You’re listening to a press conference from the Harvard T.H. Chan School of Public Health with Dr. Stephen Kissler, research fellow of the Department of Immunology and Infectious Diseases. This call was recorded at 11:30 a.m. Eastern Time on Friday, June 26.
Transcript
MODERATOR: Dr. Kissler, do you have any opening remarks?
STEPHEN KISSLER: Yeah, I just wanted to thank everyone for being here, looking forward to talking with you and hearing your questions. I know that a lot of the questions that I’ve been getting over the last couple of days have to do with the various resurgences of infections in different parts of the country and how to interpret them both in terms of where are they coming from? Why are they happening? And also in the broader sense of the epidemic. There’ve been a lot of questions about is this the second wave and what do we think about when we think about a second wave versus various peaks of infection in different places. So those are all things that I’d be happy to speak about. Of course, if you have any other questions, happy to field them as well.
MODERATOR: Thank you, Dr. Kissler. First question.
Q: Hi, Dr. Kissler, thanks for doing this. I’ve heard various explanations over the last few days about the rise in case numbers and its relationship to increased testing, as well as lower death rates of the current surge, wave, spike, whatever you wanna call it. I’m curious as to your interpretation of the relationship between those factors?
STEPHEN KISSLER: Yes, that’s a great question. So, as you say, we’ve been seeing a rise in cases in a lot of places and some of the rise in the confirmed number of cases is probably due to increased testing. But, of course, it looks like in various states, including Texas and Florida, we’ve seen a rise in the positivity of cases as well. And so when we see both of those rising, we think that that probably has to do with an authentic increase in the number of cases of disease. So there are a couple of important points, I think, to note about interpreting those data. One of which is that, you know, a number of people I’ve spoken with are comparing the rise in cases that we’re seeing now to the rise in cases that we saw sort of during this first wave, especially in New York City. And I think that that’s an OK comparison to make, but one of the key differences to keep in mind is that back then we were doing a lot less testing. So we’re probably catching these rises in cases earlier relative to the rise that’s happening than what we caught sort of in New York City. So I think that what we’re seeing is a rise in cases, but it’s a little bit earlier, sort of in epidemiological time than what we saw before. So I think that that’s a very good thing because we’re seeing this rise in cases, but we’re probably catching it earlier, which means that we have a better chance of intervening effectively than we did earlier on in the outbreak. So that’s one thing. So there’s been a question about the relationship between death rates in this new phase as well. And I think that there are also two key considerations there. So, first of all, it does seem like a lot of the cases that are happening right now are happening in younger populations. We’ve been seeing that the people who have been admitted to hospital have been of a lower median age than people who seem to be admitted in these earlier phases. That suggests to me is that it’s younger people, especially young adults, who seem to be responsible for at least this early transmission of this wave. Now, on the one hand, that’s a good thing because younger people are less susceptible to the severe outcomes of infection. But I think that as infection rises in those younger age groups, it’s really only a matter of time before it spills over into the groups of the population that are more susceptible to severe outcomes from the illness. And the last thing is that we know that there’s a fairly long delay between observed cases and fatalities. So the rise in cases that we’re seeing right now with, you know, we’re probably going to be a couple of weeks before we see that translate into a rise in mortality, especially if the early cases are predominantly in younger adults who take even longer to become seriously ill if they become seriously ill at all. So all of those things are worth bearing in mind. I think I’m going to be watching the mortality data very closely over the next week or two to see if that starts to increase, because I think that would suggest to them they’re starting to be cases spilling over from these younger age groups into older populations. It’s too soon to say if that’s will actually be the case, but I think that it’s likely.
Q: So if you were to look two weeks out, I mean, you know, Barry Bloom yesterday, emphasized something we’d heard early on in the pandemic, but which it almost seems like we’ve forgotten that, you know, you need to look at these numbers and think about two weeks from now or three weeks from now. What do you see three weeks from now?
STEPHEN KISSLER: So at the moment, it seems like there hasn’t been much, I guess, response in terms of either messaging or actually know direct political intervention to avoid these increases. With the exception of a little bit in Texas, we’ve seen sort of the pause of the reopening. So looking ahead, I think that there’s reason to believe that we could be entering another phase of near exponential growth in some of the states that are seeing increases. And so we know that earlier on in the epidemic, the number of cases could double on the order of every five to seven days. My fear is that we might be entering a similar phase. They might not rise quite so quickly as that, but, it very well might. So I think looking two weeks ahead, I think that unless something changes fairly quickly and the response that we’re in for a pretty rapid continuation of the increase in cases in these places and that the hospital admissions and especially the deaths that sort of follow along with a certain lag.
Q: Thank you.
MODERATOR: Next question.
Q: Again, thanks for doing this. Dr. Fauci had said in an interview that the administration is having intense discussions about pool testing. And I just wondered what you think of the idea of pool testing and what the shortcomings are of that and the sensitivity of that? Pooling tests to take groups?
STEPHEN KISSLER:Yes, I just cut out for a moment. So that’s fine. So I’m encouraged by the fact that they’re thinking about this, especially because by doing pooled testing, one is able to sort of shift the paradigm from testing for clinical purposes to just see if a person is infected or not, to really trying to get at what’s happening in the community, which is one of the big benefits of testing anyway. So I think that really what that marks to me is just a shift in emphasis, which is encouraging. As far as, you know, the. I think that there are good ways of dealing with the issues around sensitivity that you raise. It certainly gives you a certain type of information that’s not complete. It doesn’t give you quite as much detail as the individual level tests when you pool them. But I think that really what that marks is a shift in emphasis towards the epidemiological perspective and thinking about what’s really going on in communities versus just in particular individuals. And I think that that’s encouraging.
Q: Encouraging line or I mean, it might not be encouraging for me who wants to know my own results. What do you mean by encouraging?
STEPHEN KISSLER:So it’s encouraging in the sense that its. So, first of all, I mean, I want to make clear that by pooling tests, I think that, you know, that that shouldn’t be the way that all tests are done. And certainly I think that if someone comes to a clinical setting and requires a test in order to determine their course of care, that should absolutely be prioritized. I hope that that’s what they’re planning to do. I’m thinking more along the lines of if tests are pooled among people who are less severe in their illness as we’re starting to test people going back to workplaces, I think that for the sake of maintaining resources that those things can be effectively pooled so that we can have a sense of what’s going on in the community. Essentially, it allows you to gain more information out of a single test and to sort of use your reagents and your testing kits to get a different type of information. And so I think that as long as that’s balanced sensibly. So first of all, you know, the individual patient care really needs to be prioritized. But as long as we’re reaching the stage where we have more tests that are available that we need for individual patients who require us to get information about what their clinical course of care is going to be, and if we can use those responsibly in a pooled the way, then that will give us a lot more timely information about what’s happening in the community and that can help us determine what responses we need to take if that makes sense.
Q: So you would do like an office? Maybe everybody who works for a particular law firm would get tested together and then the firm would have a sense of whether there was any COVID within their staff?
STEPHEN KISSLER:Yeah, so let’s maybe to make this concrete. So let’s say you have an office of 100 hundred people and you have either the option of testing all 100 people at one point in time or pooling five people together and testing them multiple times. I think pooing people together and testing them multiple times will give you a lot more information because that would allow you to see if infection has entered into the community and if you get to shut down. So you can do the same sort of very similar – you gain more by that same number of tests by testing people over time. Because if you just tested a single point, then that tells you something about how many people are infected. But then that doesn’t really give you any sense of what you might need to do into the future. So it’s that tradeoff that the pooling allows you to address.
MODERATOR: Next question.
Q: Hello. Thank you, Dr. Kissler. My question is regarding what are the factors that determine that a certain vaccine is more advanced than others and the factor that put a certain vaccine in a privileged position to end a pandemic? And actually, I do not understand why some researchers are like why those at Oxford saying that are too close to find a vaccine and like that next autumn and others saying that the vaccine will not be able to reach to the people until next year. What are the factors that demand their decisions?
STEPHEN KISSLER: Right. So the timeline for vaccine development, the mix of the scientific hurdles that need to be overcome to develop the vaccine, and especially the regulatory hurdles that then need to be overcome to license the vaccine to prove its safety and its efficacy. And then finally, the logistical challenges that involve scaling up the production of the vaccine so that there are enough doses to go around. So those are sort of three different things, each of which can cause varying levels of delays towards the development of the vaccine. So we’ve been hearing a lot about the Oxford vaccine, for example, and it seems like they’ve really overcome a lot of the scientific hurdles that are required. So when we think about vaccines being more advanced, that’s sort of what we’re talking about, is how far are we along through these different phases? So I think that there’s still work on that vaccine to be done in humans to determine both its safety, its efficacy, the extent to which it both reduces the probability of becoming ill and importantly, the probability of reducing onward transmission. So those are all answers that we’re still trying to gain questions to, but we’re a little bit further along in the development phase for that particular vaccine than we are with many others. So so hopefully, hopefully that addresses the first part of your question. I’m happy to go into more of it. If you’d like to hear more. So one of the other important considerations, though, when we were thinking about vaccines is that vaccines can work in very different ways. And some of the preliminary evidence from the Oxford vaccine suggests that it’s able to reduce the severity of illness for the people who get the vaccine, but that it may not be especially effective in reducing onward transmission. Essentially, you can still spread the illness if you become infected, but you’re much less likely to become seriously ill yourself. Now, as far as I can tell those that’s based on information that that was not done in humans and that was done in primate trials. And so that still needs to be verified in humans if that’s the case. It’s certainly good that we have that vaccine. But the problem is that it won’t get us any closer to that threshold of herd immunity in the population to prevent the pandemic from spreading. So it’s definitely a step in the right direction and it could become a very important tool in our kit to avoid the worst outcomes from this illness. But, of course, many of the other vaccines that we have, for example, let’s take, for example, the measles vaccine that both prevents illness, but it also prevents you really from becoming seriously infected and spreading the infection to others. So that can sort of have this compounding effect in both reducing severity and also preventing onward transmission. And so when we’re thinking about vaccines to bring the pandemic to an end, the Oxford vaccine won’t necessarily do that if those same previous findings from the primate trials hold true in humans. But it will definitely have an effect in making the illness less severe, which will definitely be a very good thing.
Q: Regarding the second wave, you have a certain perspective in that regard?
STEPHEN KISSLER:So there’s, we’ve sort of loosely been thinking about second peaks and second waves. So what we’re seeing right now, I think, are multiple peaks of infection in various places that seem to be largely driven by the phases of reopening. And so essentially, people are mixing with one another. And so we’re starting to see rises in infection. And so I think that we’re probably in for a phase in which we’re seeing those sorts of peaks and sort of infections bubbling up and then hopefully being controlled and cases coming back down in places across the country and around the world. Now, I want to distinguish that from what we often think about as a second wave. And a second wave is the way that I conceptualize it as a really a large resurgence of infection that would affect lots of different parts of the country around the same time. And that would be driven by things like changes in the seasonal ability of the virus to spread. Sort of the same reason why we see rises in flu cases, rises in the other coronaviruses in the wintertime. And that’s something that we’ve seen in previous flu pandemics as well. Both in 1918 and 2009, transmission sort of reduced a little bit over the summer. But then there was a large increase in infection in the fall. And so that’s what we think about as the second wave. Now, for a second wave to happen, there need to be enough people in the population who are still susceptible to infection for that wave to occur. As far as we can tell from the antibody tests that we’ve done, there are still probably enough people in the population for such a second wave to occur. So I think that that’s still a very real possibility. Certainly not a guarantee. I guess the alternative is that we will sort of continue to see these rises and falls in cases across the country for the coming months and that we won’t really see this concerted second wave, but it’ll just sort of be this bubbling along over time. But I do think that there’s good reason to believe that this larger second autumn and winter time wave is still a possibility. And it could very well happen, but it would be sort of a different beast than what we’re seeing right now.
Q: I’m sorry, I have just one last question, please. What are the main differences between this COVID-19 pandemic and other pandemics in the world?
STEPHEN KISSLER: There are a number of pandemics that one can bring to mind. So I think the closest analog is that we know of the things that we’ve learned the most from are the previous flu pandemics. As I mentioned. So in 2009, the as far as we can tell, that influenza strain was not as transmissible as SARS-CoV-2. And that’s referring to the reproduction number, which seems to be somewhere between one and two for the flu pandemic, whereas for SARS-CoV-2, it’s a two and a half to three and a half. So it’s it’s it seems that this pandemic is more transmissible. And I think that that’s part of why we haven’t seen those cases sort of trail off in the summer as much as we did in 2009. That’s really one of the key differences for transmission. There are all sorts of real important clinical differences in the sense that SARS-CoV-2 is also more clinically severe than the 2009 H1N1 flu was. But as far as epidemiology, that’s one of the key differences. There are, of course, other pandemics we can think about. HIV was also a pandemic that was spread, of course, in a very different way. But nevertheless, all of these pandemics are spread through transmission between individuals and spread around different countries in the world and hit different communities in very different ways. And so I think that those are some of the things that we can learn from the previous pandemics that we’ve seen.
Q: Thank you.
STEPHEN KISSLER: Thanks.
MODERATOR: Next question.
Q: Hi. Thank you so much for doing this. I appreciate it. I have a question about contact tracing. So our biggest county here in Arizona seems to be doing like case mediated contact tracing rather than sort of traditional contact tracing. So unless the case is high risk, public health doesn’t call them, but instead texts them an online form to fill out with their personal information, as well as information about close contacts. And then contacts are also not called, but they might be sent a symptom tracking system. So is that enough or is more thorough contact tracing and phone calls needed? And if so, what? And why? I mean, cases are really spiking in the county at this point. So my sense is more is needed. But obviously, I don’t know.
STEPHEN KISSLER: Right. I think that, you know, certainly more would help. I think that I’m not as up on this literature as I would like to be. But it anecdotally from conversations I have had with people in this area, it does seem like it’s easy to reach people. It’s easier to sort of change behavior and to communicate information when somebody is individually contacted by human contact tracer rather than just sent information. And so I think that we have lots of examples from around the world of how contact tracing can vary. I think that what’s being done there is is important and it might be all that’s really possible within the logistical constraints of contact tracing is hugely resource intensive. One of the problems is that, you know, I think the hope with the first wave of infections that we’ve seen was that we would, through physical distancing, be able to bring cases down to a level where that individual level intensive contact tracing was possible because there would be few enough cases that you could really follow up each one. And we never really reached that point, unfortunately. So I think that we’re kind of left with some of these stopgap solutions in terms of contact tracing. So it’s much better than nothing. But I think that it’s far from ideal.
Q: OK. Thank you.
MODERATOR: Looks like we might be all set for today. Dr. Kissler, do you have any other comments? Final thoughts before we go?
STEPHEN KISSLER: No. Nothing further. Thanks for the questions.
This concludes the June 26 press conference.