We report here the novel finding that HIV-negative factor (Nef) protein is present in considerable numbers of peripheral blood mononuclear cells (PBMCs) from viremic HIV-infected patients not on antiretroviral therapy (ART) and also in patients receiving virologically suppressive ART, though to a smaller degree Interestingly, these Nef-positive PBMCs constitute predominantly uninfected bystander cells These results may explain systemic pathology in HIV patients, even in those receiving ART

Intracellular Nef Detected in Peripheral Blood Mononuclear Cells from HIV Patients

Loss of function mutations in the human immunodeficiency virus (HIV) negative factor (Nef) gene are associated with reduced viremia, robust T cell immune responses, and delayed acquired immunodeficiency syndrome (AIDS) progression in humans. In vitro studies have shown that mutations in the Nef dimerization interface significantly attenuate viral replication and impair host defense. However, in vivo, mechanistic studies on the role of Nef dimerization in HIV infection are lacking. Humanized rodents with human immune cells are robust platforms for investigating the interactions between HIV and the human immune system. The bone marrow-liver-thymus-spleen (BLTS) humanized mouse model carries human immune cells and lymphoid tissues that facilitate anti-viral immune responses. Here, we employed the BLTS-humanized mouse model to demonstrate that preventing Nef dimerization abrogates HIV viremia and the associated immune dysregulation. This suggests that Nef dimerization may be a therapeutic target for future HIV cure strategies.

/pdf/nef-dimerization-defect-abrogates-hiv-viremia-and-associated-36w8ex52hd.pdf

Nef Dimerization Defect Abrogates HIV Viremia and Associated Immune Dysregulation in the Bone Marrow-Liver-Thymus-Spleen (BLTS) Humanized Mouse Model.

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Nef Dimerization Defect Abrogates HIV Viremia and Associated Immune Dysregulation in the Bone Marrow-Liver-Thymus-Spleen (BLTS) Humanized Mouse Model.