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Protozoan parasites of the genus Leishmania frequently occur as opportunistic pathogens in human immunodeficiency virus type 1 (HIV-1)-infected individuals, but the mechanisms underlying protozoan growth in this context are poorly understood. Here, we demonstrate that the HIV-1 Tat protein drives Leishmania replication in primary human macrophages. We found that Leishmania growth doubled in HIV-1-infected macrophages and that anti-Tat antibodies reduced the exacerbated protozoan replication by 70%. Recombinant Tat increased Leishmania replication and overrode the leishmanicidal effect induced by interferon-gamma , allowing Leishmania replication even in the presence of this cytokine. Tat induced cyclooxygenase (COX)-2 expression and prostaglandin E2 (PGE2) synthesis, and a COX-2 inhibitor abolished the Tat-mediated augmentation of Leishmania replication. Moreover, PGE2 increased Leishmania growth, which was abrogated by anti-transforming growth factor (TGF)- beta1 monoclonal antibodies. Neutralization of TGF-beta1 reduced parasite growth in Leishmania-infected macrophages exposed to Tat by 50%. Our findings suggest that Tat generates a milieu permissive to Leishmania growth in individuals infected with HIV-1.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Increased<i>Leishmania</i>Replication in HIV‐1–Infected Macrophages Is Mediated by Tat Protein through Cyclooxygenase‐2 Expression and Prostaglandin E<sub>2</sub>Synthesis

IncreasedLeishmaniaReplication in HIV‐1–Infected Macrophages Is Mediated by Tat Protein through Cyclooxygenase‐2 Expression and Prostaglandin E2Synthesis

IncreasedLeishmaniaReplication in HIV‐1–Infected Macrophages Is Mediated by Tat Protein through Cyclooxygenase‐2 Expression and Prostaglandin E₂Synthesis