The principle findings of this study were as follows: (1) expression of the canonical Th17 cytokine IL-17 is significantly inhibited by in vitro HIV infection; (2) both in vivo and in vitro HIV infection significantly reduce IL-23-induced pSTAT3 expression which is not reversed in the setting of effective HAART; and (3) the observed reduction in IL-17 is not due to the effect of HIV infection on RORC mRNA expression in Th17 cells nor its effect on the IL-23 receptor expression. The gene discussed is IL17A; the disease is HIV infectious disease.