2020
DOI: 10.1007/s11904-020-00484-4
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Dysfunctional Immunometabolism in HIV Infection: Contributing Factors and Implications for Age-Related Comorbid Diseases

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Cited by 22 publications
(19 citation statements)
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“…Emphasis has been rightfully placed on impairments in oxidative phosphorylation in neuroHIV and degenerative diseases, such as AD 84 , 102 105 . The present pathway analysis underscores the potential contribution of disruptions of the TCA cycle and β-oxidation in the mitochondrial matrix, in which oxidative phosphorylation depends on the supply of reducing equivalents from the end-oxidation of nutrients 106 .…”
Section: Discussionmentioning
confidence: 99%
“…Emphasis has been rightfully placed on impairments in oxidative phosphorylation in neuroHIV and degenerative diseases, such as AD 84 , 102 105 . The present pathway analysis underscores the potential contribution of disruptions of the TCA cycle and β-oxidation in the mitochondrial matrix, in which oxidative phosphorylation depends on the supply of reducing equivalents from the end-oxidation of nutrients 106 .…”
Section: Discussionmentioning
confidence: 99%
“…Rising numbers of immunometabolic studies in the field of HIV-1 describe increased mitochondrial respiration in CD4 + T cells of HIV-1-infected persons with glutamine as a source for oxidative phosphorylation. These changes in immunometabolism are associated with increased expression of ROS and inflammatory cytokines, and immunometabolic dysfunction might further mediate the development of agerelated diseases (31,32). Further investigating the pathway of oxidative phosphorylation might give valuable insights into HIV-1 pathogenesis and targeting it with drugs could have a promising therapeutic potential for HIV-1-infected individuals.…”
Section: Discussionmentioning
confidence: 99%
“…However, the prevalence of cardiovascular diseases (CVDs) and CVD-related mortality has increased among PLHIV, who are up to two times more likely to present a CVD episode compared with HIV-negative individuals [7][8][9] . The pathogenesis of CVD, including hypertension, in PLHIV is a complex interaction between traditional risk factors (dyslipidemia, diabetes, smoking, and sedentary lifestyle), HIV infection (viral activity, decreased TCD4+ cell count, chronic systemic inflammation, and endothelial dysfunction), and risk factors associated with HAART (dyslipidemia, endothelial damage, carotid thickness, and lipodystrophy) [10][11][12] .…”
Section: Introductionmentioning
confidence: 99%