Short communication: human lymphotropic virus type 1 coinfection modulates the synthesis of cytokines by peripheral blood mononuclear cells from HIV type 1-infected individuals.

HIV-1 and HTLV-1 infect CD4(+) T lymphocyte but little is known about the impact of coinfection on patient's immune response. In this study we have evaluated the spontaneous production of interleukin (IL)-2, IL-4, IL-6, and IL-10 and interferon (IFN)-γ by unstimulated peripheral blood mononuclear cell (PBMC) cultures obtained from patients infected by HTLV-1, HIV-1, or both viruses. We have observed that HIV/HTLV-coinfected individuals presented significantly higher production of IL-2 and IFN-γ compared to both HIV single-infected and HTLV single-infected individuals.

Interaction of macrophages with apoptotic cells enhances HIV Type 1 replication through PGE2, PAF, and vitronectin receptor.

Phagocytosis of apoptotic cells by macrophages increases secretion of soluble mediators and generates an antiinflammatory environment. We previously reported that phagocytosis of apoptotic cells by HIV-1-infected macrophages enhances viral replication, with the participation of the cytokine transforming growth factor- beta1 and an integrin receptor. Now, we describe the role of prostaglandin E2 (PGE2), platelet-activating factor (PAF), and the integrin alphaVbeta3 (vitronectin receptor, VnR) in this phenomenon.

Depletion of CD4 T lymphocytes in human lymphoid tissue infected ex vivo with doxycycline-dependent HIV-1.

We investigated whether CD4+ T cells that do not produce HIV-1 are killed in HIV-infected human lymphoid tissue. Tissue blocks were inoculated with high amount of doxycycline-dependent HIV-rtTA. Doxycycline triggered productive infection and loss of CD4+ T cells in these tissues, whereas without doxycycline, neither productive infection nor CD4+ T cell depletion was detected in spite of the massive presence of virions in the tissue and of viral DNA in the cells.

Bystander CD4+ T lymphocytes survive in HIV-infected human lymphoid tissue.

HIV infection is associated with depletion of CD4(+) T cells. The mechanisms of this phenomenon remain to be understood. In particular, it remains controversial whether and to what extent uninfected ("bystander") CD4(+) T cells die in HIV-infected individuals.

The replication of human immunodeficiency virus type 1 in macrophages is enhanced after phagocytosis of apoptotic cells.

Clearance of apoptotic cells increases macrophage secretion of antiinflammatory mediators and might modulate viral replication in human immunodeficiency virus (HIV) type 1-infected macrophages. To study this, primary macrophages were infected with HIV-1 and exposed to apoptotic cells. It was found that phagocytosis of apoptotic cells potently enhanced HIV-1 growth.