AML1 protein interacts with Influenza A virus neuraminidase and upregulates IFNβ response in infected mammalian cells.

Gaur, Pratibha; Kumar, Purnima; Sharma, Abhinay; Lal, Sunil K

Neuraminidase (NA) is an integral membrane protein of Influenza A virus (IAV) and primarily aids in the release of progeny virions, following the intracellular viral replication cycle. In an attempt to discover new functions of NA, we conducted a classical yeast two-hybrid screen and found acute myeloid leukemia marker 1 (AML1) as a novel interacting partner of IAV-NA. The interaction was further validated by co-immunoprecipitation in IAV infected cells and in an in-vitro coupled-transcription translation system. Interestingly, we found an increase in the expression of AML1 upon IAV infection in a dose dependent manner. As expected, we also observed an increase in the IFNβ levels, the first line of defense against viral infections. Subsequently, when AML1 was downregulated using siRNA, the IFNβ levels were found to be remarkably reduced. Our study also shows that AML1 is induced upon IAV infection and results in the induction of IFNβ. Thus, AML1 is proposed to be an important player in IFN induction and has a role in an anti-viral response against influenza A virus infection.