Tobacco smoking effect on HIV-1 pathogenesis

Role of cytochrome P450 isozymes

Anusha Ande, Carole McArthur, Anil Kumar, Santosh Kumar

Research output: Contribution to journalReview article

18 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1453-1464
Number of pages12
JournalExpert Opinion on Drug Metabolism and Toxicology
Volume9
Issue number11
DOIs
StatePublished - Nov 1 2013

Fingerprint

Tobacco
Cytochrome P-450 Enzyme System
Isoenzymes
HIV-1
Smoking
Oxidative stress
Drug interactions
Oxidative Stress
Pharmaceutical Preparations
Drug Interactions
Nicotine
Lymphocytes
Macrophages
Metabolism
Neurons
Toxicity
Expert Testimony
Coinfection
Astrocytes
Monocytes

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology

Cite this

Tobacco smoking effect on HIV-1 pathogenesis : Role of cytochrome P450 isozymes. / Ande, Anusha; McArthur, Carole; Kumar, Anil; Kumar, Santosh.

In: Expert Opinion on Drug Metabolism and Toxicology, Vol. 9, No. 11, 01.11.2013, p. 1453-1464.

Research output: Contribution to journalReview article

@article{5ad2b912315e4ac4ae26adc35555de83,
title = "Tobacco smoking effect on HIV-1 pathogenesis: Role of cytochrome P450 isozymes",
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.",
author = "Anusha Ande and Carole McArthur and Anil Kumar and Santosh Kumar",
year = "2013",
month = "11",
day = "1",
doi = "10.1517/17425255.2013.816285",
language = "English (US)",
volume = "9",
pages = "1453--1464",
journal = "Expert Opinion on Drug Metabolism and Toxicology",
issn = "1742-5255",
publisher = "Informa Healthcare",
number = "11",

}

TY - JOUR

T1 - Tobacco smoking effect on HIV-1 pathogenesis

T2 - Role of cytochrome P450 isozymes

AU - Ande, Anusha

AU - McArthur, Carole

AU - Kumar, Anil

AU - Kumar, Santosh

PY - 2013/11/1

Y1 - 2013/11/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84886043288&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84886043288&partnerID=8YFLogxK

U2 - 10.1517/17425255.2013.816285

DO - 10.1517/17425255.2013.816285

M3 - Review article

VL - 9

SP - 1453

EP - 1464

JO - Expert Opinion on Drug Metabolism and Toxicology

JF - Expert Opinion on Drug Metabolism and Toxicology

SN - 1742-5255

IS - 11

ER -