Agudelo Marisela, Khatavkar Pradnya, Yndart Adriana, Yoo Changwon, Rosenberg Rhonda, Devieux Jessy G, Malow Robert M, Nair Madhavan
Department of Immunology, Institute of NeuroImmune Pharmacology, College of Medicine, AHC-I 308, Florida International University, 11200 SW 8th Street, Miami, FL 33199, USA.
Curr HIV Res. 2014;12(4):234-42. doi: 10.2174/1570162x12666140721115045.
According to a survey from the HIV Cost and Services Utilization Study (HCSUS), approximately 53% of HIV-infected patients reported drinking alcohol and 8% were classified as heavy drinkers. The role of alcohol as a risk factor for HIV infection has been widely studied and recent research has found a significant association between heavy alcohol consumption and lower levels of CD4 T cells among HIV-infected alcoholics. Although there is evidence on the role of alcohol as a risk factor for HIV transmission and disease progression, there is a need for population studies to determine the genetic mechanisms that affect alcohol's role in HIV disease progression. One of the mechanisms of interest is the dopaminergic system. To date, the effects of dopamine on HIV neuroimmune pathogenesis are not well understood; however, dopaminergic neural degeneration due to HIV is known to occur by viral invasion into the brain via immune cells, and modulation of dopamine in the CNS may be a common mechanism by which different types of substances of abuse impact HIV disease progression. Although previous studies have shown an association of D(2) dopamine receptor (DRD2) polymorphisms with severity of alcohol dependence, the expression of this allele risk on HIV patients with alcohol dependence has not been systematically explored. In the current study, DRD2 Taq1A and C957T SNP genotyping analyses were performed in 165 HIV-infected alcohol abusers and the results were examined with immune status and CD4 counts.
根据一项来自艾滋病成本与服务利用研究(HCSUS)的调查,约53%的艾滋病毒感染患者报告饮酒,8%被归类为重度饮酒者。酒精作为艾滋病毒感染风险因素的作用已得到广泛研究,最近的研究发现,在感染艾滋病毒的酗酒者中,大量饮酒与CD4 T细胞水平降低之间存在显著关联。尽管有证据表明酒精是艾滋病毒传播和疾病进展的风险因素,但仍需要进行人群研究,以确定影响酒精在艾滋病毒疾病进展中作用的遗传机制。其中一个感兴趣的机制是多巴胺能系统。迄今为止,多巴胺对艾滋病毒神经免疫发病机制的影响尚不清楚;然而,已知艾滋病毒导致的多巴胺能神经变性是通过免疫细胞侵入大脑发生的,中枢神经系统中多巴胺的调节可能是不同类型滥用物质影响艾滋病毒疾病进展的共同机制。尽管先前的研究表明D(2)多巴胺受体(DRD2)多态性与酒精依赖的严重程度有关,但尚未系统探讨该等位基因风险在酒精依赖艾滋病毒患者中的表达情况。在本研究中,对165名感染艾滋病毒的酗酒者进行了DRD2 Taq1A和C957T单核苷酸多态性基因分型分析,并将结果与免疫状态和CD4计数进行了对照检查。