Unlike pathologies such as multiple sclerosis where S. mansoni SEA seems to downregulate autoimmune inflammation mediated through IFN-γ, TNF-α, and IL-17 by inducing suppressor of cytokine signaling 3 (SOCS3)37,38 or coinfection with HTLV-I, where the Th1 type response to the virus is curbed,39 the overall profile that emerges from the innate and acquired responses in HIV/S. This evidence concerns the gene SOCS3 and multiple sclerosis.