Abstract
High prevalence of cigarette smoking in HIV patients is associated with increased HIV pathogenesis and disease progression. While the effect of smoking on the occurrence of lung cancer has been studied extensively, the association between smoking and HIV pathogenesis is poorly studied. We have recently shown the possible role of cytochrome P450 (CYP) in smoking/nicotine-mediated viral replication. In this review, we focus on the potential role of CYP pathway in polycyclic aromatic hydrocarbons (PAH), important constituents of cigarette smoke, mediated HIV pathogenesis. More specifically, we will discuss the role of CYP1A1 and CYP1B1, which are the major PAH-activating CYP enzymes. Our results have shown that treatment with cigarette smoke condensate (CSC) increases viral replication in HIV-infected macrophages. CSC contains PAH, which are known to be activated by CYP1A1 and CYP1B1 into procarcinogens/toxic metabolites. The expression of these CYPs is regulated by aryl hydrocarbon receptors (AHR), the cellular target of PAH, and an important player in various diseases including cancer. We propose that PAH/AHR-mediated CYP pathway is a novel target to develop new interventions for HIV positive smokers.
Highlights
According to the world health organization (WHO), human immunodeficiency virus (HIV) is the world’s leading infectious killer with about 40 million reported deaths since early 1980s
In addition to increased reactive oxygen species (ROS) production, these studies have suggested a strong interaction between nicotine and cytochrome P450 (CYP) isoforms, which may contribute toward enhanced HIV replication in HIV positive smokers
While the study of the effects of nicotine has gained preference, the lack of studies focused on determining the role of polycyclic aromatic hydrocarbons (PAH) in modulating HIV replication is concerning
Summary
According to the world health organization (WHO), human immunodeficiency virus (HIV) is the world’s leading infectious killer with about 40 million reported deaths since early 1980s. Cigarette smoking in particular, is highly prevalent amongst HIV-infected populations (Ueda et al, 1989). Several studies have reported 2–3 fold higher prevalence of cigarette smoking in HIV positive patients as compared to general population (Crothers et al, 2009; Tesoriero et al, 2010; Browning et al, 2013). Numerous independent factors impeding the cessation of cigarette smoking amongst HIV population have been identified. Concurrent drug use and/or history of substance abuse have been identified as critical factors governing cigarette smoking status in HIV infected individuals (Shirley et al, 2013; Pacek et al, 2014; O’Cleirigh et al, 2015)
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