HIV and aging, biological mechanisms, and therapies: What do we know?

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dc.contributor.authorGrosso, Tomás M.
dc.contributor.authorAlcamí, José
dc.contributor.authorArribas, Jose
dc.contributor.authorMartín, Marta
dc.contributor.authorSereti, Irini
dc.contributor.authorTarr, Philip
dc.contributor.authorCahn, Pedro
dc.contributor.authorClotet, Bonaventura
dc.contributor.authorSued, Omar
dc.contributor.authorNegredo, Eugenia
dc.date.accessioned2024-05-20T20:01:11Z
dc.date.available2024-05-20T20:01:11Z
dc.date.issued2022
dc.description.abstractAging, a time-dependent loss of physiological function, and its drivers are turning into a significant topic of research as the population's mean age increases. Epigenetic alterations, telomere shortening or dysfunction, mitogenic stress, oxidative stress, or accumulation of DNA damage can drive the cell to senescence: a permanent cell cycle arrest sometimes associated with a secretory phenotype and inflammatory consequences in the surrounding tissue. The amount of senescent cells grows over time in older organisms and may induce tissue inflammation and threaten overall tissue homeostasis, favoring aging. Senolytic and senomorphic therapeutics are an emerging approach to eliminate senescent cells or to block their secretory phenotypes respectively. Given that people living with HIV suffer non-AIDS comorbidities in a higher prevalence than the general population, aging is accentuated among them. Inflammation biomarkers may be helpful to assess prognosis or act as surrogate endpoints for studies of strategies focused on reversal of HIV-associated accelerated aging. This review summarizes the latest findings in aging and its major drivers, under the light of HIV infection. Since the number of older PLWH is currently rising, it will be of great importance to address and treat their age-related conditions, as well as to better decipher their biological mechanisms.
dc.identifier.otherDOI: 10.24875/AIDSRev.21000085
dc.identifier.urihttps://repositorio.huesped.org.ar/handle/123456789/984
dc.language.isoen
dc.publisherPermanyer Publications
dc.relation.ispartofseriesAIDS Reviews; 24(2)
dc.subjectAging
dc.subjectHIV infection
dc.subjectGenomic instability
dc.subjectCellular senescence
dc.subjectTelomeres
dc.subjectSenolytics
dc.titleHIV and aging, biological mechanisms, and therapies: What do we know?
dc.typeArticle

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