HIV-1 and HIV-2 infections induce autophagy in Jurkat and CD4+ T cells

Wang, Handong; Gao, Yamei; Tan, Jiying; Devadas, Krishnakumar; Ragupathy, Viswanath; Takeda, Kazuyo; Zhao, Jiangqin; Hewlett, Indira

doi:10.1016/j.cellsig.2012.02.016

Cited by 45 publications

(46 citation statements)

References 28 publications

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“…Autophagy has recently been associated with HIV-1 replication in macrophages but has also been suggested to contribute to CD4 ϩ T cell death (43,46,47,50,57). We next wanted to determine if ASP could contribute to HIV-1-induced autophagy by further addressing its induction potential.…”

Section: Resultsmentioning

confidence: 99%

Detection of the HIV-1 Minus-Strand-Encoded Antisense Protein and Its Association with Autophagy

Torresilla

Larocque

Landry

et al. 2013

J Virol

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Section: Resultsmentioning

confidence: 99%

Detection of the HIV-1 Minus-Strand-Encoded Antisense Protein and Its Association with Autophagy

Torresilla

Larocque

Landry

et al. 2013

J Virol

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“…Mounting evidence suggests modulation of autophagy in response to HIV-1 41,42 or morphine. 24 Depending on cell type, the effect of HIV-1 on autophagy varies with the course of productive infection or bystander effect of viral proteins.…”

Section: Discussionmentioning

confidence: 99%

Enhanced autophagy in pulmonary endothelial cells on exposure to HIV-Tat and morphine: Role in HIV-related pulmonary arterial hypertension

et al. 2016

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Intravenous drug use is one of the major risk factors for HIV-infection in HIV-related pulmonary arterial hypertension patients. We previously demonstrated exaggerated pulmonary vascular remodeling with enhanced apoptosis followed by increased proliferation of pulmonary endothelial cells on simultaneous exposure to both opioids and HIV protein(s). Here we hypothesize that the exacerbation of autophagy may be involved in the switching of endothelial cells from an early apoptotic state to later hyperproliferative state. Treatment of human pulmonary microvascular endothelial cells (HPMECs) with both the HIV-protein Tat and morphine resulted in an oxidative stress-dependent increase in the expression of various markers of autophagy and formation of autophagosomes when compared to either Tat or morphine monotreatments as demonstrated by western blot, transmission electron microscopy and immunofluorescence. Autophagy flux experiments suggested increased formation rather than decreased clearance of autolysosomes. Inhibition of autophagy resulted in a significant increase in apoptosis and reduction in proliferation of HPMECs with combined morphine and Tat (MCT) treatment compared to monotreatments whereas stimulation of autophagy resulted in opposite effects. Significant increases in the expression of autophagy markers as well as the number of autophagosomes and autolysosomes was observed in the lungs of SIV-infected macaques and HIV-infected humans exposed to opioids. Overall our findings indicate that morphine in combination with viral protein(s) results in the induction of autophagy in pulmonary endothelial cells that may lead to an increase in severity of angio-proliferative remodeling of the pulmonary vasculature on simian and human immunodeficiency virus infection in the presence of opioids.

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“…It has been shown that autophagy is activated in mammalian cells by a variety of viruses, including human immunodeficiency virus (HIV), varicella-zoster virus, and influenza virus H9N2/G1 (60)(61)(62). HTLV-1 and HTLV-2 were recently reported to regulate autophagy pathway in Jurkat and CD4 ϩ T cells, respectively; how- .…”

Section: Discussionmentioning

confidence: 99%

Human T-Cell Leukemia Virus Type 1 Tax-Deregulated Autophagy Pathway and c-FLIP Expression Contribute to Resistance against Death Receptor-Mediated Apoptosis

Wang

Zhou

Shi

et al. 2014

J Virol

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The human T-cell leukemia virus type 1 (HTLV-1) Tax protein is considered to play a central role in the process that leads to adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 Tax IMPORTANCEOur study reveals that Tax-deregulated autophagy is a protective mechanism for DR-mediated apoptosis. The molecular mechanism of Tax-induced autophagy is also illuminated, which is different from Tax-increased c-FLIP. Tax can be degraded via manipulation of autophagy and TRAIL-induced apoptosis. These results outline a complex regulatory network between and among apoptosis, autophagy, and Tax and also present evidence that autophagy represents a new possible target for therapeutic intervention for the HTVL-1 related diseases.

show abstract

HIV-1 and HIV-2 infections induce autophagy in Jurkat and CD4+ T cells

Cited by 45 publications

References 28 publications

Detection of the HIV-1 Minus-Strand-Encoded Antisense Protein and Its Association with Autophagy

Detection of the HIV-1 Minus-Strand-Encoded Antisense Protein and Its Association with Autophagy

Enhanced autophagy in pulmonary endothelial cells on exposure to HIV-Tat and morphine: Role in HIV-related pulmonary arterial hypertension

Human T-Cell Leukemia Virus Type 1 Tax-Deregulated Autophagy Pathway and c-FLIP Expression Contribute to Resistance against Death Receptor-Mediated Apoptosis

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