Jason Kindrachuk, PhD: Viral Shedding, Co-infection, and the Origins of SARS-CoV-2

Contagion&reg Editorial Staff

Jason Kindrachuk, PhD, addresses clinician questions about SARS-CoV-2 such as the length of infectious viral shedding and whether the virus will become endemic.

Segment Description: Jason Kindrachuk, PhD, professor of viral pathogenesis at the Medical Microbiology Department of the University of Manitoba, addresses clinician questions about SARS-CoV-2 such as the length of infectious viral shedding and whether the virus will become endemic.

This is part 2 of a 3-part interview. The first part can be found here: https://www.contagionlive.com/news/jason-kindrachuk-phd-understanding-sarscov2-in-an-emerging-virus-context

Interview Transcript (modified slightly for readability):

Contagion®: A few of these next questions are actually from our audience. We hosted a CME-certified webinar. And we were talking about what clinicians can expect if they have COVID-19 patients. We were able to answer a lot of those questions from our panelists. We had our editor in chief, Jason Gallagher, we had Carlos Del Rio, we had a few other very intelligent panelists as well.

But we didn't get to everything. And so we wanted to draw on the Q&A to spark interview questions, and at least get some of those audience questions answered down the line.

The first one would be, we know that a certain amount of viral shedding occurs after patients have left the hospital. There's different debates coming out about how long people should be quarantined, and what might be the right standard for recovery. Where does the evidence point at the moment in terms of whether this viral shedding is actually infectious after people have recovered?

Kindrachuk: I'll always put the caveat that I'm just a simple virologist, I'm not a clinician. My viewpoints may be a little bit different from what clinicians would see with their patients, but some of the data that comes out right now, or has been coming out recently suggested that, at least in terms of the infectious virus, what has been seen is that shedding seems to occur somewhere for around a week, give or take a few days on either side, once a patient becomes symptomatic, and that's what is being viewed at least as being somewhat of a standard.

Now the problem is that ultimately, I don't think we're far enough into this pandemic with enough clinical data yet to say definitively how long a person sheds for.

It comes back to the question that you raised in regards to infectious virus versus viral components, which I look at like a pinata.

If you go to a party and somebody has a pinata, you can identify what that is if somebody breaks it apart with a bat. If someone comes into the yard an hour later, they can kind of piece together that that was once a pinata, just based on the pieces that are lying on the ground. But you can't re-form that whole pinata.

RNA data suggest that the virus was once there, but that doesn’t tell us that there is still a whole virus there. And the limitation is trying to establish assays to tell us what is that correlation between the amount of RNA that we see versus infectious virus.

Contagion®: In our webinar, one of the clinical cases that we brought up was COVID-19 with a simultaneous adenovirus infection, and there's been some reports that you're seeing a lot of coinfections.

Is it possible for someone to have both influenza and COVID-19, for example?

Kindrachuk: Some of the data out of China actually suggest that that definitely is a possibility. What we don't really understand yet is what is the relationship between that coinfection versus either virus in the realm of disease severity.

What we do know, though, is that patients that tend to show more severe signs of COVID-19 may actually have bacterial coinfections, which is fairly common in severe patients with influenza. And we know for certain that bacteria will exacerbate disease in those cases.

I think we can make some general assumptions based on what we've seen from other viruses. But it's going to take a while again to piece through the data and look at the outcomes of patients to really get a feeling of whether or not there was any kind of synergistic activity.

Contagion®: Do you see COVID-19 becoming a seasonal burden as a possibility or likelihood here?

Kindrachuk: Some of this comes out of what was seen during the original SARS epidemic, because there was a small cluster of cases that emerged in 2003 or 2004. And there was some fear at that time that it may indicate that the virus had started to become seasonal, thankfully that didn't happen.

We do know prior coronaviruses that have been endemic in the population. There are 4 coronaviruses outside of SARS, MERS, and SARS-CoV-2 that have been circulating since (it’s estimated) around the 1960s. These have caused largely cold-like symptoms in most patients.

Those viruses did exhibit some signs of seasonality. But the question is, what is the driving force behind that? Is it temperature and humidity? Because it's a little bit lower temperature in the wintertime, a little bit lower humidity? Is it the proximity of people to one another? What are the driving forces behind that?

And I don't think we're quite there understanding SARS-CoV-2, whether that will be the case.

I don't think we know yet, and realistically, our biggest concern right now is let's get social distancing done. It's painful. I sympathize with people completely. But if we can try and actually curb transmission, we may end up in a situation like the original SARS epidemic, where ultimately maybe this virus will disappear. Let's do everything we can to try and mitigate spread and concerns about it becoming endemic.

Contagion®: There were early reports about there being 2 different types. Some media reports, we're calling it strains in headlines, these L and S types. Do you know if that's still considered correct, or anything else about the potential mutation and variability of this virus? I mean, I know with mutation in viruses the popular fear would be that it gets more deadly, but it tends to the other direction, right?

Kindrachuk: Right. The data is still pretty preliminary. What we've seen is that there's basically the L and S forms or strains. L seems to be the one that's found predominantly within population. I think it's about 70% versus 30%. Although S seems to be the ancestral form.

There’s discussion as to whether or not L may have been the form that was seen earlier and was more aggressive, and that S less aggressive in in terms of its transmission and its virulence.

The problem is that we don't know. A lot of this has been hypothesized based on sequencing data.

Do we have any biological data to back that up either in patients or cell culture, animal models? Again, we're not quite there yet. We will definitely be able to look at that over time.

But for right now we need to get it contained and at the same time, try and get labs around the world to be able to look at these potential differences.

Contagion®: What can you tell us about the possible evolution of the virus because there was what seemed like a bit of fake news about the virus being bioengineered from a lab in Wuhan? I guess the less conspiratorial, though still not substantiated version of that, is that it was of natural origin and then lab precautions weren't taken.

But the emerging consensus seems to be “no it, it came out of nature,” and maybe we have these animal markets involved. What's the evidence that this is a virus out of nature?

Kindrachuk: We've relied so heavily on people that are doing whole viral genome sequencing during this pandemic to try and give us some inferences on what this virus is, where it came from, and what it's going to do. We have all seen stories about what this virus is or where it came from, in particular, whether this was engineered or not.

Right now, the sequencing data simply does not provide any evidence that this was a bioengineered virus. What they've been able to do is look at the sequences to see whether there were imperfections within the sequences that would suggest that this was done through cloning procedures or bioengineering procedures. There simply is no evidence of that.

Everything points to the fact that this was something that naturally spilled over. This would not be surprising because we've seen this with SARS, we've seen this with MERS. How can there be these really low chance events that lead to something like a pandemic? The unfortunate answer is, this is how emerging viruses behave. If we go back to thinking about how they circulate, this virus likely emerged from bats.

Bats are one of the most populous mammalian species that there and one of the most diverse species. So now we have to basically say, out of all the millions of bats, there are likely small subsections of specific types of bats that are carrying this virus. But by the way, it's not that every animal within that particular species of bat is carrying the virus it's likely a tiny subset that actually carrying the virus at any one point in time.

That's where it becomes this this chance event that you have a bat which at the right time happens to pass on biological fluid to another animal that can carry the virus.

I think it comes back to our jobs as scientists to try and communicate better what we understand about spillover events, but also providing more evidence and more context, when we do things like whole genome sequencing for the public to understand what that data actually means, what the context is, and what it implies.