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Permissive factors for HIV‐1 infection of macrophages
Author(s) -
Wahl Sharon M.,
GreenwellWild Teresa,
HaleDonze Hollie,
Moutsopoulos Niki,
Orenstein Jan M.
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.68.3.303
Subject(s) - permissiveness , biology , immunology , immune system , viral replication , virology , opportunistic infection , inflammation , chemokine , virus , viral disease
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‐κB, the downstream consequences of which included augmented expression of tumor necrosis factor α 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.