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Study shows how immune systems are evolving along with COVID-19

A new study from OHSU shows that people infected by the COVID-19 virus may have immunity against new variants of the novel coronavirus for as long as 11 months following infection. This study looks at the body’s backup immune cells, which seem to be able to adapt to different variants of COVID-19. Bill Messer, a physician and a scientist at OHSU, joins us to explain the implications of this study.

This transcript was created by a computer and edited by a volunteer.

Geoff Norcross: From the Gert Boyle studio at OPB, this is Think Out Loud, and I’m Geoff Norcross.

In the year and a half that we’ve been living with the Coronavirus, we’ve learned a lot about how it moves around the world and what it does to our bodies. Becoming infected with the Coronavirus is never good, but new research shows that if you get the virus, you could be protected from variants, at least for a while. Bill Messer is a physician and scientist, and he specializes in viral infectious diseases at OHSU. He was a senior author on this new study, and he joins us now.

Dr. Messer, good to have you.

Bill Messer: Good afternoon.

Norcross: So the star of this story is something called the “memory B cell”. Can you explain what that is first, please?

Messer: Yeah, so I think a sports analogy might be the most appropriate way to describe how these memory B cells play a role in our immune response. In short, we know from a lot of media coverage that both COVID 19 disease and vaccination illicit antibodies that recognize the viruses. These antibodies arise in our body’s lymph nodes, which are the things that we often feel getting swollen in our necks when we get strep throat. In those lymph nodes, B cells, which are antibody secreting cells (or future antibody secreting cells) move in and out of these lymph nodes, and they undergo really a competent, competitive selection, based on how well these B cells stick to the pathogen that’s in the lymph node. And the B cells that stick the very best to the pathogen gets selected by our immune system to become antibody secreting cells, and they release the antibodies that we measure in our blood.

The second tier of B cells, that stick not quite as well as the first tier, get sent back into circulation as a reserve population of immune cells that are prepared to be recruited back to a repeat infection and tested again against the pathogen. And if they bind well to the pathogen that looks a little bit like, or maybe a lot like the one that they saw before, they’ll expand and start to secrete antibodies.

So the B cells are a second line of defense in our blood against repeat infection with pathogens. They arise the first time our body sees the pathogens but don’t make the cut to express antibodies. The second time we’re infected with a very similar pathogen like a variant of concern, they get recruited and again get tested against that pathogen. And if they have good activity against that new pathogen, they get selected to secrete antibodies.

Norcross: So we’ve been told all along that if we get infected with SARS-CoV-2, we do have some protection against getting it again. But we get protection against variants too, and that’s the new thing here, right?

Messer: Yeah, so one of the reasons that variants of concern are called “variants of concern” is that early in the pandemic, following infection, and then really following the rollout of vaccines, laboratories started testing antibodies from vaccine-es and people who had had COVID-19 against the variants. And one of the worrisome findings of that was that the variants seemed to have a degree of escape from the antibodies in our blood, meaning that these variants perhaps had a better chance of infecting us and making us sick if they reinfected us, even if we had COVID once or have been vaccinated once.

But those antibody studies don’t really tell a complete story. They don’t tell us what’s sitting behind the antibodies as a second line of deflection. And so, as time has passed and laboratories have had the opportunity to then examine the B cells, these memory cells, and the kind of antibodies that they secrete, what we find is that this second line of defense is actually able to secrete antibodies that do a very good job at recognizing these variants of concern, really as good as the antibodies from B cells that recognize the original variants. And so this is an additional piece of information, an additional layer of defense that we now know that our bodies have against repeat infection with SARS-CoV-2.

Norcross: To keep your sports analogy going, yay for a deep bench, right?

Messer: Right, that’s exactly right, that’s what this amounts to is a deep bench for our immune system. And I should add that this isn’t really a surprise. We know that the immune system both generates very specific responses against pathogens and that it also generates what I would call a diverse bench. And that diversity exists precisely because our immune system has learned through evolution that pathogens change, and we have to be prepared. Our immune system has to be prepared to change along with the pathogens.

And so that’s really what this deep bench is created for, is to have a reserve that can go up against the evolving pathogen toe-to-toe, or in a really fair competition, to see whether or not we can eliminate the new variant. And while it’s expected, it’s really reassuring to go to the laboratory and demonstrate that the cells are there and have this capacity.

Norcross: Of course we’re hearing about variants that are frightening in their infectiousness and even how sick they can make us. And of course there are variants that haven’t arrived yet. So how confident are you that this immune response that you described will happen, even for variants that have not appeared yet?

Messer: Right, so you raise a couple of really important points. The first is, variants of concern aren’t just variants of concern because of the antibiotics story, they’re variants of concern because they have increased transmissibility, and some of them may make us sicker. Our immune system is still prepared to respond to them immunologically, but these variants also have other features that make them worrisome for other reasons, like it’s easier to spread from person to person.

The speculative answer is that our immune system probably is still reasonably well poised to deal with the ongoing evolution of SARS-CoV-2 in a fairly appropriate manner. The more circumscribed or careful answer is that only time will tell. We really have to follow the evolution of the viruses over time to see at what pace the virus is able to move, either ahead of or really along with our immune response to it. And the honest answer is we don’t know right now. We, of course, always want to know right now. There is a desire for that kind of information. But time will tell.

There are a couple of important variables that I would point out at this point, which is the degree to which a virus can evolve like SARS-CoV-2, is really dependent on the number of people that it infects, and the number of times that it is transmitted from one person to another. The fewer number of infections, the fewer number of transmissions that take place, the fewer opportunities the virus has to evolve. Our best defense as a population, then, against the evolution of the virus remains getting vaccinated, to limit the number of opportunities for the virus to spread and infect another person.

Norcross: So still get the shots.

Messer: Still get the shots.

Norcross: If you’re just tuning in, we’re talking about new research that shows people who were infected with the Coronavirus might have an extra level of protection against variants, at least for a time. But you should still get the shot. We’re talking with Dr. Bill Messer, infectious diseases specialist at OHSU.

Dr. Messer, does this research mean that people who have been vaccinated won’t need a booster shot in the future?

Messer: Well, I don’t think that I would say that right now. It does mean that people who have had COVID-19 once do have immunity that may have a lot of features similar to vaccination. But we know a couple of things about getting vaccinated after you’ve had COVID-19. One of the groups that I work with at OHSU looked at the antibody responses of people who had had COVID-19 and then got vaccinated. And what we saw was a really massive jump in antibody titers in these people who had had COVID-19 and then were vaccinated. When I say “antibody titers,” I mean levels of antibodies in their blood. And that strikes us as really great insurance, if you’ve had COVID-19 once, you really don’t want to get it again. The best insurance that you have against not getting it again is to still get vaccinated.

We know that people who have just had COVID 19 have highly variable different levels of antibodies in their blood. But if they all get vaccinated, the vaccine tends to pull everybody up to a high level of antibody titers, irrespective of whether they were high or low antibody levels when they just had the disease. So there’s a real advantage to getting the vaccine in that context.

We did look at a couple of vaccine-es in our study, and we saw a similar effect, with an increase in the number of memory B cells in people who had had COVID-19 and then were vaccinated, as well as an increase of antibody levels which we had seen before. Now I would not call two people representative, but they tell a story that is certainly consistent with what we would expect, which is you just get even better immunity if you get the vaccine on top of your prior infection.

Norcross: I wonder what all this tells you about our bodies, the power and the complexity of the human immune system?

Messer: Yeah. So it’s, from my perspective, as a virologist and an infectious disease specialist, it’s a really timely reminder of how well adapted our body is, and our immune system is, to anticipating and adjusting to what would otherwise be unrecognized threats. And certainly that’s why SARS-CoV-2 swept through the global population because it was, to our immune system, completely new. But as long as you get it and you can get back on your feet, your immune system really takes on the task of adapting to this new pathogen in our midst. And I find it reassuring.

I think for a while we didn’t really know that this was the case. For a while, there was so much hope pinned on vaccines that we needed a reminder that these vaccines really work well because we actually have an immune system that is incredibly well adapted to work well, just evolutionarily, and that the vaccines really worked because they leverage that adaptation. And when you put a vaccine on top of a prior infection, our immune system really is taught extremely well how to recognize this pathogen and respond to it.

Norcross: Ok, well, the virus is always evolving, and so is the research. So I’m wondering what your research is going to focus on next.

Messer: I guess there are a couple of things that are worth pointing out. We are interested in studying in detail what happens with these memory B cells in people who are just vaccinated, bearing in mind that these vaccines were just rolled out literally six months ago. And one of the important findings that we haven’t mentioned in our conversations so far is that we found these memory B cells as far out as 11 months after the infection. If the memory B cells are there at 11 months out, they’re really likely to be around for a long time. Can we say the life of the person? No, but something on that order.

We’d like to know if the same is true for vaccine-es, but we need more time to pass. So we’re enrolling people who have been vaccinated and following blood samples in them over time, but enough time hasn’t passed yet to really ask the question in the same way. But that, I think, is our leading question of interest, how the vaccines imitate this natural infection process from the perspective of our immune system. Do the vaccines similarly stimulate these memory B cells to be diverse in the same manner? We hope that they do, and we have reason to believe that they should, but we don’t have enough information yet.

Norcross: Dr. Messer, thank you for updating us on this. It’s fascinating.

Messer: Yeah, well, you’re welcome, and thank you very much for inviting us to be on the show.

If you’d like to comment on any of the topics in this show, or suggest a topic of your own, please get in touch with us on Facebook or Twitter, send an email to thinkoutloud@opb.org, or you can leave a voicemail for us at 503-293-1983. The call-in phone number during the noon hour is 888-665-5865.

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