Tripanosoma cruzi (Chagas disease agent) inhibits HIV-1 replication in human macrophages at different levels.

G. ANDREANI, A.M. CELENTANO, M.E. SOLANA, S.CAZORLA, L. MARTÍNEZ PERALTA, G. DOLCINI.

Sydney, Australia, 22-25 de Julio 2007.

Congreso; 4th IAS CONFERENCE ON HIV PATHOGENESIS, TREATMENT AND PREVENTION.; 2007

International Aids Society

Objectives: Monocytes/macrophages are one of the major targets of HIV-1 infection and serve as reservoirs for viral persistence in vivo. These cells are also target of the protozoa Trypanosoma cruzi and their activation controls parasite replication. Some reported data suggest enhanced viral and parasitic replication in co-infected patients; however, no in vitro evidence about direct interaction between both pathogens exists. The aim of this work was to evaluate the effect of T.cruzi on HIV-1 replication in monocytes derived macrophages (MDM). Methods: MDM were co-infected with HIV and T.cruzi trypomastigotes (VD lethal strain) or 24h-trypomastigotes supernatants on three infection schemes: HIV 24h after T.cruzi (T.cruzi-HIV), 24h before T.cruzi (HIV-T.cruzi) or simultaneously (T.cruzi+HIV). The role of the recombinant major T.cruzi antigen cruzipain was also evaluated. T.cruzi effect on viral transcriptional activity was assessed using HIV-1∆envLuc+/VSV-G or HIV-1∆envLuc+/BaL pseudotypes by luciferase activity quantification. Parasite influence on replication of fully infectious BaL strain was evaluated by quantification of p24 antigen. MDM viability was measured by MTT assay. Results: Trypomastigotes decreased luciferase activity for both viral pseudotypes, having a lower effect on VSV-G, always being stronger in T.cruzi-HIV (p