United States: One crucial mutation of COVID-19 deadly variant JN.1 can again make it a concern for the world. The concern linked to the same was raised by health officials because the variant spread rapidly across the world last year, which shows that the virus can adapt swiftly.
While addressing the same, an expert at the Toscana Life Sciences Foundation in Italy – Emanuele Anderano, stated, “A single mutation in JN.1 was key for it to evade the antibody response, and that’s why it was able to spread globally,” according to newscientist.com.
JN.1 variant and its spread across the world
According to the reports, the subvariant of the omicron – JN.1, was identified in Luxembourg in August 2023. However, by the end of January 2024, the variant was responsible for the around 88 percent in the United States, 85 percent in the United Kingdom and 77 percent in Australia.
However, its predecessor – BA.2.86, was responsible for just more than 5 percent of known cases, globally. It is to be noted that JN.1 and its descendants were the most reported cases across the world, which forced Anderano and his colleagues to investigate how the strain can spread so fast.
When compared to the previous strain – BA.2.86, just one additional genetic sequencing in its spike protein was reported as compared to the latest strain.
Around 899 types of antibodies from the blood samples – collected from 14 people – were analyzed by Anderano and his colleagues to study the same. According to the reports, all the participants received two or three doses of an mRNA COVID-19 vaccine and had previously been infected with any of the prior variants, according to newscientist.com.
Out of the total 899, around 66 prevented BA.2.86 from infecting the cells.
Following this, the experiment was repeated with the JN.1 variant, which showed that only 23 of the antibodies prevented infection.
In the subsequent phase of their investigation, the scholars employed a computational model to simulate how the mutation in JN.1’s spike protein might have facilitated its evasion of neutralizing antibodies, which serve as barriers preventing viral entry into cells. Their findings indicated that the mutation led to the replacement of a longer amino acid, leucine, with a shorter one, serine. This alteration potentially diminished or entirely obstructed the antibodies’ ability to interact with the spike protein.
The antibodies that successfully thwarted JN.1 infection in simian cells were derived from five of the 14 blood donors. These particular individuals exhibited what Andreano describes as “super hybrid” immunity, a result of receiving three doses of mRNA vaccines, an initial infection by the original SARS-CoV-2 variant identified in Wuhan, China, followed by a subsequent infection by an omicron variant. According to Andreano, these antibodies might target other regions of the spike protein, away from the mutation site, thus preventing JN.1 infection, as reported by newscientist.com.
The research underscores the pivotal role a singular mutation may have played in enabling JN.1 to bypass neutralizing antibodies. However, Andreano emphasizes that this does not translate to an increase in the severity of illness compared to earlier variants.
This is likely due to the presence of various other components of the immune system, such as T-cells, which continue to mitigate the severity of illness even if they do not prevent infection, notes Jonathan Ball of the Liverpool School of Tropical Medicine in the UK. “Collectively, people’s immunity remains robust,” he asserted, according to newscientist.com.
The antibodies analyzed by the researchers bear similarities to those previously identified in global populations. Nonetheless, Dalan Bailey from The Pirbright Institute in the UK cautioned that the study’s limited scope necessitates replication in more extensive cohorts.