Thirdly, in another study by Cheng et al., IFNAR was blocked from weeks 6–10 post-infection (i.e., the chronic phase of infection) (127) resulting in increased viral replication correlating with elevated T cell activation, suggesting that IFN-Is suppress HIV-1 replication during the chronic phase but are not essential for HIV-1-induced aberrant immune activation (127). This evidence concerns the gene IFNA1 and infection.