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eescobar@ivic.ve WELBA104

HIV / T. gondii co-infected patients produce lower levels of IFN-γ in response to T. gondii antigens, even in the early stage of viral infection. E. Escobar, M. Alfonzo, M. Fernández , J. Camacho, Y. Roldán , B. Alarcón de Noya , M.E. de Quesada UCV / IVIC Venezuela.

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eescobar@ivic.ve WELBA104

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  1. HIV/T. gondii co-infected patientsproduce lower levels of IFN-γ in response to T. gondii antigens,even in the early stage of viral infection E. Escobar, M. Alfonzo, M. Fernández, J. Camacho, Y. Roldán, B. Alarcón de Noya, M.E. de Quesada UCV / IVIC Venezuela eescobar@ivic.ve WELBA104

  2. HIV InfectionCentral NervousSystem HIV: Neurotropic and Neuropathic MildDisturbance Fatigue Sensitive / CognitiveImpairment Motor Dysfunction BehavioralChange SevereAffection HIV-AssociatedDementia

  3. T. gondii Infection Asymptomatic in Immunocompetent Hosts TissueCysts Central NervousSystem CardiacMuscle Eye Reactivates in Immunodeficient Hosts ToxoplasmicEncephalitis Cardiopathy Chorioretinitis

  4. HIV /Toxoplasma gondii Coinfection

  5. T. gondiiStageInterconversion • Cellular Stress • Heat Shock • Presence of Nitric Oxide • MitochondrialInhibition • Extreme pH (Low/High) Control Tachyzoite Bradyzoite Reactivation • Immunodeficiency • Lack of T Cells • Lack of IL-12, IFN-γ, TNF-α • Lack of Nitric Oxide Trends in Parasitology 2002; 16(5):198-201.

  6. Objetive • Evaluate anti-T. gondii specific immune response in HIV/T. gondiicoinfected patients* * Several stages of viral infection * No HAART nor anti-T. gondii treatment • In vitro production of IFN-γ and TNF-α under parasitic stimulation was assessed.

  7. Patients and Control Groups Controls Patients HIV (-) HIV (+) C1 T. gondii (-) C2 T. gondii (+) P1 T. gondii (-) P2 T. gondii (+) A CD4 > 350/ul B CD4 200-350/ul C CD4 <200/ul

  8. Cell Culture PBMC 1 x 105cells 200 ul SATg* 1 ug/ml *Soluble Antigens of T. gondii RH strain MediumAlone RPMI, 10% FCS PHA 5 ug/ml Culture 72 hours 37°C, 5% CO2 Supernatants Citokine Determinations (Flow cytometry-CBA, Becton-Dickinson)

  9. Results

  10. IFN-γ Production

  11. IFN-γ Production under SATg Stimulation

  12. TNF-α Production

  13. TNF-α Production under SATg Stimulation

  14. IFN-γ and TNF-αProductionunderSATgstimulation • Coinfected Patients (P2) higher than P1 • Coinfected Patients Lower than Controls • Coinfected Patients Affected from early stages

  15. Conclusions • Defects in IFN-γ (and TNF-α) production in response to Toxoplasma gondii may impair anti-parasitic response in coinfected patients since early stages of viral infection • Eventual reactivation (even partial / limited) of brain parasitic latent infection may contribute to develop neurological signs and symptoms even before toxoplasmic encephalitis appears.

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