Alteraciones en la producción de citocinas en respuesta a Toxoplasma gondii aparecen desde las etapas tempranas en pacientes co-infectados con VIH-1.

Abstract

Both HIV-1 and Toxoplasma gondii are able to invade central nervous system and affect its functionality. Advanced HIV-1 infection has been associated with defects in immune response to T. gondii, leading to reactivation of latent infections and the appearing of toxoplasmic encephalitis. This study evaluated changes in the immune response to T. gondii in different stages of HIV infection. Immune response to T. gondii was assessed studying cytokine production in response to parasite antigens in HIV-1-infected/T. gondii-non-infected (P1), HIV-1/T. gondii co-infected (P2), HIV-1-non-infected/T. gondii-non-infected (C1) and HIV-1-non-infected/T. gondii-infected (C2) individuals. Patients (P1 and P2) were divided in early/asymptomatic (P1A, P2A) or late/symptomatic (P1B/C, P2B/C) according to peripheral blood CD4+ T lympho-cyte counts (>350 or <350/μL, respectively). The HIV-1 infection, from early/asymptomatic stages, was associated with significant lower production of IL -2, TNF-α and IFN-γ in response to T. gondii, when P2 patients were compared with C2 controls. These early defects may impair anti-parasitic response in co-infect-ed patients, allowing to reactivation of parasitic latent infection, enhancing the risk of CNS damage and impairment of neurocognitive functions.