Fentanyl enhances HIV infection in vitro.
Fentanyl enhances HIV infection in vitro.
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DOI：
10.1016/j.virol.2022.10.004
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发表时间：
2022-10
期刊：
影响因子：
3.7
通讯作者：
Jie Yan;Dong-hang Nie;Cheng-si Bai;Abdul Rehman;Angjin Yang;Xiaoping Mu;Yu-qing Zhang;
中科院分区：
文献类型：
--
作者：
Jie Yan;Dong-hang Nie;Cheng-si Bai;Abdul Rehman;Angjin Yang;Xiaoping Mu;Yu-qing Zhang;
由人类免疫缺陷病毒1型(HIV-1)引起的获得性免疫缺陷综合征(AIDS)在非法吸毒者中有较高的发病趋势。最近，有报道称，滥用芬太尼是一种有效的合成μ受体刺激阿片类药物，是感染HIV-1的独立危险因素。然而，增加HIV-1感染的作用机制仍然不清楚。在本研究中，我们发现芬太尼增强了MT2细胞、原代巨噬细胞和Jurkat C11细胞中HIV-1的感染。芬太尼上调CXCR4和CCR5受体的表达，从而促进病毒粒子进入宿主细胞。此外，它还下调干扰素-β(干扰素-β)和干扰素刺激基因(APOBEC3F、APOBEC3G和MXB)在MT2细胞中的表达。我们的研究结果表明，芬太尼通过上调辅助受体(CXCR4/CCR5)和下调干扰素-β和ISGs，在HIV-1感染的正向调节中发挥重要作用，并可能在HIV-1免疫发病机制中发挥重要作用。
Acquired immunodeficiency syndrome (AIDS) caused by Human immunodeficiency virus type 1 (HIV-1) has a high tendency among illicit drug abusers. Recently, it is reported that abuse of fentanyl, a potent synthetic μ receptor–stimulating opioid, is an independent risk factor for HIV-1 infection. However, the mechanism of action in augmenting HIV-1 infection still remains elusive. In this study, we found that fentanyl enhanced infection of HIV-1 in MT2 cells, primary macrophages and Jurkat C11 cells. Fentanyl up-regulated CXCR4 and CCR5 receptor expression, which facilitated the entry of virion into host cells. In addition, it down-regulated interferon-β (IFN-β) and interferon-stimulated genes (APOBEC3F, APOBEC3G and MxB) expression in MT2 cells. Our findings identify an essential role of fentanyl in the positive regulation of HIV-1 infection via the upregulation of co-receptors (CXCR4/CCR5) and downregulation of IFN-β and ISGs, and it may have an important role in HIV-1 immunopathogenesis.