Targeting TNF-Alpha in HIV-1 Infection

Author(s): Amit Kumar, Laurie Coquard, Georges Herbein

Journal Name: Current Drug Targets

Volume 17 , Issue 1 , 2016

  Journal Home
Translate in Chinese
Become EABM
Become Reviewer

Graphical Abstract:


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.

promotion: free to download

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2016
Published on: 17 December, 2015
Page: [15 - 22]
Pages: 8
DOI: 10.2174/1573399811666150615145824

Article Metrics

PDF: 89
HTML: 21