A lab technician sorts blood samples inside a lab for a Covid-19 vaccine study at the Research Centers of America (RCA) in Hollywood, Florida on August 13, 2020. (Photo: Getty Images)
The fast-spreading UK variant of the new coronavirus is powered by a set of mutated proteins that give it several advantages over earlier versions of the virus, according to a new study.
The study, posted Monday on the web site bioRxiv, finds that the UK variant appears to enter cells more effectively than previous versions of the virus. Once inside cells, the variant then churns out copies of the virus faster and delays the body’s immune response.
These strengths have allowed the variant, first discovered in September 2020 in South East England, to outcompete other versions of the virus that causes COVID-19. In April, the UK variant became the dominant version of the virus in the U.S.
So far, scientists have found that the current vaccines work well against the UK variant, and against other variants that have appeared around the world.
However, there is no guarantee that the vaccines will continue to defeat all new variants.
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“The vaccines do work, but there may be a day when they don’t and we need to be prepared for that,” said Nevan Krogan, an author of the new study and director of the Quantitative Biosciences Institute (QBI) at University of California, San Francisco.
“We’re getting a little bit of a reprieve in certain parts of the world. We need to be one step ahead of the virus. The problem has been that the virus always seems to be four steps ahead of us.”
Nasia Safdar, director of infection control at UW Health in Madison, said the new study “is interesting because it suggests there are many ways a virus can evade the host’s immune response.”
Safdar, who did not participate in the research, was less certain that mutations in the new coronavirus will render the current crop of vaccines obsolete anytime soon.
“I think there is a chance that a variant will emerge where we will see reduced effectiveness in the vaccines,” she said. “Even if it is a little bit less effective, it would still be good enough.”
UK variant contains eight mutations
From early in the COVID-19 pandemic, Krogan has worked with a large group of collaborators around the world to map out how the virus and other coronaviruses work inside the human body. The team has shown which viral proteins attack which human proteins, an effort aimed at giving scientists more ways to block or disrupt the virus.
Many researchers have focused heavily on the virus’ Spike protein, which allows it to latch onto human cells and invade them. In their latest study, Krogan and collaborators from the U.S. and Britain have found that the UK variant contains eight mutations in the Spike protein. These “almost certainly allow the virus to enter cells more effectively,” Krogan said.
While devising vaccines and treatments to attack the Spike protein can help stop or slow the virus, they may be weakened if the virus continues to mutate. The fear is that the more the virus changes, the more likely it is to develop a variant that protects the Spike protein from the current crop of medicines.
Krogan said that developing vaccines and treatments that help our own proteins offers a key advantage to the strategy of looking for ways to weaken or stop viral protein. Human proteins don’t mutate nearly as fast as viral proteins do, making them less likely to lose their edge against the virus.
The new study of the UK variant also suggests that scientists should not focus all of their efforts on fighting the Spike protein.
Krogan and his team found that the UK variant contained 23 mutations that affected five of the virus’ proteins.
Mutations in two proteins — Orf9b and Orf6 — stop the human immune system from being turned up in response to the virus. This allows the virus to outpace our immune response.
“With Orf9b, there’s more of it in the cells infected with the UK variant,” Krogan said, adding that “it’s very rare for a mutation to result in there being more of a protein, but not actually changing that protein.”
Krogan said he and his collaborators plan to apply the same methodical approach they have used with the UK variant — mapping connections between human and viral proteins — with other variants.
They plan see how mutated proteins in the South African, Indian and other variants affect both the virus and the human response to it.
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