阿片类毒品对HIV感染者PBMCs中IFN-α、ISG56、MxA表达的影响

The influence of opiate abuse on the expression of IFN-α,ISG56 and MxA in peripheral blood mononuclear cells of patients infected with HIV

目的通过检测阿片类毒品(opiates)对HIV感染者中干扰素α(interferon-α,IFN-α)、干扰素诱导基因56(interferon-stimulated gene 56,ISG56)、粘病毒抵抗蛋白A(myxovirus resistance protein A,Mx A)表达水平的影响,初步探讨阿片类毒品对人类免疫缺陷病毒(human immunodeficiency virus,HIV)复制影响的机制。方法研究对象选取美沙酮门诊、艾滋病自愿咨询检测门诊人群200名,分为4组:Opiate+HIV+组、Opiate+HIV-组、OpiateHIV+组和对照组。面对面问卷调查并采集研究对象外周静脉血,分离外周血单核细胞,采用实时荧光定量PCR法、免疫印迹法、ELISA法等检测4组人群中IFN-α、ISG56、Mx A的mRNA,蛋白表达水平,比较相关因子相对表达量的差异。结果 4组人群在年龄、性别、民族、户籍所在地、婚姻状况、文化程度及职业等人口学特征方面差异均无统计学意义(均有P>0.05)。无论是在基因还是蛋白水平上,HIV感染人群中毒品滥用者的IFN-α、ISG56和Mx A的表达水平均低于非毒品滥用者,差异均有统计学意义(均有P<0.05)。结论阿片类毒品可能抑制抗病毒效应因子IFN-α、ISG56和Mx A的表达,从而促进HIV-1的复制。

Objective To detect the effect of opiate abuse on HIV replication and the possible mechanism by analyzing the expression ofinterferon-α（ IFN-α）, interferon stimulated gene 56 （ ISG56 ） and myxovirus resistance protein A （MxA） in peripheral blood mononuclear cells （PBMCs） among human immunodeficiency virus （HIV） infected patients with or without opiates abuse. Methods A total of 200 subjects were randomly recruited from methadone treatment and voluntary HIV counselling and testing centers, and were divided into four groups ： Opiate ＋ HIV ＋ , Opiate-HIV ＋ , Opiate ＋ HIV -, and Control. A questionnaire was used to collect data on demographic characteristics. Plasma and PBMCs were isolated from blood samples of the subjects. The expression of IFN-α, ISG56 and MxA level in PBMCs were analyzed by RT-PCR,western blot and ELISA. Results There were no significant differences in gender, age, nationality, domicile, marital status, education level and occupation, and other demographic characteristics among four groups （ all P 〉 0.05 ）. Among HIV-1-infected subjects, RNA and protein level of IFN-α, ISG56 and MxA in Opiate ＋ HIV ＋ group were lower than those in Opiate-HIV ＋ group （ all P 〈 0. 05 ）. Conclusions Opiate abuse may suppress the antiviral responses of IFN-α, ISG56 and MxA to promote HIV-1 replication.