Highly active antiretroviral therapy (HAART) has dramatically extended the lifespan and
quality of life of individuals infected with human immunodeficiency virus type 1 (HIV-1). HAART
comprises of a cocktail of various pharmacological inhibitors which interfere with almost every stages
of HIV-1 life cycle. However, constant application of drugs often results in the evolution of hostpathogen
relationship resulting in the emergence of drug resistant viral strains. Drug resistant HIV-1 is
a potent threat for the humankind. Therefore, there is a constant need to search for novel therapeutic
molecules. HIV-1 infection results in the depletion of CD4+/CD8+T cells and alters the cytokine network in the infected
individuals. Tumor necrosis factor alpha (TNF-alpha), a proinflammatory cytokine, plays a critical role in HIV-1 pathogenesis.
HIV-1 utilizes the TNF-alpha signaling pathway for expanding its reservoir. Several HIV-1 proteins mimic and
regulate the TNF-alpha signaling pathway. TNF-alpha inhibitors have been used in several inflammatory pathologies with
success to some extent. In the present mini review we will discuss the role of TNF-alpha in HIV-1 pathogenesis. Furthermore
we will evaluate the TNF-alpha inhibitors as an additional therapeutic option for HIV-1 infection.
Keywords: gp120, HAART, HIV-1, Nef, reservoirs, Tat, TNF-alpha, Vpr.
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