Corona variant JN.1 could become dominant due to just one mutation

One mutation may have played a key role in the JN.1 COVID-19 variant that spread rapidly worldwide last year, showing just how quickly the virus can adapt.

“A single mutation in JN.1 was critical to evading the antibody response, and that’s why it was able to spread globally,” he says. Emanuele Andreano From the Tuscany Foundation for Life Sciences in Italy.

A subvariant of the Omicron variant, JN.1, was first identified in Luxembourg in August 2023. In late January, It accounted for 88 percentIt accounted for 85% and 77% of infections recorded in the United States, the United Kingdom, and Australia, respectively. The previous version, BA.2.86, never accounted for more than 5% of known global infections.

While JN.1 and its descendants remain the most widely reported COVID-19 variants worldwide, Andreano and his colleagues wanted to investigate how they had spread so widely. Previous genetic sequencing had pointed to additional mutations compared to BA.2.86 in the spike protein the virus uses to infect host cells.

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

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

Next, the researchers used computer simulations to test how the mutation in JN.1’s spike protein helped the virus evade neutralizing antibodies that prevent it from entering cells. They found that the mutation changed a long amino acid called leucine to a short amino acid called serine, weakening or completely blocking the antibodies from interacting with the spike protein.

The antibodies that prevented JN. 1 infection in monkey cells came from five of the 14 blood donors. Andreano says these individuals had “super hybrid” immunity, which means they had received three doses of the mRNA vaccine, been infected once with the original SARS-CoV-2 variant identified in Wuhan, China, and then been infected again with the Omicron variant. Andreano says these antibodies could bind to a different part of the spike protein away from the mutation site, and thus prevent JN. 1 infection.

The study shows that a single mutation may have been important in allowing JN.1 to evade neutralizing antibodies, but it still doesn’t cause more severe disease than previous variants, Andreano says.

He says this is likely because there are many other parts of the immune system, such as T cells, that work to block viruses that cause serious disease, even if they can’t prevent infection. Jonathan Ball “The population’s collective immunity remains strong,” he says, from the Liverpool School of Tropical Medicine in the UK.

The antibodies the researchers collected are similar to those previously found in people around the world, but they say the study is still small and needs to be replicated in larger groups. Dalan Bailey At the Pirbright Institute in the UK.