Biological ageing with HIV infection: evaluating the geroscience hypothesis

Montano, Monty; Oursler, Krisann K.; Sun, Yan V.; Marconi, Vincent C.

doi:10.1016/s2666-7568(21)00278-6

Cited by 38 publications

(24 citation statements)

References 161 publications

(241 reference statements)

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“…For example, reduced MN frequency is associated with daily fruit consumption [ 8 ]. In this sense, proper intake of micronutrients (e.g., antioxidant vitamins, selenium), regular physical activity, and other behavior interventions (e.g., UV protection, cessation of tobacco smoking, and adequate sleep/rest) can help reduce oxidative stress and HIV-related aging manifestations, including genome instability [ 1 , 2 , 17 , 56 , 57 ]. Specifically concerning micronutrients, it is essential to consider the potential deleterious effects of some nutrients, especially when used in inappropriate doses.…”

Section: Impacts Of Hiv Infection and Treatment On Chromosomal Integr...mentioning

confidence: 99%

“…People living with HIV, even on antiretroviral therapy (ART), suffer from chronic diseases and conditions associated with aging (e.g., cancer and cardiovascular and neurodegenerative diseases) at an increased rate compared to uninfected people. This indicates that HIV facilitates the occurrence of age-related diseases, independently or in association with other risk factors, potentially through the exacerbation of chronic inflammation, cellular senescence, mitochondrial dysfunction, telomere attrition, stem-cell exhaustion, DNA damage, and genomic instability [ 17 ]. Chronic inflammation is a major issue for HIV-infected individuals, and is caused by dysbiosis, microbial translocation, co-infections, and residual HIV replication, among other factors.…”

Section: Introductionmentioning

confidence: 99%

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HIV Infection, Chromosome Instability, and Micronucleus Formation

Ellwanger

Kulmann-Leal

Ziliotto

2023

Viruses

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Genome integrity is critical for proper cell functioning, and chromosome instability can lead to age-related diseases, including cancer and neurodegenerative disorders. Chromosome instability is caused by multiple factors, including replication stress, chromosome missegregation, exposure to pollutants, and viral infections. Although many studies have investigated the effects of environmental or lifestyle genotoxins on chromosomal integrity, information on the effects of viral infections on micronucleus formation and other chromosomal aberrations is still limited. Currently, HIV infection is considered a chronic disease treatable by antiretroviral therapy (ART). However, HIV-infected individuals still face important health problems, such as chronic inflammation and age-related diseases. In this context, this article reviews studies that have evaluated genomic instability using micronucleus assays in the context of HIV infection. In brief, HIV can induce chromosome instability directly through the interaction of HIV proteins with host DNA and indirectly through chronic inflammation or as a result of ART use. Connections between HIV infection, immunosenescence and age-related disease are discussed in this article. The monitoring of HIV-infected individuals should consider the increased risk of chromosome instability, and lifestyle interventions, such as reduced exposure to genotoxins and an antioxidant-rich diet, should be considered. Therapies to reduce chronic inflammation in HIV infection are needed.

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Section: Impacts Of Hiv Infection and Treatment On Chromosomal Integr...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

HIV Infection, Chromosome Instability, and Micronucleus Formation

Ellwanger

Kulmann-Leal

Ziliotto

2023

Viruses

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“…3 Division of Cardiovascular Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Bangkok, Thailand. 4 Division of Endocrinology and Metabolism, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. 5 Excellence Center for Diabetes, Hormone, and Metabolism, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.…”

Section: Abbreviationsmentioning

confidence: 99%

“…People living with HIV (PLWH) have increased rates of age-related comorbidities compared to the general population [ 1 , 2 ]. Aging characteristics are heterogeneous among PLWH [ 3 , 4 ], therefore, the identification of risk factors related to adverse outcomes with aging including cardiovascular diseases, neurocognitive impairment (NCI) and frailty has become increasingly relevant for the older PLWH population.…”

Section: Introductionmentioning

confidence: 99%

Association of Phenotypic Aging Marker with comorbidities, frailty and inflammatory markers in people living with HIV

et al. 2022

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Background Aging characteristics in people living with HIV (PLWH) are heterogeneous, and the identification of risk factors associated with aging-related comorbidities such as neurocognitive impairment (NCI) and frailty is important. We evaluated predictors of novel aging markers, phenotypic age (PhenoAge) and phenotypic age acceleration (PAA) and their association with comorbidities, frailty, and NCI. Methods In a cohort of PLWH and age- and sex-matched HIV-negative controls, we calculated PhenoAge using chronological age and 9 biomarkers from complete blood counts, inflammatory, metabolic-, liver- and kidney-related parameters. PAA was calculated as the difference between chronological age and PhenoAge. Multivariate logistic regression models were used to identify the factors associated with higher (>median) PAA. Area under the receiver operating characteristics curve (AUROC) was used to assess model discrimination for frailty. Results Among 333 PLWH and 102 HIV-negative controls (38% female), the median phenotypic age (49.4 vs. 48.5 years, p = 0.54) and PAA (− 6.7 vs. -7.5, p = 0.24) was slightly higher and PAA slightly less in PLWH although this did not reach statistical significance. In multivariate analysis, male sex (adjusted odds ratio = 1.68 [95%CI = 1.03–2.73]), current smoking (2.74 [1.30–5.79]), diabetes mellitus (2.97 [1.48–5.99]), hypertension (1.67 [1.02–2.72]), frailty (3.82 [1.33–10.93]), and higher IL-6 levels (1.09 [1.04–1.15]), but not HIV status and NCI, were independently associated with higher PAA. PhenoAge marker discriminated frailty better than chronological age alone (AUROC: 0.75 [0.66–0.85] vs. 0.65 [0.55–0.77], p = 0.04). In the analysis restricted to PLWH, PhenoAge alone predicted frailty better than chronological age alone (AUROC: 0.7412 vs. 0.6499, P = 0.09) and VACS index (AUROC: 0.7412 vs. 0.6811, P = 0.34) despite not statistically significant. Conclusions While PLWH did not appear to have accelerated aging in our cohort, the phenotypic aging marker was significantly associated with systemic inflammation, frailty, and cardiovascular disease risk factors. This simple aging marker could be useful to identify high-risk PLWH within a similar chronological age group.

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“…HIV-related age acceleration has been shown to be associated with reductions in total gray matter using epigenetic age as a biomarker for age acceleration [12]. Evidence indicates that increased and persistent senescence during HIV-1 infection contributes to chronic in ammation, immune failure and mitochondrial dysfunction [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Extracellular vesicle-Serpine-1 affects neural progenitor cell mitochondrial functions and synaptic density: modulation by amyloid beta and HIV-1

András

Serrano

Djuraskovic

et al. 2023

Preprint

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Brain endothelial extracellular vesicles carrying amyloid beta (EV-Aβ) can be transferred to neural progenitor cells (NPCs) leading to NPC dysfunction. However, the events involved in this EV-mediated Aβ pathology are unclear. EV-proteomics studies identified Serpine-1 (plasminogen activator inhibitor 1, PAI-1) as a major connecting “hub” on several protein-protein interaction maps. Serpine-1 was described as a key player in Aβ pathology and was linked to HIV-1 infection as well. Therefore, the aim of this work was to address the hypothesis that Serpine-1 can be transferred via EVs from brain endothelial cells to NPCs and contribute to NPC dysfunction. HBMEC concentrated and released Serpine-1 via EVs, the effect that was potentiated by HIV-1 and Aβ. EVs loaded with Serpine-1 were readily taken up by NPCs, and HIV-1 enhanced this event. Interestingly, a highly specific Serpine-1 inhibitor PAI039 increased EV-Aβ transfer to NPCs in the presence of HIV-1. PAI039 also partially blocked mitochondrial network morphology and mitochondrial function alterations in the recipient NPCs, which developed mainly after HIV + Aβ-EV transfer. PAI039 partly attenuated HIV-EV-mediated decreased synaptic protein levels in NPCs, while increased synaptic protein levels in NPC projections. These findings contribute to a better understanding of the complex mechanisms underlying EV-Serpine-1 related Aβ pathology in the context of HIV infection. They are relevant to HIV-1 associated neurocognitive disorders (HAND) in an effort to elucidate the mechanisms of neuropathology in HIV infection.

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Biological ageing with HIV infection: evaluating the geroscience hypothesis

Cited by 38 publications

References 161 publications

HIV Infection, Chromosome Instability, and Micronucleus Formation

HIV Infection, Chromosome Instability, and Micronucleus Formation

Association of Phenotypic Aging Marker with comorbidities, frailty and inflammatory markers in people living with HIV

Extracellular vesicle-Serpine-1 affects neural progenitor cell mitochondrial functions and synaptic density: modulation by amyloid beta and HIV-1

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