IRA FLATOW: This is Science Friday. I’m Ira Flatow. Later in the hour we’ll talk about the 50th anniversary of Earth Day. It’s next Wednesday, and due to coronavirus it’ll be a digital day of action. Just a note that we won’t be taking your calls during this pre-recorded hour of the show. First up, as the COVID-19 pandemic progresses so does the speculation, the glut of data articles and studies coming out about the virus. With all stories coming out on Twitter and Facebook and social media, it can be hard to sort through the fact from the rumor. So we want to help you fact check your feed and sort through this stories.

Last week there was a story about the risk of runners and bikers spreading the virus. And this week a report from South Korea about the reactivation of the virus in COVID-19 in patients. So how do these stories hold up, and what do they really tell us? My next guest is here to help us sort out the details. Dr. Angela Rasmussen, Assistant Research Scientist and virologist at the Columbia Mailman School of Public Health.

Dr. Rasmussen, thanks for joining us again.

DR. ANGELA RASMUSSEN: Thanks for having me back, Ira.

IRA FLATOW: Can we start with the South Korea item, where there were 116 patients who reported recovery from COVID-19 but later tested positive? There’s this idea that the virus was reactivated in them. What could be happening there?

DR. ANGELA RASMUSSEN: I’m not clear that these so-called reactivations now are that much different than what a couple of weeks ago people were reporting as re-infection. In all of these cases there have been these reports that are not supported by data– from what I have seen, in any case– that suggests that patients who have tested negative are then testing positive.

You know, I certainly can’t rule out the possibility that these patients are actually being re-infected or that the virus is somehow reactivating from being in a latent or sort of dormant state. But I think a more likely explanation is just that the test does have a certain percentage of false negatives that it can give. And we do know that people, after recovering, can continue to be positive for the virus’ RNA or its genetic material.

There are a number of viruses for which viral RNA can be found long after the patient has recovered, and they don’t actually have any infectious virus. And a recent paper that was just published studying some patients in Germany does suggest that after recovery, patients do have these sort of fluctuating levels of viral RNA that can still be detected in their tests. But that doesn’t mean that they are actually re-infected or reactivated or potentially still shedding infectious transmissible virus.

IRA FLATOW: So it’s not something like herpes that stays in your body and comes back and goes away every now and then?

DR. ANGELA RASMUSSEN: That’s correct. So herpes viruses have a very specific mechanism that allows them to basically turn off most of the viral genes and exist as sort of a genome– an episome, we call it– outside of the normal host cell genome. Then when there’s a stress or some kind of incident that provokes the virus to fire up its genes again, start expressing viral proteins, that virus can reactivate.

Coronaviruses don’t have any type of mechanism that’s known to have a latent period or reactivation events. And I would be very surprised if this virus did as well. We don’t have any reason to think it’s different from many other coronaviruses.

IRA FLATOW: There’s a lot of talk about patients recovering and developing an immunity to the virus. How are these things related?

DR. ANGELA RASMUSSEN: So we still don’t know that much about protective immunity to the virus. What we do know is that experimentally infected animals that have been allowed to recover can’t be infected with the virus– at least in the case of a study that was done in rhesus macaques, or monkeys. We also know that patients who have recovered from COVID usually have titers that are detectable of what we call neutralizing antibody. So these are antibodies that can bind to the virus and inactivate it or render it non-infectious.

Not every patient does have detectable antibodies, but it really is a minority of the patients that have been studied so far that don’t have antibodies. So the evidence thus far does indicate that most people will develop an immune response. We assume that that’s protective, but we need to do more work to find out exactly how protective it is and how long that protection lasts.

IRA FLATOW: There are reports that COVID-19 patients will show signs of improvement, and then they’ll just crash. The cycle repeats itself. And it’s due to something called the cytokine storm. What is the cytokine storm?

DR. ANGELA RASMUSSEN: So cytokine storms are actually an overreaction by the body’s immune system, and specifically inflammation. What happens in some patients, that we don’t understand, is that the immune system will really overreact. So normally when you’re infected with the virus, the inflammatory processes are really important to tell the immune system where to go, to contain and clear that infection.

Cytokine storm is when the signals that are needed to coordinate that type of response essentially lose all ability to be controlled. So rather than giving calm directions on how the immune system should go, it’s more like every inflammatory process is shouting all at the same time. And so it’s essentially immune or inflammatory chaos, and that can trigger this disease that’s actually more serious than what the virus itself causes.

IRA FLATOW: Does this storm, the cytokine storm, play any role in developing treatments or vaccines?

DR. ANGELA RASMUSSEN: So certainly people have talked about using a drug called tocilizumab. I hope I’m pronouncing that correctly. What that is is an antibody that targets a molecule called IL-6. An IL-6 is a very potent pro-inflammatory cytokines. So it’s a message that cells give to say, hey, let’s turn on inflammation. By treating with tocilizumab you’ve reduced the amounts of IL-6 so that really potent part of the cytokine storm hopefully you can reduce inflammation as well.

I believe that’s only been used so far in compassionate use circumstances– so uncontrolled essentially uses of that drug. But I would not be surprised to find out that there are clinical trials being set up and underway to test that out.

IRA FLATOW: All right. Now let me run a story by you that came out last week that was getting shared. And it was about a Belgian report that looked at how runners and bikers might spread the virus. But this wasn’t exactly a study. Where did this report come from?

DR. ANGELA RASMUSSEN: My understanding of this is a Belgian scientist or engineer who studies aerodynamics did this model of how droplets spread in certain circumstances, such as when people are running. And this was I believe first covered in a Belgian magazine. There was obviously a lot of attention paid to it. People were very concerned that it meant that if you went running you had to have at least 26 meters, I think, of space between you and other runners to avoid being exposed to respiratory droplets that can potentially be infectious.

But there was no paper and no data that was released to show how this model was developed. The original magazine article that this was described in was then translated into English and released by the author as a white paper, which is typically not what scientists usually think of when they think of a white paper, which is usually a technical description of a study or a model. To my knowledge, it hasn’t been published anywhere, so it hasn’t undergone peer review.

And I would be very skeptical of these findings, because they don’t really take into account anything that we know about how viruses are transmitted. It really is just a model of how droplets spread through the air.

IRA FLATOW: Now let me move on to another topic that was in the news or circulating. We know that COVID-19 attacks the lungs. And some researchers have been comparing this to altitude sickness and looking at treatments for altitude sickness. What’s the rationale here? Is there an overlap, possibly?

DR. ANGELA RASMUSSEN: So the rationale there is that some physicians have made the observation that this pneumonia that COVID causes does not look like typical pneumonia, in which the lungs are filled with fluid and there are actually mechanical problems with breathing, which is what mechanical ventilation, of course, helps with.

In this case, it appears that some COVID patients, at least, have lower levels of oxygen in their blood. So this is an issue less of the lungs aren’t working properly than there’s not enough oxygen getting into the blood. And that looks a lot more like high altitude sickness. But it’s really unclear that this is the case for every single patient. Some of this is based on the fact that not every patient who is put on a mechanical ventilator really has a great outcome, and patients are unable to get off these ventilators.

But I think this is just recently been appreciated, so a lot more work needs to be done to determine exactly what’s going on in these cases.

IRA FLATOW: One last question for you. We know there’s a scramble to quickly come up with a vaccine. And one way to fast track this is through human challenge trials. What happens in one of these trials, and is that a recommended way to try out a vaccine?

DR. ANGELA RASMUSSEN: Well, it’s certainly a hot topic of debate right now among scientists and physicians and bioethicists. Typically, human challenge trials are not done to test vaccine efficacy, at least not until they’ve undergone extensive preclinical testing in animals. This is really an emergency situation in which that’s even being considered.

But what happens in a human challenge trial is you would vaccinate human subjects who volunteered to be essentially guinea pigs to test the vaccine. And then you would challenge them with a dose of the virus. That would be enough for them to get infected, but ideally– and this is where the problem is– it wouldn’t kill them. The problem is we don’t know what really all of the risk factors are for getting severe COVID, and we don’t know what effect dose has on disease severity. So it’s a really tricky ethical question that I think is going to have to really undergo a lot more consideration and debate before we do it. Because the last thing we want to do is test the vaccine and end up causing a lot of injury, or potentially even killing trial subjects.

Some of the first polio vaccine trials, which were done on essentially mentally handicapped children in institutions, the Willowbrook Institution. The idea of human challenges for vaccines– they haven’t really been done since that, which is obviously unethical to do those types of experiments. I mean, I realize we’re in a desperate situation here, but I can just see so many outcomes of the human challenge trial going spectacularly and horribly wrong that I personally am not in favor of them. Although people are bringing these ethical arguments to try to minimize risk and justify it that way. So we’ll see what happens.

IRA FLATOW: Thank you very much for clearing all of this up for us Dr. Rasmussen.

DR. ANGELA RASMUSSEN: It’s always a pleasure to be here, Ira. Thank you.

IRA FLATOW: You’re welcome. Dr. Angela Rasmussen, Assistant Research Scientist and virologist at the Columbia Mailman School of Public Health.

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