Among its isoforms, IL-32γ is the most extensively investigated, with findings indicating that it can drive the host anti-HIV mechanisms to control viral infection through multiple mechanisms: (1) promotion of the production of anti-viral mediators and molecules such as IFNα/β, APOBEC, and MxA; (2) the blocking of HIV entry into the target cell by downregulating the viral target receptor and co-receptor; (3) suppression of viral reverse transcriptase; and (4) potentiation of ART activity by inducing the reactivation of latent viral infection. Here, IFNA1 is linked to viral infectious disease.