You’re listening to a press conference from the Harvard School of Public Health with Yonatan Grad, the Melvin J. and Geraldine L. Glimcher, assistant professor of immunology and infectious diseases and a faculty member in the Center for Communicable Disease Dynamics. This call was recorded at 11 a.m. Eastern Time on Thursday, March 18th.
MODERATOR: Dr. Grad, are you going to be using your camera today?
YONATAN GRAD: Oh, sure. Sorry.
MODERATOR: OK, that’s OK. Do you have any opening remarks today?
YONATAN GRAD: No, I’m happy to just jump right in with questions.
MODERATOR: Fantastic. First question.
Q: Yes. Good morning. I would like to know who was working on the question of whether the COVID vaccine prevents transmission and what do we know so far?
YONATAN GRAD: I suspect a lot of people are working on that question, and I think it’s being explored through a number of different avenues. I think some of the data coming out of Israel where we’re seeing a decline in cases where there’s been such high levels of vaccination, I think is going to be one indication of the impact of vaccines on transmission. I think we’ll also be able to learn as vaccination expands across the US. I think we’ll also be able to learn from data monitoring the levels of disease and its relationship to vaccination in those populations. So I think a bunch of people are looking at it in that way. I think also following to see in vaccinated populations what the level is. If they do become infected, then whether there is a lower level of virus. So if vaccination protects against severe disease and symptomatic disease, but if people can still become asymptomatically infected, if we see that individuals have lower levels of virus, that might also suggest that they’re shedding less. And so there would be an implication that there would be less transmissible and so it would have an impact on transmission as well. And from the data in Israel, I think we’re seeing suggestions of a strong impact on transmission. So a lot of work that I think is going on and that we’ll hear more about over the coming weeks and months.
Q: Right. What approach do you think is going to be effective in answering that? Because it seems like you’d have to either follow people for a long period of time, which kind of was a downside maybe of operation warp speed. But these are fairly shorter studies. Do you agree with that? And then what is sort of the best approach to studying this question?
YONATAN GRAD: Yeah, I think that in in the vaccine trials, it would have been great if people were regularly tested by PCR because that would have given us an opportunity to see what the impact of vaccination was, not just on symptomatic disease, but on asymptomatic disease. And then by comparing the PCR CT values, which is the cycle threshold, it’s really a reflection of the amount of virus detected. We would have been able to see whether vaccinated and unvaccinated asymptomatic individuals have different levels of virus, and it would be suggestive in terms of transmission. So, yes, I agree that that would have been great for these vaccine trials, but it wasn’t done. So in the absence of that, there are other ways we can try to get at this information. And I think looking at what happens in populations. So trying to relate as you’re vaccinating in a population, the rates observed in unvaccinated individuals, that will be a suggestion of just how much both herd effect and also generally the impact of these vaccines on transmission would be. So I think we’re going to be following epidemiologically the amount of diseases in these populations will be helpful where vaccinated people are still undergoing any kind of routine testing. So health care workers or others, if we have those data, those will also be useful in monitoring for the impact of vaccines. I think a hint will also come from looking at data not so much about from vaccinated or the impact of vaccine, but the impact of natural infection. I think we’re starting to get those data. There have been a number of reports out of the U.K., and I think there was just one out of Denmark looking at protection from reinfection, having if you have been infected and then starting to look at the CT values to get a sense of just how much virus is there when reinfected. So we’re getting a sense of that. And it’s a related question to does vaccine protect against transmission in this case, it’s how much does previous infection and immunity that it generated protect against transmission? I think those are so similar kinds of data for vaccinated individuals, I think will also be useful. And I think those will start to come out too.
Q: Do you think we’ll have more answers by the summer?
YONATAN GRAD: Oh, yeah, for sure.
Q: Thank you.
MODERATOR: I usually don’t do this, but I’m going to pop in with a quick question. Do you know anything about the design of the studies for children that I believe Moderna just started a couple of days ago? Are they doing any sort of PCR test with the kids that you know?
YONATAN GRAD: I don’t know. Pfizer has had a study going, I think, from 12- to 16-year-olds. And I think they’re also starting or have started a trial with kids. I don’t know the details of the Moderna trial. That will probably start with a question about dosing. So it’s going to be a different, I would imagine, not being a pediatrician, I’m not sure, but I would imagine they would be looking at what is the appropriate dose kind of age based dose of these vaccines first and then what is there to in order to elicit an immune response that is comparable with what’s seen in adults and then look at vaccine efficacy. Whether they’re doing this will monitor by PCR and these populations as well, I don’t know. But it seems like it would be an opportunity to try to address the question first for sure.
Q: Great. Thank you.
MODERATOR: Next question.
Q: Hi. Thanks so much. I was just hoping you could tell me a little bit about what’s happening epidemiologically right now in the US, particularly around the status of B.1.1.7. And I know there’s sort of geographic variability, but what you’re seeing?
YONATAN GRAD: Yeah. So what I’m worried about is places opening up too quickly. Right. So we’re starting to see that there is a resurgence in cases in a number of states. We had seen this massive peak over the winter and then a decline. But that decline has plateaued. And when looking at national data, that plateau actually reflects variation across states that includes some that where there’s an increase in cases. So I worry about B.1.1.7 driving that to get to your point, at least to some regard, B.1.1.7 being more transmissible. Clearly, having driven a big peak in the UK and elsewhere recently, raises concern that as we let up on the various interventions that really helped to slow the spread, we’re going to give an opening for the virus to spread further and with a more transmissible strain. We really, again, risk additional peaks. And it feels like we’re so close as vaccine starts to get rolled out that, you know, that this tension between exhaustion from the social distancing and other types of interventions, the arrival of vaccines, this tension between the desire to start opening up and the risk associated with B.1.1.7 just as placing us in a precarious position. It would be great if people could just wait a little bit longer until we get higher levels of vaccine coverage as again, I think B.1.1.7 poses a risk. I would say opening up poses a risk and B.1.1.7 exacerbates that risk.
Q: I just want to make sure I’m sort of thinking about the dynamic correctly. So basically, if the reproductive number is above one, epidemics will grow and there are all these different factors sort of in a tug of war around that like seasonality in vaccines and natural immunity and whatever interventions are still in place instead of pulling that down. But as the prevalence of B.1.1.7 increases or transmission like that’s pulling the number upright, is that kind of an appropriate way to think about what’s happening, about whether or not epidemics are going to grow or shrink?
YONATAN GRAD: So the numbers. So the effective reproductive number is influenced by as you were saying, a number of those factors. So I would say the intrinsic transmissibility. So they are not for B.1.1.7 is higher. Its estimates are it’s about 50 percent more transmissible than the previously circulating strains of SARS-CoV-2. So it we’ll pull up the reproductive number, increase contact among individuals or increased contact that provides opportunity for transmission. So as people stop wearing masks, as people return to bars and restaurants and other locations that we know are particularly risky for transmission, that will lead to an increased effective reproductive number. Keeping in place, distancing, so reducing contact and reducing opportunities for transmission and masking and so on that will reduce the effective reproductive number.
Q: Like vaccine production and like natural immunity, that also brings down the number, right?
YONATAN GRAD: Correct. My list was not exhaustive, but just where you can go to the right. So as the fraction of the population with protection increases, we should also see the effective reproductive number decline.
Q: OK, great. Thank you so much. Really appreciate it.
MODERATOR: Next question,
Q: Hello, thanks very much. I want to follow up when we talk about the number of people who are vaccinated or who have natural immunity reduces that effective reproduction number. I guess the question is, are the vaccinations going into the right people that would help to reduce that reproductive number such that we’re vaccinating people who may not have been the ones out going to bars or going to the beaches in Florida or out in public based on how we define the criteria for who could be vaccinated. Now, I guess the question is, do we vaccinate the right people to reduce that reproductive number in a way that’s going to stamp down that case number?
YONATAN GRAD: Right. So this is a question about strategy. What is your goal? Is your goal to decrease the number is you’re given a limited number of vaccines. You could either vaccinate, as you’re saying, are you trying to optimize or you’re trying to optimize the reduction in the number of deaths? If so, you can imagine there are two strategies. One is vaccinating those people at highest risk of dying to provide them with some kind of protection. And that would be one strategy. A second strategy would be vaccinating those people who are the biggest transmitters and get your case numbers down with the idea that that would provide indirect protection and thus reduce the number of deaths. So it seems like there are two strategies and you’re going to have intuition in both ways. And as my friend and collaborator Dan Larremore from the University of Colorado likes to say, when you have two conflicting intuitions, this is where mathematical models help. And this was the subject of a paper recently published in Science on Optimizing Vaccination Strategies. So what we found basically to put it into a one liner was that in most in most situations, when you think about your reproductive number, when you think about the demographics and the contacts among individuals, and when you think about your vaccine rollout, are all different things that we explored in this paper. It makes sense if your goal is to reduce deaths, to focus on vaccinating those at highest risk of dying if infected. There are some contexts where you would want to vaccinate those who are at highest risk of transmitting right to get cases down, which I think is where you were asking there. But in order to reduce deaths. But under most circumstances, when we looked at it, it seems like that on the whole, the best strategy when your vaccine supply is limited is to target those people who are at highest risk of dying to reduce the overall number of deaths. And I can put in a link to that paper.
Q: OK, thank you for answering that. So I want to again follow very good question here. There’s a number of states with the seven-day case average that’s worse than a 14-day average. And when you look at all the states and territories, that’s twenty-three places where the seven day is worse than the 14 day?
YONATAN GRAD: Meaning it’s going up?
Q: Meaning that it’s going up. Correct. For our readers. I think we have a difficult time trying to describe what we’re looking at. And are we leaving a plateau? Do you consider this, you know, numerically a wobble? Are we see seesawing? What’s the correct way to characterize what the data is tried to tell us at this point?
YONATAN GRAD: I think it’s hard for me to predict what will happen in the next seven days, the next 14 days. I worry if those it may vary by place, if those numbers of cases or hospitalizations, deaths are going up in places where we’ve seen lifting of the not from several interventions, removal mask mandates, removal of social distancing, opening up of bars, restaurants and so on. Then I would be concerned that what we’re seeing is a real increase in numbers from increased transmission and that the expectation would be that those would continue to go up because now the virus has an opportunity to spread among susceptible people. So it has to do with the overall context for where we’re seeing those numbers go up. And then the other concern is as Drew had asked B.1.1.7 were given the same it being more transmissible than prior strains, where there are opportunities for transmission B.1.1.7 will take advantage of them more than prior strains. And we’ll see it drive cases up, too. So I think concern about B.1.1.7, it’s a serious concern and one that I think further underscores the importance of vaccinating as much of the population as we can as quickly as we can.
Q: OK, and then I’m sorry, one last question if my friends here on the line will allow me, is it even relevant? I think my editors here like to think about the US in comparison to the European Union or Italy, where we track them by a week or a month. Does that still track or is it an irrelevant comparison to make now, given that our daily new cases rate is already so high?
YONATAN GRAD: I’m sorry, comparison in terms of?
Q: Number of cases in Italy or across the European Union compared to the US?
YONATAN GRAD: I see. How are we doing compared to other places in the world in terms of cases or deaths or is that right?
Q: Is it still relevant to say that we followed them by a few weeks or a month? Is that comparison?
YONATAN GRAD: The pattern observed in other places in the world is reflective of pattern seen in the US?
Q: Yes. You’re better at asking the question. Thank you.
YONATAN GRAD: No, no, no. I was receiving just to clarify for myself what you what you were asking. I think that we know just how hyper local this pandemic really is. I mean, it’s basically many local epidemics. We’re seeing states that have different patterns of spread. So although we think of the US and we can aggregate across states and think of the US as one single entity, and for some purposes it makes sense to do that, like the overall death rate and so on. I think the fact that we’ve seen such different patterns in different states governed by the community decisions on what types of interventions to put into place when and how vaccination is going, I don’t know that it makes sense to compare the entire US to what’s happening in other places. It makes much more sense to look across the US and view each of these regions as distinct.
Q: Thank you very much.
YONATAN GRAD: You’re welcome.
MODERATOR: Next question.
Q: Hi. Thanks so much. This is slightly off topic in a way, but, you know, Minnesota was the first to find one in the U.S. to document that. And in that seems like P1 has been kind of a non-issue. And I just wondered, what’s your explanation for that? Why does that variant not seem to have taken hold here?
YONATAN GRAD: I don’t know. It’s a really interesting question. You know, it seems like the initial concern based on what we’ve seen was, I haven’t seen it replicated in other places. So I don’t know what to make of it. I am worried about variants that have this E484K mutation that seems to reduce the partial vaccine escapes or natural immunity escapes. Basically, it seems to reduce the neutralization of antibodies generated from either natural infection or vaccination. So that continues to seem quite a worry. I don’t know what to make of the fact that some of the strains with that mutation haven’t really been taking off everywhere, as one might expect. It could be that the combination of you know, that mutation, plus just the extent of disease in different populations, there’s sufficient immunity to prevent it spread, or that combination of immunity plus social distancing or masking is enough to prevent it from really picking up. I don’t know. I think it’s a really interesting question and one that hopefully we’ll learn more about as genome sequencing expands. I think one of the problems in the US and other places has been we haven’t had as good genomic surveillance to really be able to tell us what the dynamics truly are. So as that ramps up, we may be able to answer that question a little bit more thoroughly. But I agree it’s an interesting and puzzling question.
Q: Thanks. Just one quick follow up, when I talked with the health lab folks here, one thing they remarked on is that that that finding came from a random sample. And I wondered you as an outsider, like, does that also strike you as interesting and does it therefore kind of point to the need for what you were just suggesting in terms of expanded sequencing? In other words, it seems like the more you do, the more you get surprised and you find things like this, but perhaps more importantly, other things that could emerge.
YONATAN GRAD: Yes, I think I’d be curious, actually, for the size of that random sample. I mean, I think this gets to something that’s been talked about now for a number of months and where I think that the federal government and the CDC are really starting to invest. And this is what should have genomic surveillance program look like. One part of it should be random sampling so that you can get a sense of what’s happening overall in a population. Another part of it should be directed sampling, particularly for people who have severe disease that will allow you to look for whether there are emergence of other known variants or new variants that are causing either more cases from a random sampling or more severe disease by comparing the strains that are causing severe disease with what you observe in a random sample, those really seem to be the main things at least we’d want to look at right now. So expanded sampling, both random and directed, will allow us to, I think, answer some of the critical questions that we’re all interested in both now and going forward.
Q: I’m sorry, one last thing on that point, the money and the relief bill last week for more sequencing, that’s something that’s a good thing, I would guess, from your perspective?
YONATAN GRAD: It’s a critical thing, not just from my perspective, but I think for all of us. I mean, investing in that infrastructure will be hugely important for SARS-CoV-2. And I think it has great long-term consequences. I think this is an infrastructure for monitoring infectious diseases that will be valuable, not just for the pandemic, but for tracking infectious diseases broadly even after we emerge from this. So I think it’s an extremely important investment for both the short term and long term.
Q: Great, thank you.
YONATAN GRAD: Welcome.
MODERATOR: I’m just going to add in real quick that Massachusetts had its first one variant case identified on the 16th, so we’ll have our little experiment going to see if it takes off or not. Next question.
Q: Thank you for your time today. You touched on this earlier, but here in Ohio, we’ve just gotten some data on the rate of genomic sequencing going on. And it’s pretty low. It’s really modest. So for one, why is genomic sequencing, why does it seem to be so scarce here? I mean, how much should states be doing? And is any state really meeting the threshold in a serious way of adequate visibility of these strains?
YONATAN GRAD: I think it’s an area that just hasn’t received much investment historically, and I think that is in contrast with what we’re seeing out of the U.K., where they have had a robust. Pathogen, broadly speaking, pathogen AMSO microbial sequencing platform for years and has really integrated that into the public health response. So, you know, it’s something where we’ve just we’ve just been behind and I don’t know of the details of how states are sequencing or how much sequencing is going on state by state, other than to say that it is really, I think, starting to improve. The CDC put out grants to support sequencing at state public health labs and in collaboration with academic labs a little while ago. And I think that has really led to a ramp up in sequencing of SARS-CoV-2 genomes. And I think that will be especially with this new fund and continue to increase. But I think we also will need is not only that the brute force of doing more sequencing, but then thoughtful approaches and strategies on how to implement that sequencing and interpret it. So as I was describing before developing approaches, that sampling approaches that will allow you to answer the questions you want to answer and to give you good estimates and robust estimates of prevalence, changing prevalence, severity of disease. All of these things will require some forethought and planning, not just sequencing, whatever you can get your hands-on convenient samples, have some value and can be interpreted to some extent. But really a deliberate sampling strategy can get you to your answers faster. So I’m hopeful that that will also be part of the genome sequencing going forward. It’s not just about the sequencing, it’s about thinking about what you’re sequencing and how to do it most efficiently and to enable answering the questions you really want to answer.
Q: And to follow I mean, do you have any sense of what rate of total samples taken need to be sequenced to have that visibility might be comfortable with, like, what, one percent of all tests or one percent of positive tests?
YONATAN GRAD: Yeah, it depends on how quickly you want to be able to find something and what you’re so, you know, we looked at this for, you know, just trying to think about this was pandemic times when we were thinking about antibiotic resistance and we were wondering about how much sampling do you need to do to pick up a new antibiotic resistance determinant prior to it becoming some fraction of the population. And there’s a similar kind of calculus that you can make here. Just how prevalent will a newly detected variant be on the relative to how much sampling you’re doing? So, you know, ideally, if you had the money and resources, you sequence all isolates, if it didn’t cost anything, that’s what you would do. But recognizing that there’s limitation and sequencing capacity and the analytic capacity, there’s going to be a lot of noise if you sequence everything. I think a number of places are targeting around five percent and to be able to do five percent of samples. But again, this gets at this question of how you want to divide that if part of your question is to be able to identify those that are causing more severe disease. You might want to split those numbers to a random sample, which can give you a sense of what’s spreading through a population and whether you have a particular variant that’s increasing and what’s causing severe disease. And so looking at those not just individuals who may be asymptomatically infected or mildly infected, but really getting a sense of which ones are responsible for people showing up in in critical care units or dying and then being able to compare those two populations so that you can understand whether what’s causing severe disease is just a reflection of what’s circulating or whether it’s one particular strain. So I think it’s going to the amount of sequencing is going to depend on the resources available, of course, and then, you know exactly how many cases you can tolerate before you pick up something new so that there’s no right answer. It’s just a question of kind of what you want to target, how many, how much, how prevalent you will accept something being before you detect it.
Q: Thank you, that’s really helpful.
MODERATOR: Next question.
Q: Hi, thanks a lot. We’re a very local newspaper, but I have a question that is a little more general. How important is it in terms of controlling the spread of variants that you don’t find out that a positive case is actually caused by a variant until maybe a week, maybe even longer after the person has tested positive?
YONATAN GRAD: I’m not sure I understand the question you’re asking, how important is it for control of variants broadly or in that specific case?
Q: The fact that it takes so long after someone tests positive and that it’s a variant? Because we don’t have the greatest contact tracing anywhere that I know of in the United States, so how important is it that it takes so long to actually identify a positive case as a matter of a variant?
YONATAN GRAD: Yeah, we can speak about B.1.1.7 as one example of this because it’s more transmissible. And it’s really, I think, you know, this gets to control of spread broadly. So the same principles apply for variants and non-variants. It’s just the same principles apply for SARS could be to what you want to try to do is, is implement art, not just pharmaceutical interventions, isolate the people who are infected, quarantine contacts, those things hold whether it’s a variant or not, and should be used for all cases being able to identify that in the population that you’re seeing an increase in variance that is useful in helping to understand which one and whether the patterns of spread or in particular populations are being able to help guide interventions or instruct whether we might need to target vaccines to particular populations or otherwise try to slow spread through reinstituting or tightening the pharmaceutical interventions. So it matters more on an epidemiological scale to influence that level of decision making. But for individual cases, I think the same principles apply no matter the strain of SARS-CoV-2 causing an infection.
Q: So if you have a case of a B.1.1.7 in a community, does that does that suggests that you might want to do more sequencing of tests in that community. I’m talking about in Cambridge, we have a certain number of B.1.1.7. We have two of the South African variant out of six in the whole state. So I’m just wondering whether that means that you’re not only targeted by severe disease, but targeted by location?
YONATAN GRAD: I see, so, yeah, I think it depends on what kind of question you want to answer. So if part of the question is to get a better sense of the local dynamics or the local prevalence, then for sure you can target your sampling, either increase the random sampling in your population, or if there are particular communities that you think are at high risk or if you’re trying to understand whether this is, it gets to what we call genomic epidemiology, and you want to understand the specific spread of variants within the population, sequencing can not only tell you about that, whether there’s a specific variant, but can help with in the right circumstance understand the pattern and nature of spread. So, again, it gets to what you want to do with that information. How is it going to help improve your public health response? Is it that you want to identify whether there is a specific event that led to a lot of spread or whether there’s a particular community that’s at high risk from spread, perhaps because of a reduction in one of the non-pharmaceutical interventions, the social distancing or so on, so that you can know that re implementing or tightening some of those restrictions might be helpful? I mean, it gets to the question of what are you going to do with that information and then how will you intervene?
Q: Thanks. Thank you very much.
YONATAN GRAD: You’re welcome.
MODERATOR: Next question.
Q: Just a quick follow up question. My sense has been that is, as a practical matter, sequencing, I want to say, never gets done in a timeline that would sort of allow some if it was me, the health department, to call me and say, hey, you’ve got B.1.1.7, you really need to stay home. That’s not really the way this happens anywhere, I don’t think. Is that right?
YONATAN GRAD: I think that is mostly right. Well, first of all, anyone with a positive test should be staying home. It’s not that we say that you should particularly stay home with one of the variants. But really, anyone who is positive should be isolating the fact that you have that someone might be infected with a variant on the individual level. One shouldn’t necessarily influence their actions. It’s just being infected with SARS-CoV-2. You should be isolating. Right. And your contacts should be quarantined. That is just general principles that hold regardless. The utility of genome sequencing on the individual level knows there are some places in which that might happen if you really wanted to track transmission or understand the nature of spread within particular exposures to really help understand whether you might know within a particular location, have an outbreak or multiple independent introductions. I mean, it can help understand the dynamics more locally and over a short time period. But from an individual level, I don’t think it will influence that or should influence at this point actions. All of the actions basically reflect infection with SARS-CoV-2 no matter the lineage.
Q: Thanks so much.
MODERATOR: Next question.
Q: Just to follow up on the genetic sequencing, are pharmaceutical companies engaged in this effort because they’re the ones developing these booster shots which are supposed to work against some of the emerging strains. So you would think logically they’d have to identify them. So I was just wondering how that works.
YONATAN GRAD: I don’t know that they themselves are involved directly in doing sequencing because there’s so much information coming from sequencing being done by other people, other groups, I mean, the identification of B.1.1.7, of P1, among others, that was that’s done by genomic epidemiology, doing the doing the sequencing and surveillance. So those have been identified in the context of public health surveillance and then further characterized by monitoring and epidemiology, as well as the response of as well as characterizing the immune response to these variants. So I don’t know that the vaccine companies themselves have been I don’t know that they’ve been involved in sequencing themselves, in part because it’s that that’s kind of covered by other groups, but they’re certainly using that information. I mean, it gets back to you as well. The first SARS-CoV-2 sequence that was generated by a combination of public health, academic group, and these companies like Moderna and Pfizer were able to start developing a vaccine based on that sequence very early on. In the same way, they’re using information being generated by surveillance and sequencing to help inform the next generation of vaccines. So I don’t know whether they’re investing directly or doing their own sequencing. But there’s plenty of other sequencing and epidemiological work that will tell them what strains to focus on next.
Q: It seems like this is a big timing issue for the rollout, for the vaccines, because I’ve heard everything from having a booster that could be a couple months, almost like a follow up follow on to the current vaccination to more like the influenza where you get it on an annual basis. I’m just wondering, which one, given the emerging situation, the fluidity of this, you know, is there one approach that makes more sense than another? Or do you think it should be coming sooner than later?
YONATAN GRAD: Oh, I don’t know. I think that the time will tell just how robust the immune response of vaccination is to two variants and whether new variants emerge that further escape from vaccine conferred or natural infection conferred immune protection. I think we’re going to wait and see whether SARS-CoV-2 is limited in its range so it can’t escape that that much more or whether it will continue to evolve away from vaccine and natural infection conferred protection. So it could be that having had a vaccine or having been infected will provide substantial protection even from variants, and that protection might be from infection at all or might be from developing severe disease or dying. And if that’s the case, it may be people say, well, if all I’m going to get is a cold and I’m not going to end up in the hospital, I’m not going to die, then maybe the immune protection that I have from this initial ground is going to be sufficient. But I think that the more conservative approach is start to develop vaccines just in case. That’s not that, just in case that it’s not that optimistic scenario and that new variants can cause just as much severe disease and death as SARS-CoV-2 has to date in naive or fully susceptible people. And then having new vaccines either is booster’s or as annual shots will be necessary. I think the strength and duration of immune protection and its relationship with emerging variants will we’ll learn over time and that will shape what the strategy will be going forward.
Q: It seems like we can count on there being more mutations, right?
YONATAN GRAD: I mean, that will always mutate. That that’s certainly the case. The question is, will it continue to have the same kind of escape from immune protection, whether that was confirmed by vaccination or natural immunity? You know, not every so whereas flu seems to evolve antigenic every year, warranting the seasonal flu vaccine, other viruses don’t have that same kind of pattern. So we’ve used basically the same measles virus vaccine since it was developed over 50 years ago. So measles also and RNA virus that that mutates, it’s just it’s antigenic range has been limited. So not every virus follows the same flu-like pattern of regular escape from immune pressure and regular antigenic evolution. So mutation for sure, but that doesn’t necessarily mean that we’re going to see the same range or same piece of antigenic evolution.
Q: OK, thank you.
MODERATOR: I have one more question coming in from Greece. And if you don’t know the answer to this, that’s fine. I’ll see if I can find somebody else for her. COVID-19 variants push Greece and many other countries in Europe into a third wave of the pandemic. The Greek government has imposed for many weeks now a third lock down schools, shops, et cetera, are closed, but it doesn’t seem to work. What is your advice and what other measures should be taken?
YONATAN GRAD: Yeah, so I don’t know the situation in Greece at all, I’m afraid, so I can’t speak directly to what’s going on or what it means that things are not working. I mean with the tempo, there’s often a delay between the introduction of lockdown measures and the reduction in cases in part. This is something we’ve learned over the course of the pandemic, that it takes a couple of weeks to see the impact of changes in societal behaviors before there are changes in case numbers, hospitalizations, deaths and so on. There is a delay. So that’s one potential explanation. But I really don’t know that the story in Greece to be able to speak to the specifics.
MODERATOR: She would also like to know how worried should we be about the new COVID-19 variant?
YONATAN GRAD: Yeah, I think that may B.1.1.7 we worry about, it’s increased transmissibility, so again, with the lifting of restrictions, it can even exacerbate any rise in cases. What we worry about, be one in seven driving more cases. And there was just a paper in Nature from Nick Davies and colleagues in the UK suggesting B.1.1.7 also causes more severe disease. So I think that is for sure worrisome. And as we’ve just been discussing, if the variants also enable escape from infection conferred by either natural infection or from vaccination. And so if they’re starting to escape from that immune pressure, then that’s also concerning because then you will increase the opportunities for spread and all of the associated ramifications.
Q: And then she had one final question, how close are we to finding a treatment for COVID-19?
YONATAN GRAD: Yes, so there are some treatments that can help that have been approved. Things like dexamethasone for people with severe diseases. It seems to help improve outcomes in hospitalized patients. Remdesivir an antiviral, fairly modest, but contributes. I know that there are individuals still companies, institutions, academic groups who are continuing to work on finding therapeutics. So, so, so treatments that can help reduce the severity of infection for people who are infected. But I don’t know where those trials stand. I can’t speak to where all of that development is and what people have tried a variety of different things that don’t seem to work. Going back to the hydroxy chloroquine and does it through my sense stories. And they know people have been looking at other types of drugs, but I can’t speak to exactly where all of those trials stand.
MODERATOR: Thank you. I think that’s it for questions. Dr. Grad, do you have any follow up, any comments before we go?
YONATAN GRAD: Thank you very much.
This concludes the March 18th press conference.