tetano
Editor, Senior Moderator
DNA Cell Biol
. 2025 Sep 19.
doi: 10.1177/10445498251379681. Online ahead of print. Polymorphism of BIK as a Host Risk Factor for Severe Influenza
Sourabh Soni[SUP] 1 [/SUP], Yohannes A Mebratu[SUP] 1 [/SUP]
Affiliations
This essay focuses on a key host factor, the protein BIK (Bcl-2-interacting killer), that influences the severity of influenza A virus (IAV) infections. Our recent research published in Proceedings of the National Academy of Sciences describes a novel IAV-BIK-β5 axis that is critical for viral replication. The study demonstrates that BIK is essential for efficient IAV replication, and its overexpression leads to increased viral loads, lung inflammation, and heightened mortality in mouse models. We also identified a single nucleotide polymorphism (SNP), rs738276, in the BIK gene's promoter. This SNP influences the basal expression of BIK, and individuals with the high-expression AA genotype are at a higher risk for severe influenza. The molecular mechanism involves the viral nucleoprotein (NP) suppressing the proteasome's β5 subunit, which leads to BIK accumulation and promotes viral replication. These findings identify BIK as a potential therapeutic target and the rs738276 SNP as a biomarker for personalized medicine.
Keywords: BIK (Bcl-2-interacting killer); host-virus interactions; influenza; polymorphism; proteasome.
. 2025 Sep 19.
doi: 10.1177/10445498251379681. Online ahead of print. Polymorphism of BIK as a Host Risk Factor for Severe Influenza
Sourabh Soni[SUP] 1 [/SUP], Yohannes A Mebratu[SUP] 1 [/SUP]
Affiliations
- PMID: 40971288
- DOI: 10.1177/10445498251379681
This essay focuses on a key host factor, the protein BIK (Bcl-2-interacting killer), that influences the severity of influenza A virus (IAV) infections. Our recent research published in Proceedings of the National Academy of Sciences describes a novel IAV-BIK-β5 axis that is critical for viral replication. The study demonstrates that BIK is essential for efficient IAV replication, and its overexpression leads to increased viral loads, lung inflammation, and heightened mortality in mouse models. We also identified a single nucleotide polymorphism (SNP), rs738276, in the BIK gene's promoter. This SNP influences the basal expression of BIK, and individuals with the high-expression AA genotype are at a higher risk for severe influenza. The molecular mechanism involves the viral nucleoprotein (NP) suppressing the proteasome's β5 subunit, which leads to BIK accumulation and promotes viral replication. These findings identify BIK as a potential therapeutic target and the rs738276 SNP as a biomarker for personalized medicine.
Keywords: BIK (Bcl-2-interacting killer); host-virus interactions; influenza; polymorphism; proteasome.