This Week in Virology has debunked the claims that there multiple strains of the virus that are either more transmissible, or more or less severe, or that your

This Week in Virology has debunked the claims that there multiple strains of the virus that are either more transmissible, or more or less severe, or that your immune system would react differently to. Here is what they had to say in episode 590[1]: Vincent Racaniello: There are a series of articles here, where there have been some claims about different circulating lineages and what that means. Are you on this, Cathy? Cathy Spindler: Right. So, there was an article that I first saw in the LA Times "Chinese Scientists Say Second Coronavirus Strain Is More Dangerous"[2]. But in that there's a link to virological.org, which we talked about another article posted there a couple of weeks ago[3], and they really debunk this and think even that this Chinese article about a second Coronavirus should be retracted. Two of the key claims that are reached by misunderstanding and overinterpreation of data and an additional analysis suffers from methodological limitations. So this long thing on virological.org goes in to the reasons why there's no real evidence for two different strains, a more severe strain and a less severe strain. Rich Condit: It also provides a nice summary of this sort of variation in sequence that's being observed in the virus over time, which is good. Vincent: Yeah, it's a good article. We'll put a link. It's worth reading, but as everyone should know, when these [indistinct] viruses, every replication cycle they sustain mutations in their genomes and the lethal ones are gone, the viruses don't reproduce, but some of them stay and if they're neutral they remain. So they can be characteristic. So the virus introduced in to the Washington area is a single introduction and then it's spread and you can tell that because it has a unique set of mutations compared to say, the Chinese isolate, but it doesn't mean anything biologically. It's just markers. Rich: And the markers are really interesting because they give you insight in to, I mean the insight that I got from observing what came out of the Washington cases is that from looking at the sequence of the virus they concluded that in fact it had been circulating for some time, and they could even get a very very rough estimate of how many cases might be out there based on the variation in sequence and the time at which the disease first showed up in a person. Vincent: I think there are some emails later about this. People are concerned that, and people suggest in these papers, at least the one here, that we're being critical of that it could be evolved to be more virulent or more transmissible. There's no evidence for that whatsoever. Rich: This is the kind of thing that... it just won't go away! Vincent: Oh, it doesn't go away... new outbreak and it comes back. Rich: Yeah, and there's no evidence. People have looked at this. We've gone over this for several.. Zika, Ebola, where's there's been variation and people point to a particular variation and they say, "This is going to make it more virulent" or something, and then the experiments ultimately get done and no. It hasn't made a difference. Vincent: And also the issue of increased transmissibility, I think this virus is already very transmissible as it is, and I think the mutations that made it effectively transmissible among humans, which happened very early on, I don't know, either in animals or in humans early on, before we knew about it, they're done, and it's going to be hard to know what they were. MERS coronavirus has never acquired those high transmissibility changes and it keeps fizzling out and then you have another reintroduction from camels but this particular SARS-Cov-2 sustained them probably early on and it's a very good transmitter. It doesn't need to get better, at least from my anthropocentric view. We never really know what viruses are selected by, but I don't think there's any evidence, and it's very hard to get that evidence. That paper tells you what you need to prove that mutations are doing something phenotypically. It's very hard to get that. Rich: It has occurred to me that people who don't think about this stuff every day might be a little confused by this discussion relative to the discussion that goes on all the time about variation in influenza virus strains, and new strains coming up and having to change the vaccine and stuff. But that's different. That's variation in the influenza virus that makes it evade the existing immunity, and those sorts of variations arise so you get circulation of viruses that you don't have as good an immune response to, but that's different than a virus making mutations that make it more virulent. It's a different story. Then they talk about it again in episode 592[4]: Alan Dove: David sends a link to a paper on possibly being two strains of SARS-CoV-2. This says, "I've seen this pop up." Vincent Racaniello: These are just basically single nucleotide polymorphisms. Dove: Oh those, yeah. Rich Condit: This is the paper where they were talking about an S-type and an L-type and one maybe being more pathogenic than another and blah blah blah blah. Basically, yes, there's variation in the virus. It doesn't necessarily mean anything. Racaniello: No. They have no evidence that's it's functionally of any importance at all. No. But he does say "this virus has now conducted many human-to-human transmissions. Have we discovered mutations that enhance transmission? Welcome to evolution." Well, the problem is you need to have the virus before it started transmitting efficiently among people. Right? And we don't have that and I'm not sure we ever will. But then maybe you could look at it and see what changes occur. And I'm not sure you could ever do anything about it because you can't infect people and we don't have a good animal model for transmission so, no. Unfortunately we won't be able to know about that. And in episode 596[5]: Rich Condit: So the second question is the doctor asking.. It's basically, can the virus mutate so you wouldn't be immune to it? And our understanding, my understanding with SARS-CoV-2 now is that there's no evidence that it's going to undergo what we call antigenic drift, right, that it will be SARS-CoV-2 for the foreseable future, and once you mount an immune response to that you'll be immune to it and there won't be, as far as we know, new strains coming up to which you will not be immune. These things, the human coronaviruses seem to be pretty stable over time. Yes, they can accumulate mutations but they are of essentially no consequence. Alan Dove: And as viruses go, these coronaviruses, because of the proofreading are actually more stable than a lot of other viruses. Probably what the doctor is thinking of is that this is analogous to flu, where you do see antigenic drift and antigenic shift, and where yeah, you get different strains circulating all the time. But there's no evidence, as Rich said, that SARS-CoV-2 is doing any of that. [1] - http://www.microbe.tv/twiv/twiv-590/ http://www.microbe.tv/twiv/twiv-590/ at about 13 minutes in [2] - https://www.latimes.com/science/story/2020-03-05/chinese-scientists-say-second-coronavirus-strain-more-dangerous https://www.latimes.com/science/story/2020-03-05/chinese-sci... [3] - http://virological.org/t/response-to-on-the-origin-and-continuing-evolution-of-sars-cov-2/418 http://virological.org/t/response-to-on-the-origin-and-conti... [4] - http://www.microbe.tv/twiv/twiv-592/ http://www.microbe.tv/twiv/twiv-592/ at about 1 hour and 41 minutes in [5] - https://www.microbe.tv/twiv/twiv-596/ https://www.microbe.tv/twiv/twiv-596/ at about 39 minutes in