Abstract: Influenza virus is a kind of RNA virus which is harmful to human and animal health. Its effective replication in host cells cannot be achieved without the assistance and support of host protein acidic nuclear phosphoprotein 32 family member A (ANP32A) and virus RNA polymerase. Viral RNA polymerase consists of three proteins:PB1, PB2 and PA, and the strongest interaction between ANP32A and viral RNA polymerase requires the participation of these three proteins. ANP32A is a member of the acidic leucine-rich nuclear phosphoprotein 32 (ANP32) family. It has been identified as a key host factor supporting the activity of viral RNA polymerase in the nucleus and plays an important role in Influenza virus replication. The species-specific difference of ANP32A determines the host range of viral RNA polymerase:A unique 33 amino acid sequence exists in avian ANP32A (avANP32A), but lacks this amino acid sequence in mammalian ANP32A. The 33 amino acid sequences unique to avANP32A can enhance the function of ANP32A, thus increasing the polymerase activity of Avian influenza virus (AIV). AIV cannot make effective use of short ANP32A (that is, ANP32A lacking a unique 33 amino acid sequence), so mammalian ANP32A cannot support avian characteristic polymerase activity. However, inserting these 33 amino acids into human ANP32A (huANP32A) can promote its support for AIV polymerase. Adaptive mutation of Influenza virus can also enhance the transmission and pathogenicity of AIV in mammals. E627K mutation often occurs when AIV adapts to mammals to enhance its replication ability in mammals. This review mainly introduced the effect of host protein ANP32A on replication and transcription of Influenza virus and the mechanism of adaptive mutation of Influenza virus, and briefly discussed the molecular mechanism of the interaction between ANP32A and polymerase on Influenza virus cross-species infection.

Key words: Influenza virus; ANP32A; Influenza virus polymerase