In our study, we identified that in the setting of HIV infection, C. albicans-specific CD4 T-cell responses manifest a sequential dysfunction with Th17-like functions (IL-17, IL-22 and IL-2) being impaired earlier following HIV infection as compared to Th1 functions (IFN-γ and MIP-1β) (Fig 3). This evidence concerns the gene CD4 and HIV infectious disease.