IFNA1 and infection: Subsequent studies suggested that the pp65 deletion mutant virus exhibited impaired expression of other important HCMV genes, including the immediate-early protein 2 (IE2), and found that a less-disruptive mutation of the pp65 ORF maintained viral inhibition of Type I IFN signaling during infection [32], indicating that pp65 may be more dispensable for inhibition of IFN signaling than was initially presumed.