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Immunopathogenesis of asymptomatic chronic HIV Infection: the calm before the storm

Ford, Emily S*; Puronen, Camille E*; Sereti, Irini

Current Opinion in HIV and AIDS: May 2009 - Volume 4 - Issue 3 - p 206–214
doi: 10.1097/COH.0b013e328329c68c
Early treatment: Edited by Sean Emery and Andrew Phillips

Purpose of review HIV and pathogenic simian immunodeficiency virus infection are characterized by chronic immune activation. This review addresses the factors that influence immune activation and may thus determine the rate of disease progression during the asymptomatic period of HIV.

Recent findings Immune activation stems from foreign antigen stimulation, including HIV, microbial products and coinfections and compensatory homeostatic mechanisms. Continuous immune stimulation creates a permissive environment for further viral replication, while temporarily allowing successful replenishment of the T-cell pool. Type I interferon, microbial translocation, activated (but ineffective) effector T cells, unruly regulatory T cells and inadequate T helper 17 cells all play important roles in the cycle of activation, functional exhaustion and T-cell death that leads to immunodeficiency.

Summary The asymptomatic chronic phase of HIV infection is a dynamic balance between host and virus, the outcome of which determines an individual's course of disease. Evaluation of the factors that determine the immunologic threshold of disease progression could assist in designing therapeutic strategies, including individualized timing of ART.

Clinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Bethesda, Maryland, USA

*Emily S. Ford and Camille E. Puronen contributed equally to the writing of this article.

Correspondence to Irini Sereti, MD, MHS, 10 Center Drive, Building 10, Room #11B07A, Bethesda, MD 20892, USA Tel: +1 301 496 5533; fax: +1 301 480 9978; e-mail: isereti@mail.nih.gov

© 2009 Lippincott Williams & Wilkins, Inc.