Coronavirus (COVID-19) Press Conferences
Coronavirus (COVID-19) Press Conferences

March 23, Coronavirus (COVID-19) Press Conference with Stephen Kissler

3/31/202247:268,438 words
0:000:00

A press conference from the Harvard T.H. Chan School of Public Health with Stephen Kissler, research fellow in the Department of Immunology and Infectious Diseases. This call was recorded at 12:30 p.m...

Transcript

EN

You're listening to a press conference from the Harvard TH Chan School of Pub...

research fellow in the Department of Immunology and Infectious Diseases. This call was recorded at

12 30 p.m. Eastern time on Wednesday, March 23rd. Dr. Kisler, do you have any of any remarks?

Yeah, just looking forward to speaking with you all. I've mentioned in the intro that I'm happy to talk about the BA2 wave. I recognize that it's not really a wave at this point yet in the US, but hopefully we can dig into a little bit more what things might look like while recognizing there's still a ton of uncertainty. Great, thank you. And it's been a while, so might be a little rusty with this, but we'll get right back in the saddle. All right, looks like we have a couple of

questions already. First question. Hi, thank you so much, Steven. Just wanted to add this was not specifically on your list of things that you said you could talk about today, so sorry if it's a two off subject to let me know if it is, but I just was wondering if you had any reaction to the news of the journey of seeking authorization for children under the age of six, what you thought of that

any thought should be shared? Yeah, I mean, as always, I'm most excited to just see what the data

look like. And I know that there's more data that's been collected that I haven't yet seen, but I think it's very promising. I know that one of the things that especially parents of young kids have really been waiting for is exactly this authorization for the youngest age groups. I do think that assuming that the safety and efficacy holds up well in that age group is durable over time, that it would be great to have these vaccines available for young kids.

And I think as I've mentioned before in previous calls, but I think it bears mentioning, again, now that I think it's also to bear in mind the difference between approvals and recommendations.

I think, again, as long as the safety and efficacy do you continue to hold up?

I'm very strong advocate for approving vaccines for the youngest age groups. I think that there's

a much broader conversation than that needs to be had about recommendations for kids in those youngest age groups. Just given that their risk profile from COVID-19 just differs so much from older adults. But I do think especially having those vaccines available for kids who have immune conditions that might not allow them to mount to get immune response to COVID-19, I think the vaccines could help in some of those cases who have other sorts of respiratory

conditions. I think there are a lot of kids who could really benefit from these vaccines, not to mention their families as well. So I see it as a great step in a good direction and I'm excited to see more. Do you just have a quick fall up on that? I mean, it says it's 43.7% efficacy in children's six months to two years old. And then just 37.5 and two to six, is that disappointing or surprising in any way that the numbers are not higher? I mean, in adults,

they were much higher levels of efficacy. It's difficult to compare the statistics on efficacy perfectly from one point in an epidemic to another. But it's not surprising to me that there would be differences here for a couple of reasons. One is that the immune systems and young kids differ hugely from the immune systems in older adults. But in my mind, probably the biggest thing is that the size of the dose differs quite a bit too. And so with smaller doses and young

kids, you might expect a smaller immune response as well. So I'm not surprised. But that said, the efficacy, well, it doesn't sound great, is actually roughly in line with the efficacy that we sometimes see from the seasonal flu vaccine. And that also can be very helpful for young

kids to keep them from getting really sick from the flu. So I think that there is precedent for

using vaccines of about this efficacy in young kids. And while, of course, you know, I would love to see a hundred percent efficacy in all of the vaccines that we have available, I do still think it's high enough to be pretty useful. Thanks so much. Next question. Hi, thank you so much for taking my question. I do have a few. And that's also piggybacking off of the Moderna question that was just asked. So these, this phase three trial was done during the recent Omicron wave. Do you think

that this vaccine could protect young children against BA2? I guess, you know, is there any reason to believe that it wouldn't? In my mind, no. I mean, it seems like BA2 and the previous sub-variance of Omicron, BA1, and its sub-lineages have, they interact with the human immune system in pretty similar ways. And so people who have been previously vaccinated or previously infected seem to fare pretty similarly when exposed to BA2 or BA1. So my expectation is that

even though the vaccine trials were done for the major Omicron wave in the US, we should see pretty similar results for BA2. Great, thank you. And then, I mean, when do you think that we would

See the vaccines available for young children and elementary school children?

see a surge of BA2? I guess the question would be, you know, will children get access to these vaccines

for the surge happens? Right. Yeah, so I mean, I think that, you know, at this point, the vaccines

could be made available to those younger age groups in pretty short order. This is pretty different than the initial rollout of the vaccine. It's simply because it's essentially the same vaccine just in different doses. And so the vaccine is available, it's been produced in high quantities. It's fairly widely distributed right now. So I think, you know, pending approval, it's difficult to say how long that might take, but I think that that could be pushed forward

pretty quickly. Ideally, within the next couple of weeks, probably, especially if we're expecting a surge from BA2, I think that we could see approval for young kids to get the matter in a vaccine pretty pretty soon. The question of if and when a surge is coming in and how large is also very much open, I know that we've seen major surges that are dominated by BA2 across much of Europe, but in contrast, for example, in South Africa, we saw a major BA1 wave and it's where they saw

the Omicron wave first. And now there's a lot of circulation of BA2, but it hasn't really caused

an increase in cases so much as it's sort of lengthened the decline and given that epidemic a

very long tail. And I think it's not totally clear what's going to happen in the U.S. In many ways

are experienced with Omicron, there are some similarities between both Europe and South Africa in terms of our vaccination rates are maybe a little bit closer to those in Europe, but we also did see a very intense BA1 wave and to the extent that that gives us protection against BA2, we might see dynamics somewhat more similar to what's happening in South Africa as well. So all of that is to say that I do think that it's possible to get approval of the vaccines

for these youngest age groups soon and probably soon enough to deal with whatever BA2 is going to throw at us in the coming weeks. That said, I'm still not totally convinced that we're going to see a major surge from BA2 and yeah, we'll just have to see on that. Great. Thank you. Next question. Thank you. So I have a question that's maybe a bit farther out than just

whatever might be happening with BA2. So I guess kind of into the future there's going to be these

waves and maybe they'll be seasonal and like how damaging they are will kind of be influenced by things like viral evolution and potential waning, but I guess like one thing that struck me so far

is that even between waves we've never actually gotten down to like really low levels, like I

don't know below 10,000 cases a day or something like that. And so I'm just wondering like what do you think like might the quiet periods look like going forward? Is it just that we need like a bit more experience with the virus before we can get to low levels or is it possible that there's just some of like a persistent plateau outside the waves that just kind of like solely ticks along and causes some amount of, I don't know, morbidity and mortality. Yeah, you know, it's

I really appreciate this question a lot. It's it's hard to say because this virus is in many ways is different from just about anything that we've seen previously. So I can give a couple of examples or I mean it's so it was so one of course is flu where we have seasonal outbreaks but then it reduces to very low levels in much of the US during the summertime and that's that's reflected across most temperate regions of the globe. And so one possible future that I could envision

is that with repeated exposures to SARS-CoV-2 will essentially reach a similar equilibrium point where we have large outbreaks potentially in the winter season or in times when people crowd indoors and and substantially lower cases in the summer, basically just ones that sort of reaches that that sort of cycle where it's depleting, it's basically infecting a lot of partially susceptible people during the winter but then that provides enough immunity to sort of

get us through the summer. But one reason why that might not be the case is because SARS-CoV-2 is just so incredibly infectious, especially with the rise of Omercron and so because of that it may well differ from the dynamics of flu where we do see persistent spread over the summer.

The other example that I always think about when it comes to highly infectious respiratory

viruses is measles and with measles we also tend to see really significant outbreaks at least in the pre-vaccination era with some major outbreaks in the winter time

They tended to sort of subside as well outside of the winter but that's also ...

because measles gives you much longer lasting immunity it seems than infection with SARS-CoV-2 does. So generally young kids would get measles but then they'd be pretty much protected for re-infection for the rest of their life. SARS-CoV-2 is different because we can of course continue to get re-infected by it. So in my mind the most likely scenarios that we're going to settle into a seasonal pattern of SARS-CoV-2 spread where it's going to be dominate probably in winter

months in temperate regions of the globe but that actually we're not going to get quite down to those low levels of spread over the summer and that there will be a lot of variation but it won't be quite like flu where there's almost none of it but we're going to kind of be dealing with this at some level at all times in the year. That's great. Thank you very much. Thanks.

Next question. I just wanted to get some idea given all the unknowns. Would you expect if there is a surge for this to look like among the various populations in the United States, the full vaccinated population, the partially vaccinated, the unvaccinated, the elderly versus the young? Yeah, thanks. So in many ways I think that it will likely resemble our experience with COVID-19 up until this point. One of the key things with Omicron and this goes for BA2 as well as

all other sub-lineages of Omicron is that a booster dose, so a third dose of an mRNA vaccine or

an mRNA vaccine on top of a Johnson and Johnson if that's what you received before,

really goes a long way towards helping protect you from symptomatic disease and especially from severe disease. So I think that probably the biggest delineation that I imagine seeing is that people who are boosted will probably fare better than people who are unboosted and I think that that's probably the biggest split point. We're going to continue to see. I imagine the standard increase in severity and the likelihood of hospitalization, for example, and even the mortality rate

that goes up substantially with older age groups. But it still seems to be the case that even now, you know, a few months after a lot of especially the older age groups have gotten their boosters that a vaccinated and boosted person over the age of 75, their risk is probably on the order if not lower than a unvaccinated 20-year-old. And so that's good and in many cases might be even

better. So I think that the most important thing is that even though if you control for everything,

the risk still increases substantially with age, that with vaccination and boosting, even the oldest members of our society are pretty well protected and it brings the risk from COVID-19 back in line with a lot of other risks that we tend to face or faced in the pre-COVID area from other pre-COVID time with other infectious diseases. Hope that helps a little bit. I mean, there's so many different subgroups and populations to think about here. I mean, there's

people are returning to work. I think that the question of, gosh, it's, I think it's beyond the scope of this call for me to sort of like be able to break down all of the issues, you know, the breakdown by racial and ethnic groups, the breakdown by socioeconomic groups and specific subgroups of people who may be immunocompromised or COVID-19 still poses a big risk.

Young kids who still have not been vaccinated, I think there are a lot of really important

things to distinguish there, but basically if I don't go into all of the details with those,

it's not that they don't matter, but that I think some of the biggest differences that we're going to see is being boosted, unboasted, and then continuing to see this gradient by age. Sorry, I remuited myself. I'm all sent. Thank you very much. Next question. Hi, thanks for doing this. So you mentioned when talking about the B2 weight potential wave about how there is a lot of uncertainty. And I'm wondering if you could sort of walk us through

the factors that sort of lead into that and the different variables that you're considering when trying to, you know, look ahead and figure out how severe a potential wave might be. Yeah, thanks. So the variables I usually look at when making sort of these forward-looking

projections, I guess, is first the immunity and the population as a whole.

So I am a modeler. I use models to try to understand what might happen next, but often times the best thing that we can do is compare what's happening now with what has already happened in

Other places that are similar to us.

earlier about the experience of Europe versus the experience in South Africa. So when looking at what's happening in the US, one of the things that I bear in mind when trying to compare our experience with other countries is that we have decent vaccination rates, although certainly lower than many of the more highly vaccinated countries in Europe, especially. But we have also had a lot of previous transmission of Delta of Omercron and of the even SARS-CoV-2 prior to those variants.

So all of that is contributing to you, actually quite a bit of population immunity. And so the more immunity we have in a population, and especially the more immunity we have to variants that are related to the thing that's currently circulating, the less chance that I see

of a major surge. The second major thing is really just where we are in the year. So seasonality

is certainly just a factor among many that's driving the spread of SARS-CoV-2. But I think that

one of the things that might help us as we're going into this next surge is that we're entering the spring, which seems to be sort of a low time of circulation for SARS-CoV-2 across the US. In some parts of the US, we've seen major surges sort of in the summer, especially the late summer, and then in others we've seen it more in the winter. But usually spring is sort of the time when we've seen the lower cases across the US. And so whereas we've seen BA-2 surges in

much of Europe during times of year, when you might be expecting to see a surge anyway, the increasing prevalence of BA-2 in the US is more coming along the time when we might expect to see cases declining anyway. So to sort of summarize that, I usually look at seasonality. I look at how much immunity we have, both at baseline and to things that are related to the things that's circulating now. And then the last thing to sort of measure is to sort of project severity

overall in the population number of deaths, number of hospitalizations. Really the most important

thing is the vaccination rate in the very oldest age groups, because those are the people who still tend to be at highest risk of going to the hospital. So the higher our vaccination rates are in that age group, the better chance that we have of not having major surges at our hospitals. Great, thank you. Thanks. Next question. Thanks for doing this. So kind of piggybacking off of that last question. I've been talking to

some folks right now. Obviously Europe's getting hit hard by BA-2 right now, but you know, every country is having their own experience. And sort of given that experience in Europe, what are you thinking as far as regional differences with how BA-2 hits the U.S. in which parts of the country are you more concerned about? I mean, I'm guessing it's those that may not have as much immunity either from vaccines or from exposures that may be kind of walk us through

which which states your region is your most concerned about. Yeah, so actually, you know, in my mind, my, in many ways, I'm sort of concerned about just about everywhere equally, but it's the timing of my concern that really changes. So here in the Northeast, we've, it's already the case that at least among the the viruses that we're sequencing, which is we're sequencing quite a bit here. Now, most of them, so over 50% are BA-2. And so it's often the case that once a variant passes

that 50% mark, we really start to see what it's going to do. So if it's a more trend in this

bull variant, we start to see it uptake in cases, for example. And so in many ways, I think that

it's going to be the coasts, especially the Northeast, that are going to see what's going to happen

from BA-2 first. But as has happened with most of this previous variants as well,

really nowhere has been spared. It's really just been a matter of timing. And so I think that when it comes to trying to measure the relative severity of different places, a lot of the same things are still going to hold. So certainly, if there's lower previous immunity, a place might fare worse. If there's much higher population density or higher concentration of older individuals, they may well fare worse. But none of this really differs from previous ways of SARS-CoV-2.

And I think the biggest difference that we're going to see between places is maybe not so much the severity, but just the timing. Thank you. Next question. Yeah, hi. Thanks for taking things for doing this and taking my question. I'm wondering if you can talk a little bit about the role of mathematical modeling and making predictions about the pandemic. Is it something that is most helpful in terms of

identifying patterns that could lead to surges in the future or maybe identifying

anomalies that could indicate the emergence of a new variant?

Yeah, thanks. So I think there are a number of different ways that mathematical models have been used

And plenty of ways that we've not used them as well as we would have liked as...

pandemic. But I think that at their best, there are really two main areas where models can be helpful.

The first is in making short term forecasts. So thinking about models as sort of the equivalent

of weather forecasting tools, for example, what we're trying to make a prediction over the next couple of weeks, what's going to happen in a specific community? And that could be really useful

especially for planning very short term responses. So I think that those kinds of things are

very helpful for local policy makers, for hospital administrators, for people who are trying to prepare capacity to contact tracing, to deal with an influx of patients. And so that's one area where models, I think, can be very useful. But of course, those forecasting models, as with weather forecasts, weather forecast for Connecticut is not going to be particularly useful for me sitting here in Massachusetts and we're actually not that far away anyway. So with those kinds of

forecasts, they need to be very precisely tailored to the populations that they're dealing with.

And that makes them a lot harder to sort of use broadly. So that brings in the second area where

models can be really useful, which is as sort of these contingency modeling frameworks. So there's sort of these mechanisms for asking complex if then statements. So you can say, if we vaccinate 10 more percent of our population, roughly how much do we expect the number of hospitalizations to decline in the next wave. So you can use mathematical models to sort of get these rough orders of magnitude estimates of how a certain policy change might affect the spread of an epidemic across

an entire country, for example. And then that allows us to compare different choices. We oftentimes have different choices of what sorts of policies we might be able to enact. And we want to make sure that we're using the ones that are going to be maximally effective while being minimally

intrusive or minimally costly. And so mathematical models can be really good at that for just

sort of trying to get a rough sense of which policies are the optimal ones in those kinds of scenarios. They won't give you as precise estimates because, again, we're sort of dealing with the entire epidemiological scenario and the location as a whole. It's sort of like the analog of climate modeling as opposed to weather modeling. So trying to understand what are the broad trends in the epidemiological climate over long periods of time. So models can be useful in both of those

areas. I think it's really important not to confuse the two types of modeling because usually one

doesn't behave well for the other purpose and vice versa. But those are the two areas where they've contributed most during this pandemic. Are you all set? Also, thank you very much. Next question. I I was wondering if you could expand just a little bit on the scenario you described of a sort of permanent COVID season as opposed to flu seasons in the fall. Like what that what then might look like. Is it public health departments on the county level or regional,

you know, saying like, look, I way of COVID or how do you see that playing out? And also sort of how much confidence do you have in that versus another sort of surprising variant? Like I'm the cron which, you know, we've been told is genetically quite distinct from the other ones and sort of is screwed up our expectations somewhat occurring now. Like how much on the other hand should I throw into the story. Yeah, you know, everything in the kitchen sink I guess. I mean,

this virus has managed to find a way to surprise us every turn. And so, you know, I think

with everything that I'm about to say, that's worth bearing in mind, that there could be some new variant that emerges that's quite decently related from anything that we've seen recently. That really could change a lot of this. And so, you know, that said, my sense is that with, you know, with with this, this gosh, that's really such a disheartening term, but the sort of a permanent COVID season. I mean, I do think that we're going to see substantial abs and flows

in different places at different times. One of the things that I didn't really get to talk about as much as some of the previous questions, but I think that does apply to them and to this is that, you know, we've been talking about seasonality and really seeing rises in cases during the winter months, but in, in a lot of places, especially in the South Eastern United States, I think Florida, for example, in particular, we actually have seen a lot of spread during the summer,

and I think that some of that could be down to just the time when people spend indoors. And so, wouldn't we surprise if we end up in a scenario where we actually have some kind of sort of opposite seasonality between different parts of the country, based on whether you're retreating indoors or air conditioning or for heat, because it really does seem like unmasked indoor interactions are far and away the highest risk exposures for spreading SARS-CoV-2.

So, we may settle into a seasonal pattern that looks different to different parts of the country.

Then, you know, we're also going to have some of the sporadic variation that ...

on introductions and differences in immunity and differences in age groups that will change the

timing of cases from place to place. So, actually, you know, what you suggest is kind of what I envision is that over time, we may have sort of a COVID weather report that is just roughly

tracking cases locally. I think that that's going to be probably largely based on things like

passive surveillance. So, the number of people who are seeking outpatient care for respiratory viruses that turn out to be COVID, a lot of wastewater surveillance, for example, because I think that the number of people who are sort of proactively going out to get tests is going to continue to decline for a while. And then, you know, the last thing I think that's worth

mentioning here is that we, in a lot of these discussions, we think a lot about policy changes

and whether they're going to be sort of the political and individual will to change or behavior, if cases do start to rise. And I think on that score, I'm actually a little bit more optimistic than some of the people I've spoken with lately, in that for much of the pandemic, you know, we've had policies that have certainly changed the ways that people interact. But it seems from a lot of the evidence that I've seen that oftentimes people also spontaneously change their behavior

based on how much COVID is circulating in their community. Our tolerance for COVID cases is

probably going to increase as people are increasingly immune to the virus, certainly. But I think

that in many ways, one of the best things that we can do to help manage continued outbreaks is to just continue informing people how much COVID is currently circulating in their community and make it just as accessible as the weather report. Because again, a lot of data suggests that people do tend to sort of adjust their behavior accordingly. Now, will that be enough to prevent major surges? Probably not. And then in the event of a new major variant, we will probably have to reevaluate

things as well. But as we continue to deal with COVID, and we think about sort of this permanent circulation of COVID-19 and population. I think that recognizing that there's going to be different sorts of dynamics of different places, sort of different patterns of spread across the year, the timing will look different. But because of that, making clear what's happening in any given

community at any given time, using passive surveillance is probably the best thing we can do right now.

Thank you. Next question. I'm thinking of thank you for taking my question. Just about the VA2, some countries, the increase of VA2 corresponds to the surge of cases. But in other countries, we are not. And so what do you think makes the difference, such as behavior or existing immunity? And also, I want to ask,

what is the most constructive or socially acceptable policies to mitigate or prevent future such? Great, thanks. Yeah, so I think that we're still trying to understand what exactly is causing a surge in VA2 in some countries versus not in others. I do think that it probably does come down mostly to differences in behavior and differences in immunity. One of the interesting things about this pandemic is that I think it's bringing to the fore a lot of things that

we've also known to be true about other infectious diseases. And so in that, you can have pretty vastly different rates of transmission in different locations of very similar viruses. And they might be locations that resemble one another fairly closely. So I'm thinking of the spread of the bacteria that causes, basically, strep throat and other strep to cockle bacteria, can look very different in the US and the UK. We have very different variants that spread at different times.

And it's not immediately clear why that's always the case. It probably, again, comes down to

differences in behavior and differences in immunity. So thinking about the SARS-CoV-2 case, I'm not terribly surprised that we're seeing very different scenarios in different countries, but in the question is why. So the things that sort of come to the forefront of my mind is that in many places, including the United States, but certainly many other countries across the world, behavior really has changed pretty substantially since the start of the year. After we learned

that four people who are vaccinated and boosted or who have had multiple previous exposures to SARS-CoV-2, Omakron does not seem to be as individually severe as Delta, for example. Now, of course, that's not true for people who have low levels of underlying immunity where Omakron can still continue to be extremely severe. And Omakron is still a formidable virus,

Because of the relative lower severity of Omakron relative to Delta for peopl...

previous exposures, many people are changing their behavior. And so we're seeing a lot more mixing

that's leading to a lot of surges in some cases. And then I think that it may well be that the

specific sub variant of Omakron that you were infected with prior to the VA-2 surge may affect your immunity to the current surge as well. We're still sort of dealing with sort of trying to disentangle some of that as well, but the amount of Omakron circulation that you've had as well is the specific sublineages that circulated may contribute to how much bread we see of VA-2 as we go forward. So it really is, I think, a combination of behavior and an immunity to the virus itself.

I think it's worth noting that we have had introductions of VA-2 to the United States and many other countries for quite some time. And they're really only taking off now. And so what that suggests to me is that the really does have to be some behavioral element that allows VA-2 to spread, that just the presence of VA-2 is not enough to cause a major surge. So all of that is to say, I can't really

predict what's going to happen in any given location, but I think that there are reasons that

we're starting to disentangle for why we're starting to see very different experiences with VA-2 in different places. The last thing you asked about was sort of socially acceptable ways of mitigating the spread of the virus. And I think that all of the interventions that we've been thinking about for the last couple of years really hold here, it seems like they're just as effective against VA-2 as against the Oma-Cron variant, other sub-letters of Oma-Cron. So, again, masking and distancing

and moving encounters outside to the extent that we're able to seem to be among the best things that we can do. Thank you so much. Next question? Thanks for having me. So this week or last week the CDC put out reports that said that black Americans were more, were four times more likely to hospitalized than white Americans for COVID. I'm wondering if you can talk to any sort of factors that may have been behind that rate and what sort of measures can bring that ratio down.

Yeah, thanks. So, I'm not an expert in this area in sort of the divisions, the demographic divisions, and especially the racial ethnic divisions in COVID-19 severity, but it's true that over the course of the entire pandemic, black Americans in particular have really born the brunt of this virus. The one area here that I can speak to is that earlier on in the pandemic, the research group that I'm a part of did a study to try to understand part of this of why

certain communities, and we were looking in particular in New York City, why certain communities that tended to have much higher rates of hospitalization and death. So you could imagine part of it might be due to intrinsic factors of higher rates of comorbidities, which can absolutely be in play or at now that we have the development of vaccines, it could be different rates of underlying immunity or different vaccination rates, although at that time vaccines were not available. So one

thing is basically the risk of severe illness after getting infected, but the other is just the risk

of getting infected in the first place, and one of the things that we found was that one of the big drivers of the disparities that we saw in COVID-19 outcomes across geographic locations that actually map pretty closely with different racial ethnic groups was attributable to differences in infection rates. So part of it was just due to the fact that black Americans in particular were getting infected a lot more frequently in large part because they were working in occupations that

didn't allow them to protect themselves or that weren't providing them the means to get that protection. And so I would not be surprised if a lot of this difference is actually due to these sort of enduring structural issues that make it such that are that black Americans in particular

are remain at higher risk of getting infected in the first place, and with those repeated

exposures, there's sort of even the repeated exposures build up your immunity. It also puts you at greater risk of getting infected, and each time you get infected, there is some risk of that infection being severe. So I'm certain that there are probably a lot of other factors that other people who are a lot better versus in this field can speak to, but I do know that at least for certain parts of the pandemic, a large part of this disparity is down to just who's getting infected.

And so I think we can still go a long way towards reducing transmission of those population

groups. They're most vulnerable. Thank you. We do have some books. I believe we could talk to you more in depth about that. So if you'd like to send me an email, I can connect to those people. Also, thanks so much. Sure. Um, it looks like we don't have any other questions right now,

I have one that was emailed to me.

and then we can get back to anybody else who may have a question. She said, should people be waiting

on CDC guidance to get ahead of searches or uh, intimations of searches that seem to be happening now in other countries or start taking action now, like putting mass back on and giving up in door 90 dining. Uh, and is there enough sequencing going on to attribute rising rates to be

a too specifically? Right. Yeah. So I mean, I think that in my mind, the um, one of the things

that the CDC can do well is to provide a sort of a national snapshot of what's happening with the spread of SARS-CoV-2. Um, but as we were talking about before, there can be so much difference in the timing and severity of outbreaks and given locations that um, that for what an

individual person in a specific community might need to do. Um, the CDC may not always be the best

place to look for that. So I think that looking at more local surveillance platforms, um, many states and even many cities have continued to maintain their SARS-CoV-2 dashboards. Um, and my hope is that those will continue, um, so that people can get a sense of how much transmission is happening in their community. And in my mind, those are the sorts of things that will help us understand, um, whether it makes sense to, uh, to sort of start masking up again and, um,

and think about some of the other interventions that we've been talking about, um, to be clear. I mean, I, I am still masking when I go to grocery stores and when I'm in places that are crowded where, um, the absence of a mask would not really enhance my life very much. So generally having unmasked encounters with with friends and such, but um, I don't really see the value of going to the grocery store while unmasked personally. And so I've just been keeping it on,

especially as we're starting to face these rising cases of BA2, um, relative to other variants

in the Northeast. So um, so I think part of it too is just to try to understand sort of what a

person's tolerances for these kinds of, um, interventions, um, and recognizing that, uh, that, every little bit helps. Um, so sort of, that's, that's one side of things. Um, the other was, to what extent can we know how much BA2 is actually circulating. So, um, here in the U.S. we've come actually a very long way in terms of how much sequencing we're doing. Um, so we have a much better sense of the breakdown of infections by variant. Um, and so at this point, we can actually be

pretty confident that the many of the cases that we're starting to see across the U.S. and in fact, a majority of the cases that we're seeing in the Northeast and in some parts of the California, um, are attributable to BA2. So, um, BA2 is associated with the, um, some of the surges that we're seeing and some of the sort of prolongation of this tale of the Omerkhan wave that we're seeing. Um, although being associated with it is also a different questionist, whether it's

the sole cause of these increases in cases when we've already spoken to them about how behavior and previous immunity, um, can also affect some of these things in some complex ways. But certainly it is true that BA2 is, um, the fraction of cases that are caused by BA2 is increasing and we have a very good sense of that across the U.S. Thank you. Uh, next question. Uh, sorry to double dip, but I thought I'd take advantage of how I had, um, I just want to, this month is the, you know,

two year anniversary of the pandemic declaration. And I was just wondering if you could say anything in a general way about how modeling has come along or what you've learned, are you guys any better at this now, uh, you know, and how. Yeah, thanks. Um, yeah, so we've, uh, we've learned a lot for

sure about modeling over the course of the pandemic. Um, the, the single most important thing, um,

in my mind, uh, that has happened, um, for modeling during the pandemic, uh, is that we've managed to break out of a lot of pre-existing silos and to begin working very closely, um, with people in other related fields, um, but that previously we might not have seen as so related. So I'm thinking about economists and behavioral scientists and ethicists, um, all of whom we really, you know, could have in many ways should have been working with much more closely before the pandemic, um,

but now that work is a lot more integrated. And so that reflects in the models that we build because they are a lot more mindful of, um, real human behavior. Um, we've managed to understand how people behave in the context of an epidemic, much better. We've been able to account for those in our models. We've been able to account for not just the health impact, but also the economic impact

of different interventions in models. And I think all of that has been really critical from making

the models speak to the current moment. Um, so, so yeah, so I think that certainly the models have improved and that is really reflective of a broader collaboration amongst scientists and amongst

Stakeholders in the community as well, um, that have helped to make the model...

a lot more accurate, um, and ultimately a lot more relevant to this societies that they're

aiming to serve. And is it fair to say that, uh, understand that understanding of human behaviors, one of the key things to come out of, you know, our experience here that, you know, the models did look the ones I saw back in March 2020, where these sort of thinker toy, you know, are not of this, you know, give you this line, but, but that really wasn't taking account how many people by their mobile phone usage actually stop going to the mall, which sounds like the kind of thing

you're talking about now that that role was human behavior in shaping the course of the pandemic. Yes, exactly. And a lot of the models early in the pandemic were, you know, much of that simplicity was just driven by the lack of data at that point, um, where, you know, we just hadn't really

been able to observe how people would respond to the pandemic for long enough at that point. But,

but you're right, I mean, I think I think the biggest thing really, you know, to distill all of that

is, is this greater appreciation and this greater ability to think about human behavior, um, getting a much more nuanced way. Thank you very much. Yeah. All right, and does anybody have a question? Sorry, I'll just get one more in here if very radical questions. So a question that I have sort of is about this pre-built up sort of immunity that that we've talked about. And you know that you were probably likely to get some production from

from the most recent, um, across ways. But like, do we know how much a, like, a delta infection from, like, last July would protect someone now? Or is there sort of like a lot of, like, what are sort of the, the known versus unknowns in, and sort of that population level immunity? Right. Yeah. So, um, there, there are more unknowns than known for sure, um, because there's so many different, um, uh, different ways that a person could have acquired their immunity, um,

and in a lot of cases, it's not very, very well documented. Um, so if it's a decent sense of who's been vaccinated with what and when, um, but when it comes to previous infections, it's really hard to know, um, whether a person got infected when that infection occurred and what it was with, um, and so that that really does complicate things. But sort of from a broader perspective, um, one of the things that seems to be the case is that, um, repeated exposures to SARS-CoV-2, um, especially

through vaccination, but also through previous infection, um, enhance your immunity, and they enhance not only the amount of immunity that you have, but also the breadth of the immunity that you have. So your ability to identify other sorts of viruses, because one of the reasons why the booster was so important, uh, for the Omocrine wave is that, um, getting that booster, basically, even though it was exposing your immune system to something that looked like the original SARS-CoV-2 variants,

from back in March April 2020, never the last, that additional exposure sort of helped your

immune system to see other parts of the viral spike that it may not have caught on the first time around, broadens its immune response, and it allows it to better recognize something like Omocrine, even though it hasn't seen it before. So my sense is that something like a previous delta infection

would do something similar to that, um, I think that Omocrine is about as different from delta,

um, you know, delta, and Omocrine are differ pretty substantially, but nevertheless, everything that I've seen is that, um, the, the closer the better, in terms of exposure and immunity, but still very distant things can give you quite a bit of immunity, um, cross immunity, that, uh, to variants that are fairly different from one another. All of that is, is made more complicated by the fact that the immunity does also seem to wane

over time. So a delta infection, um, from last year, for example, would have boosted your immunity to Omocrine currently, um, but it's also been declining. So a delta infection, I don't know, from November of last year would probably provide you more immunity than a delta infection from earlier in the year. Um, so there are all of these different forces moving in

different directions, but I think the most important thing here is that, uh, so far from what we can

tell, um, in a immunity against SARS-CoV-2 helps your immunity against any SARS-CoV-2 that you're exposed to, um, and that immunity declines over time, and the closer the thing is that you've been exposed to that you're trying to face if next is better, like the similarity is good, but distance is not necessarily really bad. Does that help? Yes, it does. Thank you. Thanks. All right. Uh, do we have any other questions out there? Yes. I have a question about vaccines.

There have been some reports about the impressive durability of the J&J vaccine, even though it's no longer, uh, recommended by the CDC here in the United States. Do you have any sense of

Why the durability might be better for that particular vaccine, um, since you...

about the durability of protection from natural infection? Yeah. You know, I, I, I, I don't,

and this is, this would, this would be a, a question for an immunologist. Um, I've seen, I've seen

that data as well, and it does seem that there is some enhanced durability. Um, and, uh, my sense

is that it probably just has to do with the way the immune system interacts with the specific thing

that it's been exposed to. Um, certainly J&J uses a different vaccine platform, um, and, uh, because of that, maybe the immune system just gets triggered in a different way or different

arms of the immune system get triggered. Um, and, uh, there are different parts of the immune system

that lead to different durations of immunity. Um, so really when we're training our immune system against the virus by vaccination, we're really trying to train this, um, you know, I sort of see our immune system as this sort of, uh, very complex thing that has a lot of different agents that act in our, uh, you know, that act to clear viruses in a lot of different ways. Um, and some vaccines really get it, sort of exciting one part of the immune response, but they don't really do

much to a different part of the immune response and vice versa. Um, so I think it really just comes

down to that balance of the response of which parts of the immune system got triggered by the vaccine. That's a really difficult thing to tell from the outset, um, in initial vaccine trials, um, because our understanding of the immune system is still, uh, very much, um, you know, we, we know

a lot, but there's a lot left to learn. Um, but I think that's probably the best I can do,

and maybe, uh, referring you to an immuneologist would be the next thing. Thank you. Um, any other questions? Um, looks like maybe not, uh, Dr. Kisser, do you have any final thoughts for us? Um, no, I think, uh, you've sacked just about all my information today. Thanks. This concludes the March 23rd press conference.

Compare and Explore