A new genetic variant of SARS-CoV-2, the virus that causes COVID-19, has emerged in the United Kingdom, but it's unlikely to threaten the effectiveness of COVID-19 vaccines, scientists say.
New "variants" of the coronavirus emerge as the virus makes copies of itself and picks up genetic mutations; the mutations in a given variant may or may not change how the virus infects cells or how easily it spreads, so scientists keep track of the changes to determine which ones might pose a potential risk.
Now, researchers in the U.K. have identified a new variant that has caused infections in nearly 60 local authority areas, Health Secretary Matt Hancock said Dec. 14 while addressing the House of Commons, The Guardian reported. That amounts to more than 1,100 total infections caused by the new variant, predominantly in southern and eastern England, according to a statement from Public Health England (PHE), an agency in the Department of Health and Social Care.
"High numbers of cases of the variant virus have been observed in some areas where there is also a high incidence of COVID-19," the statement noted. "It is not yet known whether the variant is responsible for these increased numbers of cases."
In other words, we don't yet know if the new variant spreads more easily than other variants of the virus. While the rising number of infections could be linked to a genetic mutation that lets the variant spread easily, it may have also become widespread by chance as infected individuals interacted with others and set off chains of transmission. In the coming weeks, both PHE and the World Health Organization (WHO) will study the new variant and track its spread to determine whether it's more transmissible, Hancock said.
Again, the emergence of this new variant is "not unexpected," Dr. Susan Hopkins, the medical adviser for the U.K.'s Test and Trace program, said in the statement. In fact, new variants of the virus have cropped up throughout the pandemic, with some infecting more people than others, Live Science previously reported.
"It's important that we spot any changes quickly to understand the potential risk any variant may pose," Hopkins said. Currently, there's no indication that the variant identified in the U.K. causes more-severe illness than others in circulation, she said. In addition, there's no evidence that COVID-19 vaccines would work differently against the variant, according to the statement.
In general, any single genetic mutation is unlikely to make COVID-19 vaccines less effective, Live Science previously reported. That's partly because the vaccines prompt the immune system to build different types of antibodies, which then target different sites on the coronavirus, Dr. Alex Greninger, an assistant director of the Clinical Virology Laboratory at the University of Washington Medical Center, told Live Science in an email.
The leading vaccines, including the now-authorized Pfizer-BioNTech vaccine, specifically target the spike protein — a pointed structure on the virus that plugs into cells to start infection — but antibodies can latch onto many different sites along that spike. If the spike develops a mutation in just one spot, the remaining assortment of antibodies can still grab hold elsewhere. That means, since vaccines generate a variety of antibodies, subtle mutations in the virus shouldn't make them less effective.
That is likely the case with the new coronavirus variant, which picked up a mutation in its spike protein, according to the PHE statement. To confirm that enough antibodies still recognize the mutant virus, scientists can run experiments in which they incubate the viral particles, vaccine-generated antibodies and cells together in the lab, Greninger said.
"If the spike protein changes such that it can at least partially evade the antibody that's trying to lock into it … then that would impair the effectiveness of the vaccine," said Dr. William Schaffner, an infectious-disease specialist at Vanderbilt University Medical Center in Nashville, Tennessee. Again, a subtle change in the spike protein likely wouldn't pose a problem, but scientists are checking anyway, he said.
In addition to looking at antibody responses, scientists can study whether the new mutations change how the virus functions, including whether it infects cells more efficiently compared with other variants. For example, in laboratory studies, some spike protein mutations enable the virus to bind more tightly to the ACE2 receptor — its preferred gateway into human cells — according to a report published Aug. 11 in the journal Cell.
However, the way the virus binds to cells in a dish doesn't always translate to how infectious it is in the wild, Schaffner said. Laboratory studies must be paired with data from real-world scenarios to determine how easily a particular variant spreads, he said. To compare two variants, scientists would need similar field data related to both; for example, one could compare the rate of spread between similar long-term care facilities, schools or cities with comparable public health restrictions in place.
When it comes to the new variant in the U.K., "we don't know that much about it yet," Schaffner said. Upcoming research by the PHE, WHO and other scientific groups should offer insight into whether the mutation has altered the virus's biology in any consequential way. Based on the more than 1,000 reported infections caused by the new variant, it doesn't appear to cause more-severe disease than other versions of the virus. However, it's still unclear whether the variant is more transmissible.
Originally published on Live Science.
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Nicoletta Lanese is the health channel editor at Live Science and was previously a news editor and staff writer at the site. She holds a graduate certificate in science communication from UC Santa Cruz and degrees in neuroscience and dance from the University of Florida. Her work has appeared in The Scientist, Science News, the Mercury News, Mongabay and Stanford Medicine Magazine, among other outlets. Based in NYC, she also remains heavily involved in dance and performs in local choreographers' work.