Consider This from NPR - The Intensifying Race Between Coronavirus Variants And Vaccines

Episode Date: February 16, 2021

There's evidence of at least seven U.S. variants of the coronavirus, while another that emerged from the U.K. is poised to become the dominant strain here by the end of March. One adviser from the Food and Drug Administration tells NPR there's a tipping point to watch for: when a fully vaccinated person winds up hospitalized with a coronavirus variant.NPR science correspondent Richard Harris reports on concerns that COVID-19 vaccines themselves could cause the virus to mutate. NPR science reporter Michaeleen Doucleff explains why the story of one COVID-19 patient may hold clues to how variants develop in the first place. For a deeper dive on variants, listen to Michaeleen's recent episode of NPR's Short Wave on Spotify or Apple Podcasts. In participating regions, you'll also hear a local news segment that will help you make sense of what's going on in your community.Email us at [e-mail] more about sponsor message choices: podcastchoices.com/adchoicesNPR Privacy Policy

The race between variants and vaccines is heating up. I think what we learned early on as we started to see variants emerge was there was the potential that this could happen, right? Peter Marks heads the FDA's Center for Biologics Evaluation and Research. He said in a webcast recently, the Food and Drug Administration is already thinking about how to fast-track new versions of existing vaccines if coronavirus variants make the old versions less effective. With the mRNA, it's very convenient because basically all you do is change a computer program and you can change the vaccine. He said some vaccines could be tweaked with relative ease, and the FDA wouldn't have to require a new round of large clinical trials.

We would intend to try to be pretty nimble with this so that we get these variants covered as quickly as possible because it is clear that they can spread pretty quickly. And in fact, just this week, scientists reported evidence of at least seven homegrown variants here in the U.S. That's in addition to variants from Brazil, South Africa, and the U.K. So far, there's no indication that any of these variants would require a new vaccine. You know that a line is crossed if you see people who are fully immunized with these vaccines

that nonetheless, when infected with a variant, are being hospitalized. FDA advisor Dr. Paul Offit. That's when the line gets crossed. And to date, that has not happened. Consider this. So far, vaccines have stayed one step ahead of new coronavirus variants. What scientists don't know is how long that will last. From NPR, I'm Adi Kornish. It's Tuesday, February 16th.

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Because there's evidence it creates more virus in a person's nose and respiratory tract, making it more transmissible. You very quickly start infecting many, many, many more people than you would have beforehand. Emma Hodcroft is an epidemiologist at the University of Bern in Switzerland. The UK variant does appear to be deadlier, according to British scientists, and that's a reversal from earlier assessments. But the fact that it's more transmissible might be an even bigger problem. Perhaps counterintuitively to some people, I think that transmissibility is probably the worst of these two scenarios. Because if something is more transmissible, then you just get it into a larger population. By the end of March, the UK variant is expected to become the dominant form in the US.

But tracking its spread will not be easy. Unfortunately, many regions are still severely undersampled, and unfortunately, the odds are that there are more lineages in our midst, sort of like a constellation of small variants. Von Cooper with the University of Pittsburgh told NPR that the U.S. is not doing a great job tracking viral variants with genomic sequencing. Elsewhere around the world, with the U.K. really leading the way in terms of the numbers of genomes that they've sequenced,

in fact, in Australia, nearly half of all cases have been sequenced. In the United States, we're around 40th among countries currently. Cooper said basically the U.S. hasn't had a coherent national strategy for doing the kind of scientific detective work needed to identify new variants. The CDC says they're working on it. So over the last three weeks or so, we've increased our sequencing about tenfold. CDC Director Rochelle Walensky said in a recent briefing, the government plans to ramp up sequencing even more over the next several weeks,

which means you'll probably be hearing about even more variants in the future. So as we look more, we're certainly going to anticipate we might find more. As of the beginning of this week, the agency had cataloged more than 1,000 cases of the U. the UK variant across 40 U.S. states. While scientists watch for emerging variants, there's also a worry that COVID vaccines themselves could drive the coronavirus to mutate. But NPR science correspondent Richard Harris reports that's not cause for alarm. Not yet, anyway. You may have heard that bacteria can develop resistance to antibiotics and, in a worst-case scenario, render the drugs useless. Something similar can also happen

with vaccines, though with less serious consequences. This worry has arisen mostly in the debate over whether to delay a second vaccine shot so more people can get the first shot quickly. Paul Binoche, a Howard Hughes investigator at the Rockefeller University, says that gap would leave people with only partial immunity for longer than necessary. They might serve as sort of a breeding ground for the virus to acquire new mutations. That's because the virus is always mutating, and if one happens to produce a mutation that makes it less vulnerable to the vaccine, that virus could simply multiply in a vaccinated individual. But even if that happens, that's only one step in the process. What's really unclear and really quite important for the virus to evolve

is whether those people that having been vaccinated and infected, whether they have sufficient levels of virus replication to pass the virus on to other people. If the vaccine keeps virus levels low, even mutated viruses, the infected person won't produce enough to spread to other people. If the vaccine keeps virus levels low, even mutated viruses, the infected person won't produce enough to spread to other people. Unfortunately, at the moment, scientists can't answer the most basic questions about this process. How much does the virus actually replicate inside a person who has been vaccinated with either one dose or two? And how effective is that vaccine at limiting infection enough so that the virus levels stay low and prevent the spread to other people? Andrew Reed at Penn State University says whatever the

answers may be, vaccine resistance, or escape as it's called, isn't nearly as scary as bacteria becoming resistant to antibiotics. I know everybody's worried about it, but I would say history tells us that vaccine escape does not erode to zero. It does not erase vaccine protection. A vaccine may become less potent, but in other cases where this has happened, it still works. It's often got very strong anti-disease properties, so you get less sick even with the viruses that are around. And this evolutionary pressure is present for any vaccine that doesn't completely block infection. So it's not just an issue for people who are between their initial shot and a booster. Many vaccines, apparently including the COVID vaccines, do not completely prevent a virus from multiplying inside someone, even though these

vaccines do prevent serious illness. I do think there are a lot of options here for trying to deal with any evolution should it occur. One thing that helps is that dozens of vaccines are being developed and more than half a dozen are already in use. One of the great things about having a lot of vaccine options is we might end up with a population which is heterogeneously vaccinated. You might get the AstraZeneca and I'm going to get one of the mRNA ones. That'll really help hinder the spread of mutants that are good at any one of those. A virus that has evolved to get around one vaccine is likely to be stopped by another, and that will limit the spread of mutant strains. Drug makers are also keeping a close eye on mutants and are already formulating new vaccines

that will be more effective if it turns out the original vaccines weaken too much. Paul Binoche says this is not a crisis. We're not going to fall off a cliff tomorrow in terms of vaccine efficacy, what we're likely to see is a slow, steady erosion of efficacy over perhaps quite a long period of time. Binar says to slow this evolutionary process as much as possible, it's important to slow the spread of the virus right now, so people who get vaccinated are at lower risk for getting infected in the first place. NPR science correspondent Richard Harris. Scientists are trying to learn more about coronavirus variants by studying the case of one extraordinary COVID-19 patient.

And this patient was a 45-year-old man who was admitted to a Boston hospital last spring. Doctors at Brigham and Women's Hospital treated him. He got better and he was discharged. But his infection never went away. This is an extraordinary individual who was readmitted over the subsequent five months for recurrence of his COVID infection and severe pneumonia. Dr. Jonathan Lee, one of the doctors who treated the man, says he was not a so-called long hauler, a person who clears their COVID infection but has lingering after effects, sometimes for months.

This man, Lee says, had a living, growing virus in his body for 154 days. That is one of the remarkable aspects of this case. And in fact, he was highly infectious, even five months after the initial diagnosis. Lee spoke to NPR science reporter Michaelene Duclef, who picks up the story from here. Lee says the man's immune system wasn't working normally. He was taking immunosuppressive drugs for a chronic illness, so his body couldn't fight off the virus very well. But Lee also wondered if perhaps the virus was taking advantage of this unusual situation. With so much time inside the man, the virus might have the opportunity to test

out different versions of itself and find more infectious versions. So Lee and his colleagues began to examine the virus's genes. I was shocked. Shocked because the virus was mutating very quickly inside the man's body. These mutations allowed it to evade his immune system to escape detection by antibodies. When I saw the virus and the viral sequence, I think I knew then that we were dealing with something completely different and potentially very important.

Completely different because the virus had a whole collection of mutations, not just one or two, but more than 20. Scientists had never seen this before during the whole pandemic. Lee and his team published the findings in the New England Journal of Medicine. The report didn't even make big news. That was November 2020. Then about a month later... A new coronavirus variant causing international concern.

As NPR's David Green reported, scientists this past December detected new genetic variants of the virus, one in the UK, one in South Africa, and then later one in Brazil. Guess what these variants have in common with the virus in the Boston patient? A sudden collection of multiple mutations in a combination that is worrisome. That's Jeremy Lubin. He's a virologist at the University of Massachusetts Medical School. He says these new variants look remarkably similar to the virus Lee and his colleagues found in their patient. They aren't the same, but they share important characteristics. They both have about 20 mutations, and they have ones that make the virus more contagious. And so right now, Lubin says, one hypothesis is that the new variants, the one from

the UK, South Africa, and Brazil, arose inside people like the Boston patient, people with these long-term infections and who are immunocompromised. Because their immune system was not working normally, they could not eliminate the virus. And over time, the virus then acquired a collection of mutations that otherwise had not been seen before. In other words, the virus used this long-term infection as a testing ground to try out different mutations and see which ones evade the immune system, become more infectious, and eventually spread more easily around the world. Science reporter Michaelene Ducliffe, who has been on top of this variant story for NPR.

For more of her work, we've got some links in our episode notes. It's Consider This from NPR. I'm Adi Cornish.