2021
DOI: 10.1016/j.alcohol.2021.04.003
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Possible mechanisms of HIV neuro-infection in alcohol use: Interplay of oxidative stress, inflammation, and energy interruption

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Cited by 1 publication
(2 citation statements)
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“…Alcohol use has been reported to increase CCR5 and CXCR4 for HIV-1 entry into immunologic cells, to dysregulate HIV-induced cytokines (e.g., TNFa, IL-1, and IL-6) and NF-kB regulating transcription of the HIV-1 long terminal repeat (HIV LTR), or to cause a metabolic shift and redistribution of energy usage toward HIV-1-infected neuroimmune cells, all of which accelerate HIV-1 disease progression. 3,4,[7][8][9][10] There can be additional molecular mechanisms by which alcohol and HIV PIs potentiate HIV-1 infection. The SET protein is an endoplasmic reticulum (ER)-associated chaperone protein expressed in many types of cells and has multiple biological functions depending on cell types, cellular location, and complex formations with other protein components.…”
Section: Effects Of Combination Of Ethanol With Ritonavir Lopinavir O...mentioning
confidence: 99%
See 1 more Smart Citation
“…Alcohol use has been reported to increase CCR5 and CXCR4 for HIV-1 entry into immunologic cells, to dysregulate HIV-induced cytokines (e.g., TNFa, IL-1, and IL-6) and NF-kB regulating transcription of the HIV-1 long terminal repeat (HIV LTR), or to cause a metabolic shift and redistribution of energy usage toward HIV-1-infected neuroimmune cells, all of which accelerate HIV-1 disease progression. 3,4,[7][8][9][10] There can be additional molecular mechanisms by which alcohol and HIV PIs potentiate HIV-1 infection. The SET protein is an endoplasmic reticulum (ER)-associated chaperone protein expressed in many types of cells and has multiple biological functions depending on cell types, cellular location, and complex formations with other protein components.…”
Section: Effects Of Combination Of Ethanol With Ritonavir Lopinavir O...mentioning
confidence: 99%
“…Alcohol use has been reported to increase CCR5 and CXCR4 for HIV-1 entry into immunologic cells, to dysregulate HIV-induced cytokines (e.g., TNFα, IL-1, and IL-6) and NF-κB regulating transcription of the HIV-1 long terminal repeat (HIV LTR), or to cause a metabolic shift and redistribution of energy usage toward HIV-1-infected neuroimmune cells, all of which accelerate HIV-1 disease progression. 3,4,7–10…”
mentioning
confidence: 99%