Lineage B.1.617 is a lineage of SARS-CoV-2, the virus that causes COVID-19.[1] It first came to international attention in late March 2021 after the newly established INSACOG performed genome sequencing on positive samples throughout various Indian states. Analysis of samples from Maharashtra had revealed that compared to December 2020, there was an increase in the fraction of samples with the E484Q and L452R mutations.[2] Lineage B.1.617 later came to be dubbed a double mutant by news media.[3]
Lineage B.1.617 has three sublineages according to the PANGO nomenclature:
- B.1.617.1 (Kappa variant), first detected in India in December 2020
- B.1.617.2 (Delta variant), first detected in India in late 2020
- B.1.617.3, first observed in January 2021[4]
Here are some of the common mutations present in the spike protein of lineage B.1.617. Not all sublineages of B.1.617 share the same mutations:
- L452R. The substitution at position 452, a leucine-to-arginine substitution, confer stronger affinity of the spike protein for the ACE2 receptor and decreased recognition capability of the immune system.[5][6] These mutations, when taken individually, are not unique to the variant; rather, their simultaneous occurrence is.[5][7] This mutation is present in all three sublineages of B.1.617.
- T478K. The substitution at position 478, a threonine-to-lysine substitution,[8] is only found in lineage B.1.617.2.[9]
- E484Q. The substitution at position 484, a glutamic acid-to-glutamine substitution, confers lineage B.1.617 stronger binding potential to the human ACE2 receptor, as well as better ability to evade hosts' immune systems in comparison to other variants. This mutation is not present in the B.1.617.2 genome.[10]
- D614G. The substitution at position 614, an aspartic acid-to-glycine substitution, is shared with other highly transmissible lineages like B.1.1.7, B.1.351 and P.1.[11]
- P681R. The substitution at position 681, a proline-to-arginine substitution, which, according to William A. Haseltine, may boost cell-level infectivity of the variant "by facilitating cleavage of the S precursor protein to the active S1/S2 configuration".[10] This mutation is present in all three sublineages of B.1.617.
https://en.wikipedia.org/wiki/SARS-CoV-2_lineage_B.1.617
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