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Expert Opin Drug Metab Toxicol. 2013 Nov;9(11):1453-64. doi: 10.1517/17425255.2013.816285. Epub 2013 Jul 4.

Tobacco smoking effect on HIV-1 pathogenesis: role of cytochrome P450 isozymes.

Author information

1
University of Missouri Kansas City, School of Pharmacy, Division of Pharmacology & Toxicology , Kansas City, MO 64108 , USA.

Abstract

INTRODUCTION:

Tobacco smoking is highly prevalent among the HIV-1-infected population. In addition to diminished immune response, smoking has been shown to increase HIV-1 replication and decrease response to antiretroviral therapy, perhaps through drug-drug interaction. However, the mechanism by which tobacco/nicotine increases HIV-1 replication and mediates drug-drug interaction is poorly understood.

AREAS COVERED:

In this review, the authors discuss the effects of smoking on HIV-1 pathogenesis. Since they propose a role for the cytochrome P450 (CYP) pathway in smoking-mediated HIV-1 pathogenesis, the authors briefly converse the role of CYP enzymes in tobacco-mediated oxidative stress and toxicity. Finally, the authors focus on the role of CYP enzymes, especially CYP2A6, in tobacco/nicotine metabolism and oxidative stress in HIV-1 model systems monocytes/macrophages, lymphocytes, astrocytes and neurons, which may be responsible for HIV-1 pathogenesis.

EXPERT OPINION:

Recent findings suggest that CYP-mediated oxidative stress is a novel pathway that may be involved in smoking-mediated HIV-1 pathogenesis, including HIV-1 replication and drug-drug interaction. Thus, CYP and CYP-associated oxidative stress pathways may be potential targets to develop novel pharmaceuticals for HIV-1-infected smokers. Since HIV-1/TB co-infections are common, future study involving interactions between antiretroviral and antituberculosis drugs that involve CYP pathways would also help treat HIV-1/TB co-infected smokers effectively.

PMID:
23822755
PMCID:
PMC4007120
DOI:
10.1517/17425255.2013.816285
[Indexed for MEDLINE]
Free PMC Article

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