The results indicated that infection with the rSIV NS1 S42P and S42P/ D92E virus readily induced relatively high levels of IFN-α and IFN-β production compared to the wt virus, which was equivalent to a 2.04- and 3.19-fold increase after rSIV NS1 S42P infection, and a 2.21- and 3.62-fold increase, respectively, after rSIV NS1 S42P/ D92E infection (Fig. 4a). Here, IFNB1 is linked to infection.