Omicron May Be Less Severe. It’s Still A Big Healthcare Problem.

IRA FLATOW: This is Science Friday. I’m Ira Flatow. For the past few weeks, we have heard that the Omicron variant seems to be less severe than the previous form– Delta. Yes, it spreads a lot faster than Delta. But if you get infected with Omicron, chances are you might feel ill, but could safely recover at home. No need for a trip to the emergency room.

But paired with the skyrocketing infection numbers across the US, what does labeling Omicron as less severe even mean in terms of public health? What about our immunocompromised peers? And with more people getting infected, will we have more long haulers, people who have lingering secondary illnesses? And what about kids, infants, and toddlers who are not vaccinated?

Here to break down Omicron severity are my guests– Dr. Michael Diamond, virologist and immunologist, Washington University School of Medicine in St. Louis and Dr. Saskia Popescu, infectious disease epidemiologist and infection prevention expert at the University of Arizona College of Public Health in Phoenix. Welcome, Michael. Welcome back, Saskia.

MICHAEL DIAMOND: Thank you.

SASKIA POPESCU: So nice to be back. Thanks.

IRA FLATOW: Nice to have you back. Let me begin, Saskia, with you. Omicron is spreading just so quickly. But what do we need to consider to evaluate how severe it is?

SASKIA POPESCU: I think it’s really challenging right now. Because it’s barely been over a month since we identified Omicron. And we’re learning about this every single day. So, first and foremost, we’re going to need more genomic sequencing to know who actually has this new variant who’s tested positive and collect more data on hospitalizations, not just within the US, but globally. One of the biggest hurdles we have right now is that we’ve got some great data from South Africa.

But the question is, is this new variant inherently less severe? Or is it because it hit a population that had been severely impacted by COVID already and there was some inherent, infection-induced immunity before? So we’re learning so much more about this every single day. And it’s very easy right now to get small anecdotal studies and information from a handful of patients and make decisions on that.

So I always stress, we need more information on hospitalizations. We need more genomic sequencing and, ultimately, time and not to jump the gun when it comes to a small cluster of cases that were studied. For example, the CDC’s new guidance was really based off of an MMWR study that was six people. That’s way too small. And we’ve barely just learned about this. So it’s going to take some time.

[LAUGHTER]

IRA FLATOW: Yeah. Because people are making decisions on the risk about what they hear in these cases.

SASKIA POPESCU: Exactly. And it’s going to take time. Yeah. And so I think we just need to be patient and wait for the data to come in a little bit.

IRA FLATOW: Michael, I know your lab at Washington University has been looking at how different variants impact the respiratory tract. And you found something interesting about Omicron and the lungs. Explain to us what you found.

MICHAEL DIAMOND: Yeah. So we’ve been interested in trying to understand whether there are differences in the ability for Omicron to infect the upper airway and the lower airway, which it seems to be what we’re seeing in humans. As Saskia alluded to, we’re seeing perhaps more upper respiratory infection and really severe lung infections.

And so to model that, we’ve been studying animal models– rodent models– mice and hamsters. And what we found in all of the different strains of mice that we tested and was multiple ones– and all of the hamsters– and this was a group through the NIH collection of investigators, so about 10 investigators independently working very quickly. In every case, we saw attenuation of Omicron in the animals, meaning that they were able to infect the upper airway, but just less frequently able to cause infection in the lung or cause pneumonia.

IRA FLATOW: Does that mean we’re seeing less scarring in the lungs, less than with the previous variants?

MICHAEL DIAMOND: I think we have to be a little careful here. Because it’s a little uncertain about extrapolating directly from animal models to humans. And I do agree with Saskia that we need additional data. Because when we do the animal models, they don’t have any pre-existing immunity. They don’t have a vaccine. They never were infected before in this particular case when we did the study.

We really need to know in humans who have never been infected, who have never been vaccinated before. Are we also seeing evidence of attenuation? And this would allow us then to make a more direct link between the animal studies and the human studies.

But as of now, we know definitively that if you have a vaccine or had a prior infection, you’re much more likely to get mild disease and not require severe interventions in a hospital. But we do not know yet in children under five that haven’t been vaccinated, even in adults that didn’t get vaccinated or infected. What is the course of disease? So I think it’s a little premature to predict exactly what’s going on. But the animal data would suggest that it may be more attenuated in the lower lung, but that needs to be corroborated.

IRA FLATOW: The tests we’ve used for COVID have largely been no swabs. But some experts are now saying that throat swabs, like how we test for strep throat, are better at picking up the Omicron variant. Does that make sense to you, based on what you found in the lab?

MICHAEL DIAMOND: Well, we certainly are able to in some of the animal models, particularly the hamster model and also even in non-human primates. Although we have not done those studies ourselves, can show that you can detect viral RNA, which is what’s used for these tests or even viral antigen in either nose swabs or in saliva.

And in fact, a number of the early diagnostic tests that were generated were saliva based. And they were done here. We implemented them at Washington University. And many schools at academic institutions and other places also use saliva-based PCR tests.

So sampling of saliva is much easier. It’s less invasive and has pretty good sensitivity. So I think that, certainly, we have evidence that a virus is present there. Whether it’s infectious in saliva is a different question, but certainly easy for diagnostic purposes.

IRA FLATOW: Saskia, let’s talk about hospitalizations. What do we know about how this big Omicron surge is impacting the health care system?

SASKIA POPESCU: Well, right now, we actually are seeing just such an unprecedented surge in cases. It’s over 247% increase in the last 14 days. So on January 5, the daily average was 585,000 new cases. But actually, that’s a running average.

So just on January 5, we saw over 704,000 new cases in the United States. And hospitalizations are also on the rise. So as reported on January 5 as well, the daily average is over 110,000 new people hospitalized, which is a 58% increase over 14 days.

So the numbers are growing every single day. This is really challenging. Because right now, even though we’re hopeful that Omicron means less severe disease, the issue is that we’re having staffing shortages. Nearly 20% of hospital facilities are reporting critical care staffing shortages.

And a lot of this is a result of staff getting sick and needing to call out. So you see that changing CDC guidance, also, about people able to return to work after five days or work while they’re in isolation with a mask on. And I think that’s really indicative of a staffing shortage across the US.

So hospitalizations are on the rise for patients, but also really straining the health care system in the winter, which is already one of our hardest seasons in health care. Because we have influenza, and respiratory viruses, and the fact that people have been avoiding medical care, because of COVID for a while or challenges to get medical care. So this is a really hard, unprecedented time. We’re moving into the third year of this pandemic. Health care workers are exhausted. And now, they’re getting sick. And we’re having staffing shortages. So our hospitals are severely strained.

IRA FLATOW: How much of that strain on the hospital system can be attributed to people who go to the hospital, but don’t need to go to the hospital?

SASKIA POPESCU: That’s a tricky question. That data will likely take time for us to understand. But right now, during the winter months, of course, you have a lot of people, as I mentioned, who have been maybe avoiding health care. Because they’re nervous about COVID, or it’s just been already so overwhelmed.

So we always see– I call them the worried well– people that maybe don’t need an emergency department. But maybe that’s their only access to care. Or maybe they’re very stressed, because they don’t feel well. We’re in the middle of this huge surge. And they want to get seen to know if they have COVID.

So that data point is hard to really understand. But we are seeing very busy emergency departments and especially with the staffing shortages coupled with testing shortages. People are really struggling to get tested for COVID, whether they feel that they have it, because they have symptoms or they’ve recently been exposed.

So, often, that leads people to go to emergency departments or other health care facilities, like urgent cares to try and get seen just to get tested. And that’s amplifying the strain. But right now, I can tell you from years doing this, hospitals get so stressed during the winter months. It’s just our busiest season. And it’s very, very stressful when you have staffing shortages and you’re in the middle of this very severe winter surge of COVID.

MICHAEL DIAMOND: Ira, if I can add a comment, I think there’s a couple points. And I totally agree. One thing is that in the emergency room, I think there is a certain percentage of people who may test positive for COVID who certainly are worried which way their illness is going to go. Are they going to get worse? Are they going to need an emergency visit?

And so they actually pre-empt it and just show up. Because they have major concerns, especially if they’re elderly or immunocompromised in any way. And this creates tremendous burden on the emergency department. Because then they’re not able to, in addition to all of the COVID patients, see their normal patients.

And as Saskia alluded to, in the winter months there’s many other illnesses that are occurring, flu and otherwise, in addition to all of the other trauma– cardiac, whatever other systems are compromised in individuals that require hospitalizations. The second thing is that at least in our hospital, and I’m sure in many across the country, we have stopped doing elective surgeries now in order to save beds and save staff to take care of COVID patients.

And of course, this is an issue. Because people may need surgeries. Although they may not be emergency, but they need to delay them. And this creates a problem for dealing with their current medical issues. So there are a lot of ramifications of having large numbers of infections that you’re not able to control. Because people aren’t vaccinated, or the vaccines aren’t working as effectively.

IRA FLATOW: I want to talk about kids for a moment. Because I know that there are more kids in hospitals now, during this Omicron surge than there have been before. Dr. Fauci said it may be overcounting. Because these kids may be in the hospital for something else. And while they’re there, they get tested and turns out they have infections. Do we know what is happening there, Saskia?

SASKIA POPESCU: I really, truly think it’s a little premature for us to understand. It’s going to take a few more weeks. Because again, this is the busiest time. When we were working in peds, you have so many kids coming in with respiratory illness already.

So it’s not surprising to see them getting tested, whether they’re coming in for another illness, surgery, or just feeling a little run down. And they end up testing positive for COVID-19. So I think that is a possibility. But in terms of Omicron, it’s still very early for us to understand its impact on pediatric patients.

IRA FLATOW: And speaking of pediatric patients, what about infants in daycare? I’m talking one to four-year-olds. Aren’t they still very vulnerable? Because they don’t have any vaccinations.

SASKIA POPESCU: Entirely. And I think that’s probably our biggest hurdle right now is that we’re focusing on boosters in adults and now encouraging them in children. But we have an entire age group that is unable to be vaccinated. And they’re back in school. They’re back in daycare. So they’re more likely to get exposed, but also when you add that to the holidays where everybody is gathering. And we are seeing so many exposures as a result of holiday parties and gatherings.

So I stress so much that it is so early in our understanding of Omicron and what that means for adults’ immunity and infection, but also children. But overwhelmingly, I think it’s important that we acknowledge vaccines have been very helpful and effective, even if we see a little bit of decreased efficacy against infection over time. For those who are truly vulnerable and unable to be vaccinated, it does pose a risk. But we just don’t know what that means for children right now.

IRA FLATOW: Michael, many of us who take COVID seriously are concerned about the possibility of long COVID where people have health complications weeks and even months after they’ve recovered from the virus. Is it too early to tell how Omicron and long COVID could mix?

MICHAEL DIAMOND: Ira, it’s a great question. And I think it’s in the back of our minds, both as infectious disease physicians, scientists, and otherwise. The short answer is we just don’t know. It is way too early to know. We don’t really fully understand long-haul COVID syndrome in the context of historical SARS-CoV-2 isolates in COVID-19.

In other words, why some people get it, and why some people don’t. It appears that certainly it’s in greater frequency in people who get severe disease. But it also occurs somewhat sporadically in people who didn’t have very severe disease. So then if you think about it in that way, then if it did occur in Omicron and we have larger numbers of people who get infected, it is possible we may be setting ourselves up for a large amount of it.

However, the reality is we just don’t know. And we don’t know all of the factors that lead to this clinical manifestation. And so until we really do, we’re not going to be able to predict this. So I would say that at this point, we need to watch out for it. We need to assess what’s going on. But it’s very difficult to predict whether Omicron is going to cause it at all. And if it does, whether it’s with less frequency or greater frequency. And so this is something that– I think it’s just too early.

IRA FLATOW: This is Science Friday from WNYC Studios, talking about the Omicron risk. And looking forward, what kinds of studies on Omicron would you like to do in your lab? What do you need to know? What do you want to know?

MICHAEL DIAMOND: Well, I think one of the things that we really want to know is, why is the virus more transmissible? And is it because it’s infecting the upper airway much, much better? Or are there other properties of the virus that enable it to be spread more easily?

For example, it’s more stable in certain types of droplets than other types of droplets. It has an ability to infect certain types of cells in the upper airway better in addition to what we know is its ability to evade antibody responses. So there are multiple factors that affect transmissibility of a virus. And I think we’re still at the very early stages of beginning to understand why Omicron appears to spread so much faster than even the other variants, such as Delta.

IRA FLATOW: Some people have expressed a fear that Omicron and Delta could mix together and form a superbug. Do you have that fear, Michael?

MICHAEL DIAMOND: Well, I would say that coronaviruses have the potential to recombine. And what that means is you can take one virus and another virus. And if a person or an animal, if it was a reservoir, got co-infected, some of the genetic material could exchange.

So that’s one mechanism of evolution of this virus in addition to just accumulating mutations. Because it’s RNA-dependent RNA polymerase, which allows it to generate its new RNA. It has some error capacity. So I would say it is possible that the virus could swap some gene segments or regions of it. But so far, we have not seen that in large scale. But it’s certainly something that we’re looking out for.

Saskia earlier alluded to the fact that we need to do and expand our genomic sequencing capacity to track, to see. How is Omicron changing in real time? So this needs to be done so that we can evaluate whether any types of these recombinations are occurring. So far, nothing like that has occurred. It is theoretically possible.

IRA FLATOW: Saskia, I give you the last word. Give us your takeaway point you want to leave our audience with when it comes to the severity of Omicron.

SASKIA POPESCU: I would say hold tight. You’re going to be seeing so much information coming in, as you already have, in the coming weeks and months about Omicron. Because we’re getting it anecdotally, small little bits, small studies. And to understand this means building a mosaic out of all these data points to get a better picture of what this new variant means in terms of transmission, but also disease severity.

So take it with a grain of salt and know that it takes time for us to understand these things. In some ways, we’re building the bridge as we cross it. But we have years now of data supporting us. And it’s just important to be patient and to not just see a single study and hit the panic button. We’ll get through this together.

IRA FLATOW: Dr. Michael Diamond, virologist and immunologist at the Washington University School of Medicine in St. Louis and Dr. Saskia Popescu, infectious disease epidemiologist and infection prevention expert at the University of Arizona College of Public Health in Phoenix, Arizona. Thank you both for taking time to be with us today.

MICHAEL DIAMOND: Thank you.

SASKIA POPESCU: Thanks so much.

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