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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. by Shivkumar Biradar; Yash Agarwal; Antu Das; Sherry T. Shu; Jasmine Samal; Sara Ho; Cole Beatty; Isabella Castronova; Robbie B. Mailliard; Thomas E. Smithgall; Moses Turkle Bility is a scholarly article available to read on EtoBox.

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## Abstract BackgroundLoss 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. Importantly, Nef persists in antiretroviral therapy-treated chronic HIV-infected individuals. 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. ResultsHere, we demonstrate that nef deletion abrogates HIV viremia and HIV-induced immune dysregulation in the BLTS-humanized mouse model. Furthermore, we demonstrate that preventing Nef dimerization abrogates HIV viremia and HIV-induced immune dysregulation in the BLTS-humanized mouse model. We als

Author

Shivkumar Biradar; Yash Agarwal; Antu Das; Sherry T. Shu; Jasmine Samal; Sara Ho; Cole Beatty; Isabella Castronova; Robbie B. Mailliard; Thomas E. Smithgall; Moses Turkle Bility

Publisher

Research Square Platform LLC

Published

2021

Language

EN