Abstract
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.
Original language | English (US) |
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Pages (from-to) | 43-50 |
Number of pages | 8 |
Journal | Virology |
Volume | 577 |
DOIs | |
State | Published - Dec 2022 |
Keywords
- Acquired immunodeficiency syndrome
- Fentanyl
- Human immunodeficiency virus
- Opioids
- Reactivation
ASJC Scopus subject areas
- Virology