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Published online before print July 22, 2003

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(Journal of Leukocyte Biology. 2003;74:726-735.)
© 2003 by Society for Leukocyte Biology

Viral and host cofactors facilitate HIV-1 replication in macrophages

Sharon M. Wahl^*,1, Teresa Greenwell-Wild^*, Gang Peng^*, Ge Ma^*, Jan M. Orenstein and Nancy Vázquez^*

^* Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland; and
Department of Pathology, George Washington University School of Medicine, Washington, D.C.

¹Correspondence: Building 30, Rm. 320, 30 Convent Drive, MSC4352, NIDCR, NIH, Bethesda, MD 20892-4352. E-mail: smwahl{at}dir.nidcr.nih.gov

Human immunodeficiency virus type 1 (HIV-1) infection of CD4⁺ T lymphocytes leads to their progressive loss, whereas HIV-1-infected macrophages appear to resist HIV-1-mediated apoptotic death. The differential response of these two host-cell populations may be critical in the development of immunodeficiency and long-term persistence of the virus. Multiple contributing factors may favor the macrophage as a resilient host, not only supporting infection by HIV-1 but also promoting replication and persistence of this member of the lentivirus subfamily of primate retroviruses. An encounter between macrophages and R5 virus engages a signal cascade eventuating in transcriptional regulation of multiple genes including those associated with host defense, cell cycle, nuclear factor-B regulation, and apoptosis. It is important that enhanced gene expression is transient, declining to near control levels, and during this quiescent state, the virus continues its life cycle unimpeded. However, when viral replication becomes prominent, an increase in host genes again occurs under the orchestration of viral gene products. This biphasic host response must fulfill the needs of the parasitic virus as viral replication activity occurs and leads to intracellular and cell surface-associated viral budding. Inroads into understanding how HIV-1 co-opts host factors to generate a permissive environment for viral replication and transmission to new viral hosts may provide opportunities for targeted interruption of this lethal process.

Key Words: opportunistic infections • cDNA expression array • p21 • SLPI • Vpr

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