IFN-γ was associated with protection against liver fibrosis in human infection with S. mansoni,29 and both IFN-γ and T-bet have been identified as factors restraining severe granuloma pathology associated with IL-17 responses in mouse models of S. mansoni infection.30,31 Although we could not discern differences between HIV+SM+ versus HIV+SM− individuals in the IFN-γ response to innate stimuli, the frequency of IFN-γ+ CD8 T cells and IFN-γ+TNF-α+ CD4 T cells in response to HIV was significantly enhanced in coinfected individuals. The gene discussed is CD4; the disease is Granuloma.