Abstract
Epidemiological studies have demonstrated that the use of methamphetamine (METH), a sympathomimetic stimulant, is particularly common among patients infected with HIV. In vitro studies have determined that METH enhances HIV infection of CD4+ T cells, monocyte-derived dendritic cells, and macrophages. In addition, animal studies have also showed that METH treatment increases brain viral load of SIV-infected monkeys and promotes HIV replication and viremia in HIV/hu-CycT1 transgenic mice. However, the mechanisms (s) of METH actions on HIV remain to be determined. In this study, we investigated the impact of METH on intracellular restriction factors against HIV and SIV. We demonstrated that METH treatment of human blood mononuclear phagocytes significantly affected the expression of anti-HIV microRNAs and several key elements (RIG-I, IRF-3/5, SOCS-2, 3 and PIAS-1, 3, X, Y) in the type I IFN pathway. The suppression of these innate restriction factors was associated with a reduced production of type I IFNs and the enhancement of HIV or SIV infection of macrophages. These findings indicate that METH use impairs intracellular innate antiviral mechanism(s) in macrophages, contributing to cell susceptibility to the acquired immune deficiency syndrome (AIDS) virus infection.
Keywords: HIV, Interferon, Intracellular restriction factors, Macrophages, METH, microRNAs, SIV, Interferon regulatory factor, Interferon regulatory, IFN, JAK-STAT.
Current HIV Research
Title:Modulation of Intracellular Restriction Factors Contributes to Methamphetamine- Mediated Enhancement of Acquired Immune Deficiency Syndrome Virus Infection of Macrophages
Volume: 10 Issue: 5
Author(s): Xu Wang, Yizhong Wang, Li Ye, Jieliang Li, Yu Zhou, Sinem Sakarcan and Wenzhe Ho
Affiliation:
Keywords: HIV, Interferon, Intracellular restriction factors, Macrophages, METH, microRNAs, SIV, Interferon regulatory factor, Interferon regulatory, IFN, JAK-STAT.
Abstract: Epidemiological studies have demonstrated that the use of methamphetamine (METH), a sympathomimetic stimulant, is particularly common among patients infected with HIV. In vitro studies have determined that METH enhances HIV infection of CD4+ T cells, monocyte-derived dendritic cells, and macrophages. In addition, animal studies have also showed that METH treatment increases brain viral load of SIV-infected monkeys and promotes HIV replication and viremia in HIV/hu-CycT1 transgenic mice. However, the mechanisms (s) of METH actions on HIV remain to be determined. In this study, we investigated the impact of METH on intracellular restriction factors against HIV and SIV. We demonstrated that METH treatment of human blood mononuclear phagocytes significantly affected the expression of anti-HIV microRNAs and several key elements (RIG-I, IRF-3/5, SOCS-2, 3 and PIAS-1, 3, X, Y) in the type I IFN pathway. The suppression of these innate restriction factors was associated with a reduced production of type I IFNs and the enhancement of HIV or SIV infection of macrophages. These findings indicate that METH use impairs intracellular innate antiviral mechanism(s) in macrophages, contributing to cell susceptibility to the acquired immune deficiency syndrome (AIDS) virus infection.
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Cite this article as:
Wang Xu, Wang Yizhong, Ye Li, Li Jieliang, Zhou Yu, Sakarcan Sinem and Ho Wenzhe, Modulation of Intracellular Restriction Factors Contributes to Methamphetamine- Mediated Enhancement of Acquired Immune Deficiency Syndrome Virus Infection of Macrophages, Current HIV Research 2012; 10 (5) . https://dx.doi.org/10.2174/157016212802138797
DOI https://dx.doi.org/10.2174/157016212802138797 |
Print ISSN 1570-162X |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4251 |
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The development of a safe and effective vaccine that impedes HIV-1 transmission and/or limits the severity of infection remains a public health priority. The HIV-1/AIDS pandemic continues to have a disproportionate impact on vulnerable and under-served communities in the USA and globally. In the USA, minority communities that have relatively ...read more
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