It is clear that SARS-CoV-2, the agent of the Covid-19 epidemic, is here to stay. Like influenza, an easily transmissible respiratory virus, SARS-CoV-2 mutates to evade the immune system of those who have been previously vaccinated, infected, or both.
KP.2 belongs to a group recently characterized as the FLiRT variants. This name is derived from the technical designations of two critical mutations in their spike proteins: the F456L mutation and the R346T mutation. As with JN.1, many spike protein mutations in KP.2 are also present in earlier variants of concern, including E484K and N501Y. These variants, known as the Alpha and Beta variants of SARS-CoV-2, were first detected in early 2021.
In the receptor-binding domain, just one change from JN.1 could significantly impact F456L, which may enhance ACE2 binding affinity or decrease antibody binding efficiency. I have noted the extensively mutated N protein. Mutations at R203K and G204R have been present in most virus variants during the pandemic and are likely to enhance the rate of viral replication. Although these mutations are identical to those in JN.1, the N protein continues to play a crucial role in the virus's pathogenicity.
In fact, there are numerous synonymous mutations scattered throughout KP.2, but gathering data on these mutations is much more complex than collecting data on amino acid mutations.
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Source: TeenVogue - 🏆 481. / 51 Read more »