Study unravels the molecular mechanisms underlying influenza B virus pathogenicity

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Announcing a new article publication for Zoonoses journal. Influenza B virus is a significant respiratory pathogen responsible for seasonal influenza. In recent years the B/Yamagata lineage has demonstrated a rapid increase, predominantly featuring the neuraminidase (NA)N342K mutation. This study determined the impact of the NAN342K mutation on the pathogenicity of influenza B virus and elucidate the underlying mechanisms.

Gene fragments with specific mutations were generated using site-directed mutagenesis PCR, resulting in recombinant viruses (rAH127 and rAH127/NAN342K). C57BL/6 mice were infected to evaluate the impact of amino acid mutations on virus pathogenicity. Body weight, survival rate, virus replication, and lung pathology were compared among the groups. NA enzyme activity was assessed to determine the mechanisms underlying the effects of amino acid mutations on the pathogenicity of influenza B virus.
The NAN342K mutant virus exhibited significantly increased NA enzyme activity (3.19-fold) and viral replication capacity in MDCK cells (6.76-fold) compared to wild-type virus. These changes led to enhanced pathogenicity in

The NAN342K mutation likely enhances virus replication and pathogenicity by increasing NA enzyme activity. These findings contribute to understanding the molecular mechanisms underlying influenza B virus pathogenicity and have implications for targeted therapeutic strategies.

Source:
Journal reference:

Chen, Q., et al. (2023). NAN342K Mutation Enhances the Pathogenicity of Influenza B Virus in Mice. Zoonoses. doi.org/10.15212/zoonoses-2023-0013.

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