The new coronavirus variant JN.1 may have become dominant due to a single mutation

One mutation may have been crucial for the JN.1 variant of COVID-19 that spread rapidly around the world last year, showing how quickly viruses can adapt.

“The single mutation in JN.1 was the key to evading antibody responses, which is why it was able to spread around the world.” Emanuele Andreano At the Tuscany Life Sciences Foundation, Italy.

JN.1, a variant of the Omicron variant, was first identified in Luxembourg in August 2023. accounted for 88 percentwhich accounts for 85% and 77% of recorded infections in the United States, the United Kingdom and Australia, respectively. Its predecessor, BA.2.86, never accounted for more than 5% of known infections worldwide.

JN.1 and its descendants remain the most commonly reported COVID-19 variants worldwide, and Andreano and his colleagues wanted to investigate why it has spread so widely. Genetic sequencing had previously shown that the spike protein the virus uses to infect host cells has additional mutations compared to BA.2.86.

To learn more, Andreano and his colleagues analyzed 899 antibodies from blood samples taken previously from 14 people who had received two or three doses of an mRNA COVID-19 vaccine and had been confirmed to have been infected with an earlier variant.

The researchers added each of these antibodies to a dish of monkey cells along with the BA.2.86 SARS-CoV-2 virus. They found that 66 of 899 antibodies were able to stop BA.2.86 from infecting the cells. When they repeated the experiment with JN.1, only 23 antibodies were able to block infection.

The researchers then used computer simulations to test how a mutation in JN.1’s spike protein helped it evade neutralizing antibodies that block the virus from entering cells. They found that the mutation, which replaces a long amino acid called leucine with a shorter one called serine, weakened or completely blocked antibodies from interacting with the spike protein.

The antibodies that prevented JN.1 infection in monkey cells were collected from five of the 14 blood sample donors. These individuals had “super-hybrid” immunity that arose from three doses of the mRNA vaccine, one infection with the first SARS-CoV-2 variant identified in Wuhan, China, and then a second infection with the Omicron variant, according to Andreano. These antibodies may bind to other parts of the spike protein away from the mutation site and prevent JN.1 infection, Andreano said.

The study suggests that a single mutation may have been key to allowing JN.1 to evade neutralizing antibodies, but it still doesn’t cause any more severe disease than previous mutations, Andreano said.

That’s probably because there are many other parts of the immune system, such as T cells, that, although they cannot prevent infection, do work to stop the virus from causing severe disease, he said. Jonathan Ball “Overall, people’s immunity remains strong,” said the professor at the Liverpool School of Tropical Medicine in the UK.

The antibodies the researchers found are similar to those previously found in populations around the world, but the study is still small and needs to be replicated in larger groups, the researchers said. Darran Bailey At the Pirbright Institute, UK.