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(Journal of Leukocyte Biology. 2000;68:303-310.)
© 2000 by Society for Leukocyte Biology

Permissive factors for HIV-1 infection of macrophages

Sharon M. Wahl, Teresa Greenwell-Wild, Hollie Hale-Donze, Niki Moutsopoulos and Jan M. Orenstein

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 Medical Center, Washington, DC

Correspondence: Sharon M. Wahl, PhD, NIDCR, NIH, 30 Convent Drive, MSC 4352, Building 30, Room 332, Bethesda, MD 20892-4352. E-mail: smwahl{at}dir.nidcr.nih.gov

Immunodeficiency, the consequence of HIV-1 infection, predisposes the host to opportunistic infections. In turn, opportunistic pathogens influence target cell susceptibility to HIV-1 infection and replication. Although the advent of highly active antiretroviral therapy (HAART) has altered these sequelae, co-infections may prevail in some parts of the world and in failed HAART regimens. Moreover, immune activation as occurs in tonsil and non-infectious mucosal inflammatory lesions may also be associated with proximal sites of viral replication. These connections between enhancement of HIV-1 infection and activation/inflammation warrant further elucidation of the factors promoting permissiveness to HIV-1 infection. Using the opportunistic pathogen Mycobacterium avium as an in vitro model, we demonstrated that co-infection facilitated HIV-1 infection of monocyte-macrophages by multiple pathways. M. avium activated NF-{kappa}B, the downstream consequences of which included augmented expression of tumor necrosis factor {alpha} and CCR5 receptors, both permissive for sustaining HIV-1 infection. Pronounced viral replication in lymph nodes co-infected with M. avium and HIV-1 paralleled these in vitro findings. Furthermore, reduction in viral burden is associated with treatment of infected or inflamed tissues, underscoring the link between immune activation and viral replication.

Key Words: Mycobacterium avium • nuclear factor {kappa}ß • viral replication




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