TNF and HIV-1 infection: Therefore, it was remarkable that co-infected patients, even in early stages of HIV-1 infection, had produced significantly lower levels of IL-2, TNF-α and IFN-γ under SATg stimulation, associating HIV-1 infection with early defects in the response against T. gondii, which could impair the control of latent infection in the CNS, allowing limited reactivation, that is, not associated with toxoplasmic encephalitis, but capable of generating cumulative damage and functional impairment, even in the asymptomatic stage of HIV-1 infection.