in a lab environment to actually work on and develop vaccines.

ERIC VERDIN:  The classical vaccine, the first vaccines that were generated, consisted of taking a virus and making it multiply in a laboratory setting. And when you do this, the virus essentially becomes disabled. It can still replicate, but it is hobbled, it becomes less fit.  You can then put it back into people, and eventually this virus does not induce the full disease but still induces immunity. This is how the first polio virus was generated. Another way is to actually create the virus and inactivate it. You heat it, for example, and then you actually administer it to people. They see it as a virus, even though it’s not able to divide, and they still mount an immune response. Now these are the original way of making a vaccine.

Today, we do this, typically, with specific sub-units of the virus, so we can express one viral protein or two that we know are the most important, and actually inject those in people. And, the last way to develop a vaccine is that   we can actually inject the viral RNA or the viral DNA directly into people, generating protein. So all of these methods are currently being explored. There are lots of biotech companies, large and small, actually pursuing each of these approaches. Hopefully, one of these will pan-out and will yield an effective vaccine.

MODERATOR:  Beyond today’s pandemic, how can we instill preventative self-maintenance of health as a way to decrease the toll of future pandemics? Should we change how we live?

ERIC VERDIN:  Great question, and I think we should look at what has happened in some Asian countries, and what is happening in the US and in Europe. There has been, over the last 40 years, a global disinvestment in a field that we call public health. Public health is the science of understanding how do epidemics happen, how do we monitor for them, and once they start, how do we control them, how do we snuff them out? It turns out that for the last 30 to 40 years, the science of epidemiology and the science of public health or public health systems have not gotten needed attention. These represent significant investments, obviously, but they pale in comparison to the amount of money that we have to spend now. So an ounce of prevention in this case is just exactly what we need.

For example, think about what will happen when we come out of our lockdown, which will happen progressively in the next few weeks, hopefully, the next month or two. We are going to need to identify everyone who has been infected. We are going to need to identify everyone who is productively infected. So we will need these tests. But not only the test. Once we identify positive people, we will need to do something called contact tracing. That means that if a person emerges as positive for COVID-19 we will need to identify everyone who has been interacting with this person in the last two weeks, notify them and isolate them. That’s the only way we will be able to control this virus in the absence of a lockdown. And so it’s been estimated that we’re going to need to hire close to 300,000 people just for the US, alone, to do contact tracing.

And, obviously, we don’t need such a workforce on a long-term basis, but if we had had a stronger public health system, we might have been able to prevent this right from the beginning. And I think, hopefully as a society we will learn the lesson and move into the future with a reinforced public health system. Because the thing to remember about this pandemic is that there will be more of them. There are thousands of viruses lurking in animals in different places of the world, waiting to jump into humans and to cause similar or worse problems. I won’t say we should count our blessings with this current virus, but this is not the worst virus that we could end up dealing with. There are other potential pathogens that could be worse.

MODERATOR:  How did this virus jump from animals to humans and is it a public health issue to try to stop that from happening in the first place? And I think climate change could be involved in all of it.

ERIC VERDIN:  With regards to climate change, I think we know that we’re in the process of disrupting ecosystems that have been in place for long periods of time. When we disrupt ecosystems, there are untoward consequences that can happen. I am not suggesting that the coronavirus is linked to this, but there are many ways in which global warming is thought to lead to such possibilities in the future.

Now, how did the virus jump in this case? It is thought to be from a bat. We knew beforehand that bats contain these coronaviruses and many others pathogens. So there’s still a potential for others. In this case, it is thought to have occurred during a market sales, but it could happen with a kid going into a bat cave and being bitten by a bat.

So I think we will never be completely immune to the fact that viruses can jump from other animal species to humans. I think this has happened. This is how the HIV epidemic started. It started from a chimpanzee virus that jumped into humans and this will happen again. So I think trying to suppress all of the jumping events is almost impossible.

What we can do is to mitigate what happens when the jump has occurred by stopping the spread of disease. And this, for example, is what we did in the case of Ebola, in the case of SARS, which was also a coronavirus, we were able to stop it a number of years ago. For some reasons, we were not able to stop this one. I think, hopefully, we will learn our lesson and be more prepared.

MODERATOR:  In Marin County, where we are, as of today we had 171 diagnosed cases and 121 people recovered. Do the people who recovered have antibodies that might be used for a treatment or in vaccine development?

ERIC VERDIN:  That’s a very good question. This is another one of the therapeutic modalities that I have not discussed yet. So we are actively working on developing drugs to treat the people who are infected. We are working on vaccines. But we also have the antibodies. As I mentioned earlier, some of these antibodies are neutralizing. That is, if you were to receive them from someone who had survived an infection, you might actually be protected immediately without having to wait the three weeks to one month that it normally takes you to create antibodies after being vaccinated. So that’s one possibility, and there are efforts in this direction. But this method obviously involves some really big complications because you need to identify all of the infected people, you need to extract their blood, you need to purify the immunoglobulin, which is the antibodies. It’s a very complicated and expensive process.

Another approach is to look at those people who have survived an infection and who have created these antibodies and to identify the most potent and specific antibodies. And then using genetic engineering, we can actually produce the antibodies in factories. This approach has actually been used against HIV, and there are now a number of really highly neutralizing antibodies that one can administer to patients and they actually will suppress the infection. I know that this type of research is underway. It is one of the many approaches that are being pursued, but we don’t know which one will eventually be successful.

MODERATOR:  There was a question about folks who are appear to be immune to the coronavirus. Is there something to be learned from them, as well?

ERIC VERDIN:  Yes, absolutely. Again, in the HIV field, where I worked for a number of years, we knew there was the whole gamut. Some people actually were exposed to the virus and could not be infected. We identified the receptors, and some people actually carried a mutation in this receptor. We can expect that some people in the human population have a mutation in the SARS-CoV-2 receptor and will therefore, be immune. We also know, in general, younger people tend to have fewer serious manifestations of the disease. Why that is, we don’t fully understand. This is something that we intend to study. I think we can expect the whole gamut and this is what we see with many viruses.

One important aspect is the size of the inoculum, or viral load that someone is exposed to. In virology this is known to be one of the key determinants of pathogenesis of disease. That is, you know, for some viruses, a small inoculum might actually not yield a very significant disease, whereas a larger inoculum will yield a much more significant disease. We have preliminary evidence that this might be the case in COVID-19.

MODERATOR:  I’m assuming that there are folks that are watching this webinar who are dealing with chronic conditions and are on medications. Maybe some of them are anti-inflammatory conditions like rheumatoid arthritis. What should people do when they look at the pills they take every day and they wonder, ‘Gosh, what should I do? Are these good for me now or are they bad for me now?’

ERIC VERDIN:  I think they should continue taking their medicine. They should closely consult with their physicians. This subset of people who have chronic conditions, I would argue, are the last ones we should experiment on with drugs that are currently rumored to work. We heard the case of a person who actually took a dose of hydroxychloroquine and actually died from an arrhythmia.

So if you have already existing condition, you are at increased risk for the complication of this virus, but you might also be at increased risk for the complication of the drugs that you will take. So I would argue that everyone should really closely consult with their physician. And until we have strong evidence, this is not a time for self-experimentation or taking chances on a non-proven drug.

We know that drugs can be miracle and many drugs that have been developed actually have incredibly positive effect. But there is no drug that comes without any side effect, none. And so when you decide to take a drug, I think you always have to ponder, ‘Am I willing to live with the potential side effects?’ And in a case of hydroxychloroquine, for example, or azithromycin, two drugs that have received the largest amount of publicity with their potential effect on the virus, these drugs carry significant potential complication in terms of the heart rhythm troubles. And so I would urge caution. It’s not the time to experiment on anything.

MODERATOR:  Does hot weather make COVID-19 more containable or is that a myth?

ERIC VERDIN:  At this point, it’s a myth. Where is the myth coming from? It turns out that a number of viruses exhibit what we call seasonality, and flu is the best example. The flu tends to occur more during the winter months. No one knows why, by the way. A number of hypotheses have been advanced. Maybe people are more together and in an enclosed space during the winter. That’s, clearly, the case for the flu. In the summer, it’s quite rare to see flu cases.

There is currently, unfortunately, no evidence of any seasonality in COVID-19. We should have seen it already. Although, you know, there are some areas where the virus appears to be relatively low, and some of these areas are more in the southern part of the country. There are also some exceptions, like Louisiana. Right now, Louisiana, which has hot weather, is actually suffering one of the worst epidemics. So I would say, so far the consensus is that the seasonality is not evident.

MODERATOR:  What’s happening with the collaborations and the science?

ERIC VERDIN:  Yes, and I think when you have Nevan Krogan on in a  couple of weeks, I think it would be great to follow this up with him. For those of you who are not in science, you might not notice, but it is an intensely competitive affair. We are humans, we are passionate about our ideas. Scientists sometimes collaborate, but also compete fiercely. What I have seen in the case of the COVID-19 and this coronavirus, it’s really the opposite. And the collaboration that we have with Nevan Krogan and his group, and Melanie Ott from the Gladstone has just been the most open collaboration that I have ever seen. There are a large number of groups, I don’t know the exact number.  Nevan will say that that there are hundreds around UCSF, the Buck, and others. People come to meetings, they share their very preliminary data. They share their reagents.

So I think everyone recognizes this is not a time for fierce competition. This is a time for collaboration and bringing a solution to the problem as fast as we can. And, in some way, it is a new way to do science. I find it incredibly refreshing. And I think it will change the way in which we work in the future, and, hopefully, this will be one of the good things that will come out of this pandemic.