Fewer Coronavirus Antibodies May Not Mean Less Immunity

IRA FLATOW: This is Science Friday. I’m Ira Flatow. Chances are your news feed is still filled with ever-changing stories related to the COVID-19 pandemic. So what should you be paying attention to?

Well, it’s time to fact-check my feed, with Dr. Angela Rasmussen, a virologist at the Mailman School of Public Health at Columbia University, joining me again to help fact-check your feed. Thanks for joining us today, Angela.

ANGELA RASMUSSEN: Always a pleasure to be here, Ira.

IRA FLATOW: Let’s begin with something that’s always being asked [INAUDIBLE]. That is, what is the state of vaccine developments? There have been some really-interesting initial reports this week. Hopeful news?

ANGELA RASMUSSEN: Definitely hopeful news. It’s still preliminary news, but it’s very promising. So on Monday, a study was released of the phase 1, 2, trial results from the Oxford vaccine. And last week trial results were released from the phase 1 trial of the Moderna vaccine. And both vaccines appeared to induce robust immune responses.

Both of them also met acceptable safety profiles. Neither of these actually show that the vaccine works, or that it’s effective at protecting people from either being infected or protecting them from severe disease. But it’s a very promising start. So it’s great news that we can move forward with the phase-3 clinical trials that will actually show that these vaccines are effective, as well as safe.

IRA FLATOW: When you say vaccines, do you expect that– if there are successful ones– we may have competing, or if not competing, just different vaccination choices?

ANGELA RASMUSSEN: I think that that is definitely a possibility. So there are over 100 different candidates in the vaccine-development pipeline right now. These are just two of them, that are furthest along in the process. And this process has been greatly accelerated, to say the least, compared to the clip that vaccine-development a normally precedes at.

So there’s a very good chance that the vaccines that are furthest along may not be the best vaccines in terms of their efficacy. For example, these vaccines may not protect against being infected, but they may protect against severe disease– which is still a huge public-health benefit, and would be tremendously important in terms of stopping the trajectory of this pandemic. But that said, for longer-term immunity, we may want a vaccine that is completely protective against even being infected.

So I think it’s a great idea. Also, in terms of availability, having more than one vaccine that is being manufactured, potentially, by a different process means that there might be more doses available for more people. And it’s really critical that we get a critical mass of people vaccinated.

So having multiple options is really a good thing. I don’t think it’s so much a vaccine race, in that there’s going to be one winner. I think there may well be multiple winners of this vaccine race.

IRA FLATOW: Speaking of vaccines, there have been some troubling stories that have said that the antibodies from a COVID infection may not stay around for very long. What’s the science on that one?

ANGELA RASMUSSEN: So we have seen a correlation with disease severity and antibody titers. And people who have milder or asymptomatic infections with SARS coronavirus 2 tend to have lower antibody titers in general. And then these appear in some people to decrease over time.

I think people have really misunderstood this. Because this is really the way the immune system works, is that after you become infected there’s a peak at which you have higher antibody titers. And then they normally naturally decrease. Not having detectable antibody titers doesn’t mean that you don’t have immune protection.

So antibodies are made by a type of immune cell called B cells. And when you become infected with the virus, you develop memory B cells. These B cells are secreting amounts of antibody over a period of time. And that does decrease after a while, but those cells are still there. And presumably, if you’re exposed to the virus again, they will rapidly become reactivated and start making more antibody.

So we don’t have any evidence that suggests that this type of immunity doesn’t last at all. We also have some more evidence that T cells are probably very important for controlling infection. And people do have memory T cells that are generated from infection. As several studies have now shown, people also have T cells– memory T cells– from other coronavirus infections. So the common-cold coronaviruses that infect people, that can cross-react, potentially, with SARS coronavirus 2.

So there’s more than one type of immunity. There is there is more going on in the immune system besides just neutralizing antibody titers. And so far this evidence, while it’s something to watch– and we need to understand protective immunity better for this virus anyways– it doesn’t necessarily mean that you are less immune, or that you don’t have any immune protection against reinfection.

There’s also no evidence that people are being reinfected. At least there’s nothing documented that shows that people have been reinfected, which does suggest that most people who get SARS coronavirus 2 infection probably have some level of protective immunity.

IRA FLATOW: Yeah, that was my next question. Because my feed has been full of ideas of, can you get reinfected? Stories of people can can, cannot. And you’re saying at this point there’s no evidence that people can get reinvented.

ANGELA RASMUSSEN: Yeah. So this is something that has been, I think, very confusing. And it’s something we really don’t know much about. But there has been some work done to actually determine if people are reinfected.

So we have already seen since, really since February, there have been reports of people who test negative. They recover from SARS coronavirus 2, or COVID- 19, and then they test positive again. And the South Korean CDC actually investigated this. They took almost 300 people who had been negative after recovering– confirmed cases that tested positive again.

And they did two things. First they, did an epidemiological study, where they talked to all the people that they’d been around since recovering, and determined that there were no new cases of transmission that were linked to these people who then tested positive again– suggesting that they’re actually not transmitting the virus to anybody.

They also did a virology study, in which they looked at whether or not these people were actually shedding infectious virus. And they found in 0 cases out of, I think, 285 that nobody had infectious virus. So that likely suggests that people who test positive again, those tests are detecting residual virus that hasn’t yet been cleared– but virus that’s not infectious, importantly.

So we don’t really have any documented evidence of reinfection in those cases. There have been reports of people who have recurrent symptoms, or who have persistent symptoms that don’t go away. And we’re just starting to understand why that is. There could be cases– and we’ve seen this for other viruses– notably Ebola virus. We discovered during the West African outbreak that in some people Ebola virus can persist in certain tissues– so-called neurologically privileged sites, where they can essentially hide-out from the immune system.

So we don’t know if that’s going on with this virus. And it’s a possibility that we need to look into. It’s also possible that people– the so-called long haulers, who have recurrent or persistent symptoms, are actually suffering from inflammatory conditions that were triggered by the initial infection. But that doesn’t necessarily mean that they’ve become reinfected, or that their infection has reactivated, or has reemerged, essentially, in those people. We just really need to know a lot more about it.

IRA FLATOW: A lot of discussion these weeks about going back to school. And one of the talking points you often see from people in favor of schools opening for in-person instruction is that, quote, “kids don’t get it,” or, “kids don’t pass it as much as others.” What do we know about kids and COVID?

ANGELA RASMUSSEN: Well, we know that kids certainly get it. Not only do kids get it, but they can have the same viral loads as adults– including adults in the highest-risk group– so adults 80 and over. So kids are definitely not resistant to infection. They are susceptible to infection, and they can be infected.

The data is a little more conflicting about how frequently children transmit the virus to others. However, there have been documented cases of people contracting the virus from infected children in their household. So kids can transmit it.

We also know that kids do have– at least symptomatic children– have infectious virus that they’re shedding in their nasal secretions. So there is certainly the possibility for children to transmit it. We definitely need to have more information about whether or not they transmit it as readily as adults do, and what the basis for that is.

But certainly, children are not immune to this virus. They are not resistant to this virus, and they can be infected with it. And in some cases, they can actually become very sick and die from contracting this virus.

IRA FLATOW: Also, in my feed, there’s a lot of conversation about the definition of aerosol– the virus is airborne. What’s the difference? What does the research show?

ANGELA RASMUSSEN: So this has been incredibly confusing, even for subject-matter experts. Oftentimes when virologists say aerosol or droplet, they might mean something different from what an infection preventionist might mean, or what somebody who studies fluid aerodynamics or engineering might mean. But what we do know is that short-range, airborne transmission of this virus does occur. And we’ve known that for a while.

So there have been several studies showing situations in which the virus probably was transmitted by inhalation of particles. Now, what size those particles are– whether they’re floating around, or whether they’re ballistic– meaning that they are propelled from the person who’s dispersing them into the environment– that remains sort of an open question.

But there’s definitely situations. There is a restaurant in Guangzhou, China in which virus was probably spread downwind from an air conditioner– an infected person sitting in front of that air conditioner. There was a call center in South Korea that was a crowded office environment, in which people in the same office became infected, but people on the rest of the floor did not. And there was the Skagit Valley Choir, in which people were practicing physical distancing, but they were singing– and presumably propelling a lot of droplets or aerosol particles out into the environment– and a number of people became infected.

That shows us that short-range airborne transmission of the virus is something that occurs, and it’s more likely to occur in enclosed or crowded indoor spaces. The good news is that long-range aerosol transmission probably does not occur, or at least does not occur frequently. And an example of this would be something like measles, where if you are secreting infectious particles, they can get into the HVAC system or the air ducts and be transmitted over long distances through the air.

It doesn’t appear that this virus is transmitted in that way. We have no epidemiological evidence suggesting that people in one room are capable of producing droplets that infect people in another room, that’s connected by the same HVAC system. So the good news there is that we can essentially take the same precautions that people have been recommending since the spring. And that is to avoid enclosed spaces, to avoid crowds.

Practice physical distancing, wear a mask, and practice good hand hygiene. All of those things should still be effective at reducing transmission risk.

IRA FLATOW: Just a quick note, that I’m Ira Flatow. And this is Science Friday, from WNYC Studios.

There have been stories that there are multiple strains of the virus circulating, and maybe that’s why it affects people differently. What’s the science about that?

ANGELA RASMUSSEN: So this comes from a pretty-sensationalistic media coverage of a paper that was recently published, that showed that the dominant variant of the virus circulating in the United States has a mutation in the spike protein. That’s called D614G.

And all this means is that there was a mutation in the virus genome that caused an aspartic acid in the spike protein to be replaced with a glycine. This is not in the receptor-binding domain of spike, so this has no effect on how the virus gets into cells, we don’t think. But nonetheless, the authors of this paper suggested that this mutation is making the virus more transmissible.

And since then, a few studies have come out in cell culture suggesting that this mutation confers a benefit for infectivity– meaning that in cell culture viruses with G instead of D, or glycine instead of aspartic acid, are more capable of infecting cells in that culture dish.

What this doesn’t mean is that this virus is somehow more transmissible. And that was really the crux of the initial media coverage of this– that because the strain or variant is dominant in the US and Europe, that means that there is some sort of evolutionary selection occurring that is giving this virus an advantage, by making it more contagious. Oftentimes viruses behave differently in cell culture than they do in the real world. So while this is something certainly to look for, there are other explanations for why this is dominant.

For example, we know that there have been a number of importations into the United States from Europe. And this strain was dominant in Europe. It may be what we call founder effects– which is just that because more of that virus started the epidemic here in the United States, there was just more of it.

So this is something that we really need to look for. And really the best way to do this, probably, is by looking at transmission and pathogenicity, or the ability of this virus to cause disease, in different animal models. That’s how we can really determine if in vivo, in humans or in animals, that this mutation confers any kind of difference in transmissibility or pathogenicity.

IRA FLATOW: We also heard the president say, again, that one day the virus might just, quote, “disappear.” I mean, do viruses just disappear? And I guess as an extension of that, do you think that we should expect this virus, in one form of another, to just hang around for months, days, years, and maybe get lessening of power over that time?

ANGELA RASMUSSEN: Well, I think that’s an excellent question. And the second part of that, we just don’t know. It’s possible that this virus may become endemic, if we develop a safe and effective vaccine– which, obviously, there’s a number of vaccine candidates in the running right now– that will change things. But viruses don’t just disappear.

Even when we are able to control an epidemic and a virus doesn’t reemerge– and a good example of this is SARS classic. SARS classic didn’t just disappear. It went away because we employed active epidemiological interventions to prevent the spread, and we were able to contain it. It has not reemerged, and we’re not really entirely sure why that is– probably because somebody has not come into contact with the reservoir species that is circulating SARS classic in the wild.

So viruses can go away, but they don’t just arbitrarily disappear. They usually go away because we employ active public-health measures to get rid of them. And a key tool in this is going to be vaccination. The only viruses that we’ve successfully eradicated– smallpox and rinderpest, which is an agricultural pathogen, has been through concerted vaccination campaigns. And so if we want this virus to just disappear, we’re going to have to do work to make that happen.

IRA FLATOW: We’ve also heard– and my inbox has been full of debate about whether they want to take a new vaccine– whether they would trust a new vaccine, given their distrust of the government these days.

ANGELA RASMUSSEN: I think that this is a huge concern. And it can’t be understated the damage that has been done in terms of sowing distrust between public-health officials and the public. I firmly believe that you can’t have public health without the engagement of the public. And this is a huge problem.

I’m very concerned that people might not get the vaccine. And not only people who are really staunch anti-vaccine advocates, but also people who are just concerned about the speed and the accelerated approval process that these vaccines are undergoing.

IRA FLATOW: Well, as always, I want to thank you, Angela, for taking time to help fact-check my feed.

ANGELA RASMUSSEN: It’s my pleasure, Ira. Anytime.

IRA FLATOW: Dr. Angela Rasmussen is an associate research scientist and virologist at the Mailman School of Public Health, Columbia University in New York.

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