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Macrophages and HIV-1

Cobos-Jiménez, Viviana; Booiman, Thijs; Hamann, Jörg; Kootstra, Neeltje A.

Current Opinion in HIV and AIDS: September 2011 - Volume 6 - Issue 5 - p 385–390
doi: 10.1097/COH.0b013e3283497203
Innate immunity: Edited by William A. Paxton and Teunis B.H. Geijtenbeek

Purpose of review Macrophages play an important role in HIV-1 pathogenesis and contribute to the establishment of the viral reservoir responsible for continuous virus production. This review will discuss new insights into HIV-1 infection in macrophages and the effect of infection on immune function and pathology.

Recent findings New cellular factors interacting with various steps of the HIV-1 replication cycle, such as entry, integration, transcription, and assembly of new viral progeny, have been identified. Cellular and viral microRNAs have been shown to regulate virus replication, promote viral latency, and prolong cell survival. Interference with innate immune functions, like phagocytosis, autophagy, cytokine production, and T-cell activation by HIV-1 has been found to contribute to virus replication and latency. Growing evidence indicates an important role of infected macrophages in a variety of HIV-1-associated diseases, including neurocognitive disorders.

Summary Under combined antiretroviral therapy (cART), HIV-1 continues to persist in macrophages. Better understanding of HIV-1 infection in macrophages may lead to new adjunctive therapies to improve cART, specifically targeting the viral reservoir and ameliorating tissue-specific diseases.

Department of Experimental Immunology, Sanquin Research, Landsteiner Laboratory, and Center for Infectious Diseases and Immunity Amsterdam (CINIMA) at the Academic Medical Center of the University of Amsterdam, Amsterdam, The Netherlands

Correspondence to Dr Neeltje A. Kootstra, Department of Experimental Immunology (M01-107), Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The NetherlandsTel: +31 20 5668291; fax: +31 20 5669756; e-mail:

© 2011 Lippincott Williams & Wilkins, Inc.