To further understand the attenuation mechanism dependent on the amino acid residue at G333 on aspects of viral infection and IFN responses in astrocytes, we investigated the tropism for astrocytes using a recombinant HEP-Flury strain (rHEP; Glu333) and a single amino acid mutant HEP333R strain (Arg333) in vitro. This evidence concerns the gene IFNA1 and viral infectious disease.