What the immune response to the coronavirus says about the prospects for a vaccine

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With a number vaccine candidates against the corona virus sharing promising results in clinical trials and a growing number of studies elving into our mean response to infection. The spotlight has turned once again. On the body's defense mechanisms. I think two questions that really relate to the ability of the vaccine to protect us and our ability to fight off a second infection and so that is the quality of the immune response and the duration of the immune response this week. I'm joined by professor. Eleanor riley from the university of edinburgh to dove into these questions and more. I'm nichole davis. Welcome to science. Weekly ellena you came onto the podcast in july and talk to us about immunity and covid nineteen specifically the relationship between antibodies and immunity. So let's start with a recap on the major players in the immune system that are of interest when it comes to an immune response and potentially immunity so antibodies are protein molecules that are produced by immune cells kobe cells and these cells live in our spleen and narrow and they secrete antibodies off. They've been exposed to a foreign organism such as virus. There are two types of cells that produce. Antibodies on short-lived cells that produce. Antibodies for a few weeks national to the first line response and then some of those cells transition into lonely cells that goto a bone marrow and can produce antibodies for months years. Possibly even to case and then on top of antibodies. have that can kill virus. Infected host cells t cells the two types of t cells one of which we think of such of the conductor of the orchestra of the immune system and these kotei health cells and they very much help the b. cells to make antibodies produce. Growth factors may direct the direction in which the be cells developed and they will still give them signals to turn into cells and then there are the cdte cells and they actively kill virus infected cells and then Antibodies can also bind to these specific cells and help them to kill cells so they recognize little bits of virus on the infected cell bind to the infected so and kill it and then there are cells which are less specific cells that we call macrophages are neutral fills and they just recognized that. Something's not quite right with the cell. They don't necessarily recognize the infected with the virus and they kill it actually or bits of the immune system work together a little bit like you need a whole orchestra to make a good tune when you need all of these cells working together to make a good news arms. And i know you said in july that at that point it was too early to tell how quickly people were losing their antibodies. And we've got to remember here that it's a relatively new virus. What's the latest research saying that seems to have been some movement on that now. What we're seeing is if you all the data together. There's an early peek in the antibodies wants. Lots and lots of antibodies are produced to mop up all virus. That's in your body and then as that virus goes away the antibodies start to decline a little bit. Because you don't need them any antibodies anymore and they settle into a of steady class. O of antibody production. And that's very typical. This kind of two phase response the only peak lots of antibodies followed by sort of standing level of antibodies. That nick for a long time. That's very typical of an antibody response and it sort of relates to the short lived long lived cells. You have lots of short-lived cells making lots of antibody that off and then the long lived cells who that fewer in numba keep on producing. Antibodies for much longer so yes. Let's talk about these long-lived b. cells in the no said the t. cells. What is research telling us about what happens to them and how. How long do they hang around for. So we don't have much data on those are actually quite difficult to look at in humans. They tend to live in the bone marrow for example not very accessible and so we tend to rely on mathematical modeling of the change in the dynamics of the antibody concentration to predict what's going to happen even though we haven't actually been able to see it because it hasn't gone on long enough so the moment the infants is that we have suggests that things are probably okay these cells behaving as we expect them to the was one pay published early on suggesting may be a little bit of a fault with the production of these long midsouth. But i'm not sure that that's been replicated in other studies. I think i saw a preprinted study. That hasn't been peer reviewed yet. Which jested that these visas and t so's lost for at least six months is that. What are the problems here in terms of measuring this so we only have six months data at the moment and the virus really hasn't been around that long so what we can say the moment. Is that the cells assisting for as long as we are able to measure them at the moment obviously in six months or another twelve months time. We'll be able to go back to those people and say have they still got those cells. Yes or no. But in the meantime just looking at the change in the dynamics of the response and mapping it onto what we know the other viruses. My prediction is that these that there will be some long lift immunity to this virus. He said there might be some long term protection. How long term are we talking here. I mean i've seen a lot of people saying well current viruses such as that of course common code some codes of course by coronavirus is of course the protection only lasts for say a year or so. Do we think that our protection against the corona virus that causes covid nineteen mike baxter timeframe or or could it be longer. I think it's very difficult to say at the moment. Say all of the data. We have suggests that these antibody responses are going to be at least as long lived as response of corona viruses. And possibly i might think even probably going to last longer your immune response tends to be proportional to the level of threat that you face so the common cold corona viruses really only colonize our upper respiratory tract so on nose throat and so the virus doesn't go very deep into apology and we make rather grief that effective noon response nose and throat that controls it this coq nineteen causing virus goes much deeper into our bodies it goes down into our lungs into bronchial and therefore the immune response tends to be stronger and they struggle we call systemic immune responses do tend to last longer because they are recognizing that there is a more serious threat that has to be dealt with. Do we know if factors like ethnicity gender age factor in the scale of the immune response. She said stronger. Immune response to your first. Infection is is more likely to me. You have great protection against the second infection. Those factors correlated at all. There's very little day to so far on ethnic differences in the immune response the data. That's coming after the vaccine trials suggests that there aren't any major differences in at between ethnic groups in terms of whether the vaccine protects them will not but we haven't yet seen lab data on their antibody responses with at t cell responses. There is a lot of genetic variation in the immune response. People be aware that some people unfortunately have very severe genetically determined immunodeficiencies. That's just the tip of the iceberg of genetic variation in the immune response and some of those differences do have geographical and ethnic components to that certain genes that either make good or bad immune response on more common or less common in groups countries. But we don't yet know if any of that is going to influence really the totality of their immune responses. We just don't have any evidence much by age. It feels like ages is. It's very important given that the older you are the more risque from caveat nineteen so there are two components to that one is whether you are able to make an immune response again's a virus. You've never seen before and there is. I think really quite good evidence that you ability to make a completely new immune response does decline as you get older. The other component is that a lot of the disease we say in coke nineteen excessive inflammation. And there's also evidence that we get older with less good controlling inflammation so it's a little bit of a double whammy as we get older way are less able to make an immune response to a new virus such as the covid nineteen virus and if we then get the viral infection where less good at controlling the inflammation that it causes a so we know there are several different vaccines. Which looking very promising. You have the rene vaccines at you have vaccines which used a chimp. Virus to bring genetic material from the corona virus into cells. The question is is the immune response that generated the same as it would have been to a natural infection and do the t. cells and so on hang around in the same way. The vaccine is just a tiny component of viruses this spike protein which is on the surface of the virus and so if you vaccinated with spike protein. You make antibodies in tesol responses just to that protein. If you get the virus itself then you get many many more pro teams that you're exposed to a new may make antibodies to some of those. So you responded more limited but you might also say that your response is more focused because it's actually antibodies to spike coaching a really important for neutralizing the virus so the vaccine in juices a narrow immune response but one would hope it would also be focused on therefore stronger on the base the matter and would it be expected that this will provoke a stronger. Immune response natural infection. I've heard some people say that actually vaccine can producer a strong response it coun- if they initial infection is quite mild say with virus like sauce covy to which induces very mild infections in some people i would expect the vaccine to tobacco to jason mewes which is much stronger than you would get after nascent dramatic or mild infection. People get serious dose of coca to make a very strong immune response. And i doubt if the vaccine it doesn't need to be any strong national adopt if it is when it comes to and viruses the coups common code. It's been some concern that these viruses somehow elude the memory b cells. and so. that's why even though we have thousand cells to to the common cold viruses. We will often get reinfected with them. I wonder if they're those same concerns about the coronavirus behind covid nineteen so there is a little basic data. There's one paper that suggests that the sauce kofi to virus that causes covid nineteen disables particular pathway in the b. cell response leading to a poor long term memory response but these experiments done in the lab in a in a in a petrie dish. And i think it's too early to know if that's really what happens in humans so i think we do need to be a little bit cautious and we need to be aware that it might happen. Good news is that the proteins that are believed to cause that problem are not present in the vaccine so even if it's a problem in natural infection it shouldn't be a problem with a vaccine

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