IRA FLATOW: This is Science Friday. I’m Ira Flatow.

The race continues to understand the inner workings of COVID-19, find treatments, and develop a vaccine. And it all threatens to bury us in an avalanche of new scientific research, some of it good, some of it preliminary, thin, or with conclusions unsupported by the actual evidence. This isn’t necessarily a bad thing. Scientists are collaborating with an intensity never seen before.

But if your social media feed is anything like mine, you are being bombarded with a confusing number of claims. And many don’t have good or maybe any research behind them. So what better time, ladies and gentlemen, for another edition of “Fact-Check Your Feed,” where we debate, discuss, and debunk all that stuff clogging your inbox. And we’re starting out with a video that went viral on Facebook and YouTube last week, though it’s now been taken down.

The Plandemic video made bombastic claims about the coronavirus. But, as my next guest is about to explain, many were either baseless or flat out false. Here with me again is Dr. Angela Rasmussen, assistant research scientist and virologist at Columbia’s Mailman School of Public Health. Welcome back, Angela.

ANGELA RASMUSSEN: Thank you so much for having me back, Ira.

IRA FLATOW: Let’s start with that viral video. What’s incorrect in the claims made there?

ANGELA RASMUSSEN: Almost everything.

[LAUGHING]

That video pretty much from the– actually, the moment I hit play, I started shouting, oh my god, I can’t believe that they are saying this. Both the researcher who is interviewed in that video, Judy Mikovits, as well as some of the circumstances of her prior career as a scientist, as well as the things that she’s actually saying about coronavirus and vaccines, are completely incorrect, beginning with really her history.

So she made news by publishing a paper about 10 years ago that suggested that a mouse retrovirus was a cause of chronic fatigue syndrome. And it turned out that that was a laboratory contaminant that caused those results to happen. So the paper ended up being retracted. And she was later fired by her employer, which was a research institute in Nevada, and was arrested then because she actually took a laptop and several lab notebooks and some data from her office to Southern California.

So the whole thing is kind of a mess. But it doesn’t actually have anything to do with her being silenced for being a truth teller. And in fact, she is not a truth teller because in that video, she says a whole number of things that are just flat out untrue.

IRA FLATOW: She says Ebola was made in a lab in the 1980s.

ANGELA RASMUSSEN: Yes. And that’s easy to disprove. Ebola actually emerged naturally in the country of Zaire at the time, now the Republic of Congo and the Democratic Republic of Congo, in Africa. So we knew about Ebola before the ’80s. And it did infect people.

She also claimed that we’ve never successfully made a vaccine for an RNA virus, which is not true. So many of the vaccines that we’ve known about and have worked for years, including polio, the measles/mumps/rubella vaccine, influenza vaccines– those are all RNA viruses with very effective vaccines.

IRA FLATOW: What do you think is the most important claim that needs to be debunked here?

ANGELA RASMUSSEN: There’s two really important claims that need to be debunked. One is that coronavirus pandemic was planned and it has something to do with vaccination. And the second is that vaccines are inherently unsafe and ineffective.

So she claims that she’s not anti-vaccine. But she claims also that vaccines are immune therapies when, in reality, vaccines can be used that way. But they’re typically used as preventative measures. And it’s very dangerous, I think, to circulate the idea that vaccines or any hypothetical vaccine that will be developed against SARS-coronavirus-2 is all part of this dangerous conspiracy to kill people because then people might not get the vaccine. And getting that vaccine will be key to us resuming our normal lives. And these types of vaccines now we’ve already seen with measles vaccine denial, for example– that one consequence of this is actually people can be very seriously ill. And people can die.

IRA FLATOW: One of the claims that you mentioned from this viral video is one we keep hearing from politicians also. And that is that the virus was made. And a listener, James, called into our VoxPop app with a question.

JAMES: Scientists have always said that most likely, the virus came from bats in the wild and transferred to a intermediate host animal. What’s the evidence? How do scientists know that the virus is natural versus from a laboratory?

IRA FLATOW: That’s a good question. How do scientists know that it was emerging naturally and not made in a lab?

ANGELA RASMUSSEN: So we have several pieces of evidence that suggest, first of all, that this virus wasn’t made. And it’s also highly unlikely that this virus escaped accidentally from a lab, which has been another origin theory that’s been put out there.

So by analyzing the genome of this virus, there are genetic features that would be observable if this virus was actually made from one of the reverse genetic systems that we know exist for betacoronaviruses. So one way that viruses– virologists can study viruses is by using these reverse genetic systems, which is basically a way to store all of the information you need to make the virus on a piece of DNA. And if you are going to engineer a virus or do any kind of genetic engineering, you need to have access to one of these reverse genetic systems. There are telltale sequences associated with these reverse genetic systems. And none of them are part of this virus, SARS-coronavirus-2’s, genome.

So that’s one very strong indicator that this virus emerged naturally. Another feature of the virus genome that has to do with the polybasic cleavage site and the spike protein is something that we haven’t seen before. So it would be very, very unlikely that somebody would spontaneously engineer a polybasic cleavage site with this particular sequence because computer modeling shows that this sequence would actually be predicted as sub-optimal. And it’s very unlikely that somebody would just decide to use a sub-optimal polybasic cleavage site sequence when they could use one of the other ones that are already known for other betacoronaviruses.

So the evidence, just by looking at the genome and analyzing the genome, strongly, strongly suggests that this virus emerged naturally. And one of the problems with the way that this has been presented in the public discussion is that people seem to think that it’s either– only one of two things could have happened. It could have come out of a lab by accident or it could have emerged from this wet market in Wuhan.

And the reality is we know that people who live near bat caves in China– actually, a number of them have antibodies to other bat SARS-like coronaviruses. So there are many circumstances in which people might be exposed to these viruses just in the course of their normal daily lives. And in fact, that serology data suggest that this happens with a fair amount of frequency. So it’s entirely possible that any number of natural encounters with either a bat or their droppings or another animal, potentially, that was infected with SARS-coronavirus-2 was actually the event that led to this rather than an escape from a lab.

IRA FLATOW: Now, these aren’t the first examples of falsehoods that have gone viral during this pandemic. Why do you think that people are latching onto so many things that are demonstrably incorrect now?

ANGELA RASMUSSEN: So one of the things that scientists think about a lot is how to deal with uncertainty. And I think that the general public, when facing something that’s completely new like this that scientists don’t know what to make of this– there’s so much that we don’t know about this. We know far less than what we actually do know about this virus, which has only been known to us for the last 5 and 1/2 months. I think that the general public has a lot of difficulty dealing with this uncertainty, with the fact that we actually just don’t know very much about this. And we’re working as hard as we can to find out. But I think people’s natural response to this is to try to find explanations. And scientists would call this developing hypotheses.

The problem is separating a hypothesis from the evidence that we actually have to prove that that hypothesis is true. And while most scientists are credible, most scientists are also very careful to gauge– to make people aware of the limits of our knowledge.

IRA FLATOW: Moving on to another piece of research making the rounds, coronavirus has been seen in the semen of at least– what– six people, including a couple in recovery from the virus. Does this hint that, like Zika, it may be sexually transmitted?

ANGELA RASMUSSEN: So it’s something definitely that we should look into. But it doesn’t necessarily indicate that coronaviruses can be sexually transmitted. So this study was a very small report showing that six patients who were recovering from confirmed cases of COVID had viral RNA in their semen. That doesn’t necessarily suggest that they had enough actual infectious virus in their semen to transmit it by that route.

And one thing that would also be a big factor in this is whether receptors, receptor distribution of ACE-2, would allow, actually, sexual transmission to be a route of transmission. We know for Zika and Ebola virus that the viruses can persist in the testes of infected men. The Ebola outbreak in particular– we learned this in a very unfortunate way when a person who had recovered from Ebola ended up sexually transmitting it to two different women, who both died.

So it definitely has huge public health implications if COVID can be sexually transmitted. But showing that there’s just RNA in the semen is a far cry from showing that sexual transmission is possible.

IRA FLATOW: Yeah. That’s what I was going to ask. What kind of research would it take to actually understand that virus is sexually transmitted?

ANGELA RASMUSSEN: So I think there’s a couple different approaches you can take to this. One is to just look for infectious virus in the semen of people who are RNA-positive. If there’s no infectious virus there or there’s very, very low levels of it, that certainly indicates that sexual transmission is probably less of a risk.

Another way to look at this is by looking at epidemiology and are there patterns of transmission in populations that suggest that sexual transmission might be occurring. So to my knowledge, there is no evidence that there is, first of all, infectious virus in the semen or that there are clusters of transmission that suggest a pattern associated with sexual transmission. So until we have that type of information, it’s really hard to say whether this is something we need to be worried about or not.

IRA FLATOW: I’m Ira Flatow. This is Science Friday from WNYC Studios.

We talked about this story I’m going to bring up a bit last week. But I want to come back to it from a virology point of view. And that is the claim that COVID-19 has been mutating to become more, much more, infectious. Why is that wrong?

ANGELA RASMUSSEN: So COVID-19 or SARS-coronavirus-2 viruses– RNA viruses, including coronaviruses, mutate every time they copy their genomes. So that is basically because the enzymes that do the copying make mistakes. And those mistakes don’t get corrected.

Sometimes, those mistakes will confer an advantage to the virus. Sometimes, they do nothing. Sometimes, they are actually detrimental to the virus. When they confer some type of advantage, then that mutation can be selected for and undergo what we call positive selection evolutionarily.

Sometimes, though, there are other things called founder effects where, basically, a mutation gets into a population early on. And just because it lucked out and was there first, it ends up being the dominant strain in that community.

So the paper published or the preprint last week that showed that there was a mutation in the spike protein that became dominant throughout the US and in some other places could be from either of those things. That preprint suggested that it is associated with increased transmissibility. And it’s worth noting that, while that may be the case, that study does not indicate that that is actually true. In order to determine that and the functional effect that a mutation will have, you actually need to do studies to see if that mutation is linked to increased transmissibility, perhaps in an animal model, or increases in viral fitness.

And there’s a really good example of this happening with the Ebola outbreak in West Africa. It turned out that that virus, when they looked at it in cell culture, actually did. That mutation conferred some fitness advantages, meaning the virus can replicate more efficiently and infect cells better. But when they tried it out in animals, it had no effect on pathogenesis, or the ability of the virus to cause disease.

So we need to be really cautious about the way we talk about the functional implications of these mutations for viruses. It definitely deserves a closer look. But we can’t conclude that it’s increasing transmission just based on sequence analysis alone.

IRA FLATOW: And then we also keep hearing people talking about herd immunity, but maybe with the wrong definitions.

ANGELA RASMUSSEN: So the way that we’ve induced herd immunity, meaning that enough people in the population are immune that a virus cannot establish itself and spread in that population– the way that we’ve done that historically is with vaccines. You make, basically, the majority of people unable or not susceptible to a given virus– viral pathogen. And then that virus won’t spread in that community. So we prevent it.

In this case, people are talking about herd immunity now as if, like, let’s infect everybody with this potentially lethal virus. And once everybody gets infected with it, we’ll all be immune. And that is a terrible way to approach herd immunity.

The main reason that vaccines have been such incredibly powerful public health tools is that they allow us to get that immunity without having to suffer the deaths that will happen if we were actually infected with those viruses themselves. So I think it’s really, really dangerous to talk about herd immunity as let’s just reopen up and infect everybody.

IRA FLATOW: We’re now in month five since the coronavirus first started really making itself known around the globe and right here in the US. Is debunking getting easier or harder for you? Are you seeing more misinformation or less?

ANGELA RASMUSSEN: I’d say probably more, although it’s been a pretty steady stream from the beginning of this. A lot of the times, I see the same sort of thing get recycled over and over again in different ways.

So the origin of the virus is a great example. Early on in the pandemic, like in February, a lot of people were saying, oh, this is a biological weapon. And then Kristian Andersen and colleagues published a paper that outlined the genetic evidence why this is probably not a biological weapon. And in fact, it’s not a biological weapon. So then it went away for a little bit and then came back in the form of this laboratory accident origin theory.

So these same stories keep getting brought back or resurrected with just slightly different twist on them. And it’s– it does, honestly, get pretty exhausting trying to argue about these all the time.

IRA FLATOW: Yeah. And that is all the time we have. But keep sending us your questionable stories on Science Friday VoxPop app. And we’ll be back to fact-check it with Dr. Rasmussen in a future show. As always, Angela, you’ve been terrific. Thank you for taking time to be with us today.

ANGELA RASMUSSEN: Thank you so much for having me. I always love coming to Science Friday and talking about this with you, Ira.

IRA FLATOW: You’re welcome. Dr. Angela Rasmussen, assistant research scientist and a virologist at Columbia’s Mailman School of Public Health, in New York–

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