In vivo effects of methamphetamine on HIV-1 replication: A population-based study

Jiang, Junjun; Wang, Minlian; Liang, Bingyu; Shi, Yi; Su, Qi-jian; Chen, Hui; Huang, Jiegang; Su, Jinming; Pan, Peijiang; Yu, Li; Wang, Hong; Chen, Rongfeng; Liu, Jie; Zhao, Fangning; Li, Ye; Liang, Hao

doi:10.1016/j.drugalcdep.2015.12.027

Cited by 24 publications

(22 citation statements)

References 41 publications

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“…In vitro studies suggest that METH enhances HIV-1 replication in various HIV-1–permissive cells, including monocyte-derived macrophages and dendritic cells [57, 58]. METH has also been shown to increase replication of the feline immunodeficiency virus in astrocytes.…”

Section: Discussionmentioning

confidence: 99%

Identification of whole blood mRNA and microRNA biomarkers of tissue damage and immune function resulting from amphetamine exposure or heat stroke in adult male rats

et al. 2019

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This work extends the understanding of how toxic exposures to amphetamine (AMPH) adversely affect the immune system and lead to tissue damage. Importantly, it determines which effects of AMPH are and are not due to pronounced hyperthermia. Whole blood messenger RNA (mRNA) and whole blood and serum microRNA (miRNA) transcripts were identified in adult male Sprague-Dawley rats after exposure to toxic AMPH under normothermic conditions, AMPH when it produces pronounced hyperthermia, or environmentally-induced hyperthermia (EIH). mRNA transcripts with large increases in fold-change in treated relative to control rats and very low expression in the control group were a rich source of organ-specific transcripts in blood. When severe hyperthermia was produced by either EIH or AMPH, significant increases in circulating organ-specific transcripts for liver ( Alb , Fbg , F2 ), pancreas ( Spink1 ), bronchi/lungs ( F3 , Cyp4b1 ), bone marrow ( Np4 , RatNP-3b ), and kidney ( Cesl1 , Slc22a8 ) were observed. Liver damage was suggested also by increased miR-122 levels in the serum. Increases in muscle/heart-enriched transcripts were produced by AMPH even in the absence of hyperthermia. Expression increases in immune-related transcripts, particularly Cd14 and Vcan , indicate that AMPH can activate the innate immune system in the absence of hyperthermia. Most transcripts specific for T-cells decreased 50–70% after AMPH exposure or EIH, with the noted exception of Ccr5 and Chst12 . This is probably due to T-cells leaving the circulation and down-regulation of these genes. Transcript changes specific for B-cells or B-lymphoblasts in the AMPH and EIH groups ranged widely from decreasing ≈ 40% ( Cd19 , Cd180 ) to increasing 30 to 100% ( Tk1 , Ahsa1 ) to increasing ≥500% ( Stip1 , Ackr3 ). The marked increases in Ccr2 , Ccr5 , Pld1 , and Ackr3 produced by either AMPH or EIH observed in vivo provide further insight into the initial immune system alterations that result from methamphetamine and AMPH abuse and could modify risk for HIV and other viral infections.

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Section: Discussionmentioning

confidence: 99%

Identification of whole blood mRNA and microRNA biomarkers of tissue damage and immune function resulting from amphetamine exposure or heat stroke in adult male rats

et al. 2019

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“…Finally, METH use is significantly associated with higher plasma viral loads when compared with patients not abusing METH. These effects are independent from antiretroviral therapy (17)(18)(19)(20).…”

Section: Hiv Infectivity In Neural Progenitor Cellsmentioning

confidence: 98%

Methamphetamine increases HIV infectivity in neural progenitor cells

Skowrońska

McDonald

Velichkovska

et al. 2018

Journal of Biological Chemistry

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HIV-1 infection and methamphetamine (METH) abuse frequently occur simultaneously and may have synergistic pathological effects. Although HIV-positive/active METH users have been shown to have higher HIV viral loads and experience more severe neurological complications than non-users, the direct impact of METH on HIV infection and its link to the development of neurocognitive alternations are still poorly understood. In the present study, we hypothesized that METH impacts HIV infection of neural progenitor cells (NPCs) by a mechanism encompassing NFκB/SP1-mediated HIV LTR activation. Mouse and human NPCs were infected with EcoHIV (modified HIV virus infectious to mice) and HIV, respectively, in the presence or absence of METH (50 or 100 μm). Pretreatment with METH, but not simultaneous exposure, significantly increased HIV production in both mouse and human NPCs. To determine the mechanisms underlying these effects, cells were transfected with different variants of HIV LTR promoters and then exposed to METH. METH treatment induced transcriptional activity of the HIV LTR promotor, an effect that required both NFκB and SP1 signaling. Pretreatment with METH also decreased neuronal differentiation of HIV-infected NPCs in both and settings. Importantly, NPC-derived daughter cells appeared to be latently infected with HIV. This study indicates that METH increases HIV infectivity of NPCs, through the NFκB/SP1-dependent activation of the HIV LTR and with the subsequent alterations of NPC neurogenesis. Such events may underlie METH- exacerbated neurocognitive dysfunction in HIV-infected patients.

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“…METH at pharmacological concentrations exerts a direct immunosuppressive effect on dendritic cells and macrophages [23, 24]. Also, enhancement of HIV infection [1, 7, 8] and replication of the virus inside of macrophages [35, 36] are excellent examples of how METH can modify the pathogenesis of an infectious disease. Active METH-using HIV-infected persons have higher viral loads than those who never used the drug or recently used the drug [1].…”

Section: Discussionmentioning

confidence: 99%

Capsular specific IgM enhances complement-mediated phagocytosis and killing of Cryptococcus neoformans by methamphetamine-treated J774.16 macrophage-like cells

Aslanyan

Ekhar

DeLeon-Rodriguez

et al. 2017

International Immunopharmacology

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Methamphetamine (METH) is a powerful and highly addictive stimulant that affects the central nervous system of users in the United States and worldwide, and its consumption is associated to the acquisition of HIV and AIDS-related infections. METH enhances cryptococcosis in mice, an opportunistic infection caused by the encapsulated fungus Cryptococcus neoformans. Due to its ability to survive within macrophages, C. neoformans is an ideal model to study pathogen-macrophage interactions. METH abrogates normal macrophage function, which might contribute to the higher rate and more rapid progression of infections in drug abusers. Hence, we investigated the role of complement and specific IgM to C. neoformans capsular polysaccharide on the function of J774.16 macrophage-like cells after exposure to METH. We found that complement and IgM significantly promotes complement-mediated phagocytosis of C. neoformans by J774.16 cells in comparison to co-incubation with complement alone. IgM enhances the expression of complement receptor 3 on the surface macrophages treated with the drug. Also, IgM-increased macrophage phagocytosis of C. neoformans may be associated with upregulation of GTPase-RhoA, a key regulator of the actin polymerization signaling cascade. Fungal cells incubated with complement and IgM in the presence of METH demonstrated higher number of cells per aggregate, a possible explanation for their enhanced ingestion by phagocytes. IgM increased killing of yeast cells by macrophages by inhibiting the alkalization of the phagosome and stimulating the intracellular production of nitric oxide. Together, our findings suggest that IgM stimulates the effector functions of macrophages against opportunistic pathogens in the setting of drug abuse.

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In vivo effects of methamphetamine on HIV-1 replication: A population-based study

Cited by 24 publications

References 41 publications

Identification of whole blood mRNA and microRNA biomarkers of tissue damage and immune function resulting from amphetamine exposure or heat stroke in adult male rats

Identification of whole blood mRNA and microRNA biomarkers of tissue damage and immune function resulting from amphetamine exposure or heat stroke in adult male rats

Methamphetamine increases HIV infectivity in neural progenitor cells

Capsular specific IgM enhances complement-mediated phagocytosis and killing of Cryptococcus neoformans by methamphetamine-treated J774.16 macrophage-like cells

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