Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors

Abstract Background Methamphetamine (METH), a potent addictive psychostimulant, is highly prevalent in HIV-infected individuals. Clinically, METH use is implicated in alteration of immune system and increase of HIV spread/replication. Therefore, it is of importance to examine whether METH has direct...

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Autores principales:	Yu Liu, Feng-Zhen Meng, Xu Wang, Peng Wang, Jin-Biao Liu, Wen-Hui Hu, Won-Bin Young, Wen-Zhe Ho
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	Methamphetamine Human immunodeficiency virus Interferon-stimulated genes Monocytes Biotechnology TP248.13-248.65 Biology (General) QH301-705.5 Biochemistry QD415-436
Acceso en línea:	https://doaj.org/article/782e61a2422e42c3a01f37859d6dc0fa
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spelling	oai:doaj.org-article:782e61a2422e42c3a01f37859d6dc0fa2021-11-14T12:31:46ZMethamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors10.1186/s13578-021-00703-42045-3701https://doaj.org/article/782e61a2422e42c3a01f37859d6dc0fa2021-11-01T00:00:00Zhttps://doi.org/10.1186/s13578-021-00703-4https://doaj.org/toc/2045-3701Abstract Background Methamphetamine (METH), a potent addictive psychostimulant, is highly prevalent in HIV-infected individuals. Clinically, METH use is implicated in alteration of immune system and increase of HIV spread/replication. Therefore, it is of importance to examine whether METH has direct effect on HIV infection of monocytes, the major target and reservoir cells for the virus. Results METH-treated monocytes were more susceptible to HIV infection as evidenced by increased levels of viral proteins (p24 and Pr55Gag) and expression of viral GAG gene. In addition, using HIV Bal with luciferase reporter gene (HIV Bal-eLuc), we showed that METH-treated cells expressed higher luciferase activities than untreated monocytes. Mechanistically, METH inhibited the expression of IFN-λ1, IRF7, STAT1, and the antiviral IFN-stimulated genes (ISGs: OAS2, GBP5, ISG56, Viperin and ISG15). In addition, METH down-regulated the expression of the HIV restriction microRNAs (miR-28, miR-29a, miR-125b, miR-146a, miR-155, miR-223, and miR-382). Conclusions METH compromises the intracellular anti-HIV immunity and facilitates HIV replication in primary human monocytes.Yu LiuFeng-Zhen MengXu WangPeng WangJin-Biao LiuWen-Hui HuWon-Bin YoungWen-Zhe HoBMCarticleMethamphetamineHuman immunodeficiency virusInterferon-stimulated genesMonocytesBiotechnologyTP248.13-248.65Biology (General)QH301-705.5BiochemistryQD415-436ENCell & Bioscience, Vol 11, Iss 1, Pp 1-9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Methamphetamine Human immunodeficiency virus Interferon-stimulated genes Monocytes Biotechnology TP248.13-248.65 Biology (General) QH301-705.5 Biochemistry QD415-436
spellingShingle	Methamphetamine Human immunodeficiency virus Interferon-stimulated genes Monocytes Biotechnology TP248.13-248.65 Biology (General) QH301-705.5 Biochemistry QD415-436 Yu Liu Feng-Zhen Meng Xu Wang Peng Wang Jin-Biao Liu Wen-Hui Hu Won-Bin Young Wen-Zhe Ho Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors
description	Abstract Background Methamphetamine (METH), a potent addictive psychostimulant, is highly prevalent in HIV-infected individuals. Clinically, METH use is implicated in alteration of immune system and increase of HIV spread/replication. Therefore, it is of importance to examine whether METH has direct effect on HIV infection of monocytes, the major target and reservoir cells for the virus. Results METH-treated monocytes were more susceptible to HIV infection as evidenced by increased levels of viral proteins (p24 and Pr55Gag) and expression of viral GAG gene. In addition, using HIV Bal with luciferase reporter gene (HIV Bal-eLuc), we showed that METH-treated cells expressed higher luciferase activities than untreated monocytes. Mechanistically, METH inhibited the expression of IFN-λ1, IRF7, STAT1, and the antiviral IFN-stimulated genes (ISGs: OAS2, GBP5, ISG56, Viperin and ISG15). In addition, METH down-regulated the expression of the HIV restriction microRNAs (miR-28, miR-29a, miR-125b, miR-146a, miR-155, miR-223, and miR-382). Conclusions METH compromises the intracellular anti-HIV immunity and facilitates HIV replication in primary human monocytes.
format	article
author	Yu Liu Feng-Zhen Meng Xu Wang Peng Wang Jin-Biao Liu Wen-Hui Hu Won-Bin Young Wen-Zhe Ho
author_facet	Yu Liu Feng-Zhen Meng Xu Wang Peng Wang Jin-Biao Liu Wen-Hui Hu Won-Bin Young Wen-Zhe Ho
author_sort	Yu Liu
title	Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors
title_short	Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors
title_full	Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors
title_fullStr	Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors
title_full_unstemmed	Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors
title_sort	methamphetamine facilitates hiv infection of primary human monocytes through inhibiting cellular viral restriction factors
publisher	BMC
publishDate	2021
url	https://doaj.org/article/782e61a2422e42c3a01f37859d6dc0fa
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Methamphetamine facilitates HIV infection of primary human monocytes through inhibiting cellular viral restriction factors

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