This process can cause rapid shifts in the viral function. For example, reassortments of flu strains circulating in pigs, birds, and humans led to the H1N1 flu pandemic. Unlike influenza, however, coronaviruses possess no physical segmentation to undergo reassortment.
Coronaviruses can experience some shifts in function through a process known as recombination, when segments of one viral genome are spliced onto another by the enzyme making the viral copy. Understanding these evolutionary dynamics of SARS-CoV-2 is vital to ensure that treatments and vaccines keep pace with the virus.
For now, the available vaccines are effective in preventing severe disease from all the viral variants. Filling in these blanks could help us learn how to protect ourselves in the future. All rights reserved. The pace of evolution Mutations may happen randomly, but the rate at which they occur depends on the virus.
The wide world of viruses Mutations drive evolution, but they are not the only way that a virus can change over time. Share Tweet Email. Why it's so hard to treat pain in infants. This wild African cat has adapted to life in a big city.
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Animals Wild Cities Morocco has 3 million stray dogs. Meet the people trying to help. Do vaccines for viruses need to be updated when variants arise? Is that true with all viruses? Some people are trying to develop a universal influenza vaccine, to try to target the antibody generation toward a part of the molecule that cannot change without making the molecule not work anymore. But I think the evidence is that the variants are not escaping the vaccine dramatically. And of course, that also depends how quickly we can get this vaccination round to complete—how many different variants are going to emerge by the time most people are vaccinated.
The coronavirus definitely is not going to be like that. But if it does become endemic and it circulates in the population all the time, then there is a chance that a slightly different virus might emerge and we may need a booster. Another question is, as people become immune thanks to vaccinations, is that going to be a strong pressure on the virus? Variants may emerge because people are immune to the old virus.
Taylor McNeil can be reached at taylor. Skip to main content. By Taylor McNeil. June 9, Are there different varieties of virus genomes? And how do mutations happen? Are they different in DNA vs. We could say that a certain mutation occurred in England in this month and that virus strain started to spread. And we could trace back where viruses came from based on these unique mutations, but none of them really changed the way the virus itself replicated.
It's only now that we're getting into some of these variants that are changing the way the virus behaves in the population. And again, that's just a really small set of all the mutations that accumulate in these viruses. Well, you can't prevent the virus from mutating, but what you can do is limit the virus's spread, and in that way you reduce the chances that a mutation can emerge that is going to help the virus infect humans better. Say, for example, it's a one in a million chance that a mutation will be advantageous to the virus.
If you let the virus replicate itself , times, odds are that the advantageous mutation will occur. But if you limit the overall replication of the virus to 1, times, then it's much less likely that the random advantageous mutation is going to occur.
And I think we're seeing that now across the U. It's only spreading in unvaccinated people. So the strength of vaccination in terms of not only protecting people, but now limiting the emergence of other variants by reducing the overall replication of the virus in the population is clearly seen.
Essentially it's telling us that that original strain—which surprised us with how well it was able to spread in the human population—still has room for improvement. The basic Darwinian principles of natural selection are in play now.
The virus is changing to be able to spread better in the population, and when it gets better at spreading, it becomes the dominant virus—and we're seeing that occur over and over again. So clearly this virus came in with a good ability to replicate in humans, but it's finding ways to get better and become more of a human pathogen as opposed to what we used to call a zoonotic pathogen.
This probably means it's going to be a human pathogen for some time to come. My lab has spent a lot of time studying influenza, and many of the same types of experiments that we do with SARS-CoV-2 give us very different results than the same experiment done with influenza. So while those two viruses spread in the same way and are causing disease in the respiratory tract, they do things in very different ways.
And so it's going to be very important for us to understand how two respiratory viruses can cause such different disease at the molecular level. While there's already been thousands of papers published on SARS-CoV-2, I think we've only scratched the surface in terms of understanding how this virus is causing damage in people—we don't really understand that in any detail. Comparing it to other respiratory viruses is going to be something that's really, really important for us to do because, again, that's going to tell us different signatures that we may need to look for in animal viruses that may tell us whether or not an animal virus is potentially a human pathogen.
But I would emphasize the important thing, which is the vaccines are still working, and the vaccines are working against the delta variant—particularly the mRNA vaccines.
If you've gotten the full course of mRNA vaccine, you've got pretty good protection against these variants.
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