 Hello and welcome to NewsClick. Today we have with us Dr. Satyajit Rat and we will discuss what we have been doing right through COVID-19 and what things look like today. We're going to discuss WHO's announcement that antibodies are there for at least three months. Now a lot of people have interpreted this to mean that after three months maybe the antibodies are not there in the body and therefore infections can reoccur and there have been some isolated cases of where people have talked about reinfections. So Satyajit, antibodies will not be there, it's not what WHO has said. So should you clarify what they really mean and what are the results they're talking about and what does it mean for vaccine-induced immunity as well? So unlike many other times on this one I'm going to be a little more optimistic sounding than than usual. So here is what- A rare change for you, right? Thank you for appreciating it. So here's what happens. The virus comes in and as we've discussed there isn't one thing called immunity that is triggered. There's a whole number of interlinked but separate responses of the body that are activated in response to the virus reinfection. One of those is an antibody response. Now the data that have accumulated, the evidence that has accumulated over recent months which is what the WHO note is referring to have generally begun to show the following. Number one, they are showing that most people who are infected, the overwhelming majority, more than 90% of people who are infected with SARS-CoV-2 make antibody responses. Secondly, the overwhelming majority of these people who have made antibody responses stay antibody positive meaning their antibodies persist in their bodies for at least months. This is what WHO is saying. This is underlined by WHO because there were initial worries and fears that even in the first three months there may be substantial fractions of people, percentages of people who will go from being and having antibody to not having antibody. The general indication seemed to be that that's not a large fraction of people. What happens after three months is not that everybody's antibody just shuts off. What happens is we begin to get a lot of variation. In some people it will go, antibodies will persist, in some people they will not, in some people they will decline by six months, nine months, whatever. All of this is unsurprising to people who have been studying coronavirus immunity. Remember, this is not coronavirus. This is just one coronavirus. There is a range of its cousin, coronavirus, is that we are familiar with. The fact that antibodies against any coronavirus infection don't last for very long times uniformly in everybody is not surprising to people who study coronavirus infections and immunity, other coronavirus infections and immunity. They are common cold. The common cold coronavirus. We have many situations where the same common cold coronavirus causes an infection in the same person twice in a year because the antibodies have disappeared. Now, so this is the background of the WHO note. It is not to be interpreted as everybody's antibody is disappearing at the end of three months. It is to be interpreted as for three months, most people will retain antibodies. After that, it will vary from person to person, how long the antibodies stay. So that's one point. A second point that's useful to remember is that, as I said, antibodies are not the only immune response against the virus. There are, there is another category of immune response called T-cells. These are the two cells who come and actually kill the infected cells. So, these are much harder to test for. So there is even less evidence about them. But that evidence says that people who have become antibody negative have still been shown to have T-cell responses. Now, neither of these, neither the antibodies that have been tested nor the T-cells that have been tested are proven to be protective. Okay. They're there, but it doesn't mean they're causing what is called protective immunity. Exactly. On the other hand, clearly we do have situations where even if I lose antibodies, that doesn't mean I have lost all triggered immunity. I still have T-cells. So if they work to protect, then I have some protection. So it's quite possible that there is a sort of messy situation where we don't know how much of the immunity is protective. We know some of the immunity is short-lasting, but some of it is likely to last longer. And each one of us is likely to have some variable combination of these things. In this, also there are what are called B-cells, which are supposed to be memory of the infections and trigger then the protective immune response. So absolutely, right? And nobody has tested those either. In fact, even though T-cells have been tested, memory B-cells haven't been tested at all except for one set of evidence that I've seen. So we don't know. But the bottom line is, and here's where I'm going to sound optimistic as a guess. My guess is that because of this, most people who have the infection once are likely, even if they are reinfected, to have milder illness. Coming to the question of reinfections, there are also some examples you've been talked about where reinfections is said to have occurred. Now, in the very large number of cases which are there in the world today, and we have the total number is really very large, number of reinfections of this kind reported that really you can count with the fingers of our hands. So effectively, it seems a rare occurrence. But could you explain that the chances of reinfection or at least within five, six months is why it is so rare and this is likely to be only an outlier? So this is going to be a very unsatisfactory answer because it's essentially going to say that in none of the cases of reinfection that have been anecdotally described, do we actually know that it's reinfection? And here's why we don't know. How do we know that there's infection? Because you test the fluid and you find virus viral irony. Let's not even worry about whether that's whole infectious virus or not. You find viral irony. You test 15 days later, you find that you test 15 days later, you don't find it. Then a month later, you test, you find. Now, is this reinfection or is it just that one of these tests was just technically not right and missed finding the viral irony? Most of the reinfection stories we hear fall in this category. And therefore, in most of them, it's at the moment impossible to distinguish between the possibility that it's an infection and the possibility that these people are that very small and interesting and important minority who clear virus very, very, very, very, very, very slow. The cases have been up to nine months that the virus stays in the water. So therefore, it's more likely to be that kind of an outlier than a reinfection outlier. It's certainly as likely to be that as this. So both hypotheses stay and it's difficult to say which is which. And since we've been saying that this is as much about the substance of science as about the politics of science in society, let me take a moment to explain how we would differentiate between the possibility that this is simply a continuing infection versus that it's a reinfection. So if you had the entire viral RNA sequenced, then between two samples, if there was sequence continuity, it's the same virus. But if the second sample is clearly different in sequence from the first sample, because you were quieted from somebody else in whom the virus has changed in the meanwhile differently, then you have true reinfection. So the way to ask the question to people who talk about reinfection is, are there viral sequencing data from before the negative test and after the negative? Much more difficult to. Much more difficult. Coming to the other issue, which of course is hanging in the background of all this, is the efficacy of the vaccine. That how long will it be assuming the vaccine is successful and we have enough number of cases for us at least to sound optimistic at this stage? Assuming one or two or more of the vaccines will become effective. The question remains for how long? Now, does it mean that after three months, they won't be effective? That after six months, they won't be effective? Or what is the likelihood using your crystal ball as an immune system expert? What would be the crystal ball that you would consult and what would it say? So Praveen, I am enjoying myself today, because this is my second one of sounding optimistic. And after a very long time of not sounding optimistic. Not our viewers, that this is not an usual occurrence, that we get him optimistic twice in a show. I mean, one itself is a big thing. Go ahead, it's funny for the interruption. So here's the issue. When you have a virus infection, we have an immune response absolutely. But the virus has gotten selected in a sort of mutual evolution, where the virus that is infecting us successfully has figured out at least a little bit of how to deal with immunity. Simply because a virus strain that cannot deal well with immunity will get propagated poorly. So a viral variant that deals somehow with immunity will be preferentially propagated and in proper Darwinian evolution, that's the strain that will come to dominate. Now, if that's the case, then the likelihood is that SARS-CoV-2 has ways of fiddling with the immune response. But SARS-CoV-2 is not what we are putting into the vaccine. Remember, we've been discussing a variety of vaccine design technologies in all of which we take one protein of SARS-CoV-2 and simply get the body to see the protein and to make an immune response against it. We don't put a live SARS-CoV-2 virus into the body as a vaccine. So none of the tricks that SARS-CoV-2 is using to fiddle with the immune response are included in the vaccine. So the fact that SARS-CoV-2 infection may lead to short-lived immunity is not telling us that the vaccines that we are designing will also necessarily lead to short-lived immunity. Now, the vaccine technologies may have their own limitations because of which some anti-vaccine responses will last less long than other anti-vaccine responses. But the fact that SARS-CoV-2 antibody responses may not be long-lived is no pessimistic guarantee that vaccine responses are going to be short-lived. For all we know, vaccine responses will be respectively linked. That optimistic point made, let me add a pessimistic footnote, which is that my expectation is that the first-generation vaccines which will come up as we've been discussing by the end of this year, my guess is that they will not be great vaccines. They will work. They will be useful. But they will not provide 100% protection, but they'll provide some protection. They'll not be very long-lived, but there'll be reason. But that's not going to be because SARS-CoV-2 is short-lived immunity. So to develop more effective vaccines, perhaps we need to see five, ten vaccines operating, then find one of the good points of them, and then come to what? And then tweak them and come to a second generation. So the second-generation vaccines are likely to give us a better handle on the epidemic, but the first generation should really act to promote what is called the herd immunity. There are also some arguments that the herd immunity may be required, maybe only 20%, 30%, 40%, is there any basis to this? Or these are all seat of the pants guess what the people are doing. So I'm losing count of how many times I'm saying this. Herd immunity is not a strategy. It's not a tactic. It's an outcome. When we reach herd immunity, we will discover that we have reached herd immunity by looking back and saying, oh, the outbreaks are subsiding, we seem to have reached herd immunity. Let us now examine what the correlates of herd immunity are. We're not going to be able to plan for herd immunity like that. So let's not even be discussing herd immunity as though we can decide on a number and aim for it. That's oversimplifying our tactics and strategy. I think here we should sort of step in a little and talk about that. This is something that I have also looked at because mathematically the propagation is human to human contact and it is not a uniform issue that this percentage of this population, you get a herd immunity. It's really how human beings connect and they connect obviously differently. And therefore, as you say, the statistical fact that you've got it at 25, 30, 40 or 70% is merely the artifact of the propagation of human being, human interactions as much as disease interactions. So effectively, therefore, there is no mathematics which can predict this at any stage. That kind of mathematics maybe once we have quantum computers, we might be in a better position to do it. But our current computational methods do not lead to the solution of this kind of problems. And whoever has tried it, even for small population size, say in a town, even that, the predictions have not worked very well. So I think I get what you're saying. Even this R0, the preoccupation of R0, etc., all these are statistical artifacts of historical data rather than prediction looking forward. Do I sort of summarize what you have sent? Absolutely. And so let me add a non-mathematical footnote. Take an example of one of the parameters that is commonly being discussed in the context of herd immunity, which is zero prevalence. Yeah. Estimates of what percentage of people have in the past few months been exposed to the virus. You do this by looking for antivirus antibodies. And the numbers are widely varied. But here's, and let me underline the problem connecting to what you were saying, non-mathematically. Let me give the example of Pune. There was a structured zero survey done. A couple of weeks back, results were announced this past few days. There are neighborhoods where 60% people have been previously exposed to the virus. There are neighborhoods where only 30% have been exposed. Both these neighborhoods are in Pune city. Am I going to calculate the percentage exposure of Pune as the average of these? That doesn't mean anything. So let me make my favorite point about the virus does not understand administrative sociopolitical boundaries. The virus works in populations that connect to each other, that breathe on each other, that talk to each other. And because none of us is hermetically sealed off from anybody else, no group that has achieved so-called herd immunity will have stably achieved herd immunity if it's surrounding communities have not achieved herd immunity. I mean, it's a very interesting proposition statistically can be average. It is what is called a statistician delight that if your fringe, if your head is in the fringe and your feet are on the oven, then your body temperature on the average is quite comfortable. So it's the same problem that you average widely dissimilar figures. And after the average, you say, you know, hey, we've got 30% and the virus seems to have stopped transmitting, which could be due to a whole range of different reasons. And then you say, you know, that means 30% gives us herd immunity, which is nonsense. And as you said, that in any population, there are at least then the 30% antibody population, you can still have 70% of the people who can have infections and it can start all over again. Yes. With this, I think we have come to the end of our discussion on rather optimistic notes given by Dr. Rath that we have possibilities of a vaccine, which will be much longer lasting than what the three month figure WHO has given. And we can hope to see improvements in the vaccine over time. And therefore, the so-called herd immunity that people have been talking about may be reached, but with vaccines, not the way people thought that by infecting each other. Thank you, Satyajit, for being with us, spending this time to explain to our viewers what all of this gobbledygook, quite often it is really gobbledygook means. And even doctors seem to be confused by the immune system. And therefore, we need your shall we say deciphering, cracking the code to so to say, over all of this means. This is all the time we have news click today. Do keep watching news click and also visit our website.