Targeting TNF-Alpha in HIV-1 Infection.
Fiche publication
Date publication
janvier 2016
Journal
Current drug targets
Auteurs
Membres identifiés du Cancéropôle Est :
Pr HERBEIN Georges
Tous les auteurs :
Kumar A, Coquard L, Herbein G
Lien Pubmed
Résumé
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.
Mots clés
Anti-HIV Agents, pharmacology, HIV Infections, drug therapy, HIV-1, drug effects, Humans, Paracrine Communication, drug effects, Tumor Necrosis Factor-alpha, antagonists & inhibitors
Référence
Curr Drug Targets. 2016 ;17(1):15-22