Longitudinal study of surrogate aging measures during human immunodeficiency virus seroconversion

Leung, Janice M.; Fishbane, Nick; Jones, Meaghan J.; Morin, Alexander M.; Xu, Stella; Liu, Joseph C. Y.; MacIsaac, J.L.; Milloy, M.-J.; Hayashi, Kanna; Montaner, Julio S. G.; Horvath, Steve; Kobor, Michael S.; Sin, Don D.; Harrigan, P. Richard; Man, S. F. Paul

doi:10.18632/aging.101184

Cited by 27 publications

(26 citation statements)

References 52 publications

(61 reference statements)

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“…13 Telomere shortening during HIV seroconversion has also been reported in a smaller sample (n = 31), using a different telomere length assay and an extended time gap (2 years) between preseroconversion and postseroconversion sampling. 16 Our study confirms this and demonstrates that rapid telomere shortening occurs quickly after HIV seroconversion, and faster than after HCV seroconversion.…”

Section: Discussionsupporting

confidence: 88%

Rapid Decrease in Peripheral Blood Mononucleated Cell Telomere Length After HIV Seroconversion, but Not HCV Seroconversion

González-Serna

Ajaykumar²,

Gadawski³

et al. 2017

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Section: Discussionsupporting

confidence: 88%

Rapid Decrease in Peripheral Blood Mononucleated Cell Telomere Length After HIV Seroconversion, but Not HCV Seroconversion

González-Serna

Ajaykumar²,

Gadawski³

et al. 2017

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…Although telomere shortening has been shown in acute infections in experimental animal models (Asghar, Hasselquist, et al., 2015; Asghar et al., 2016; Ilmonen et al., 2008), such effect has not been reported in humans. Previous studies have shown that chronic viral infections (i.e., HCV, CMV, and HIV) accelerate cellular aging in humans, as reflected by shorter telomere length and elevated CDKN2A expression (van de Berg et al., 2010; Gianesin et al., 2016; Leung et al., 2017; Pathai et al., 2013; Robinson et al., 2013; Zannetti et al., 2006). Furthermore, genome‐wide association studies (GWAS) have linked CDKN2A to many age‐related pathologies, including susceptibility to frailty and increased risk of coronary artery disease, myocardial infarction, type 2 diabetes, and Alzheimer's disease (Jeck et al., 2012).…”

Section: Discussionmentioning

confidence: 99%

“…In this study of acute malaria infection, we find distinct dynamics of cellular aging not observed during chronic infection (van de Berg et al., 2010; Gianesin et al., 2016; Leung et al., 2017; Pathai et al., 2013; Robinson et al., 2013; Zannetti et al., 2006). After successful treatment and in the absence of new infections, the effect on cellular aging markers was largely reversed as reflected by lower CDKN2A expression, higher telomerase activity, and gradual restoration of telomere length in peripheral blood of travelers from three months postinfection up to one year.…”

Section: Discussionmentioning

confidence: 99%

Cellular aging dynamics after acute malaria infection: A 12-month longitudinal study

et al. 2017

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SummaryAccelerated cellular aging and reduced lifespan have recently been shown in birds chronically infected with malaria parasites. Whether malaria infection also affects cellular aging in humans has not been reported. Here, we assessed the effect of a single acute Plasmodium falciparum malaria infection on cellular aging dynamics in travelers prospectively followed over one year in Sweden. DNA and RNA were extracted from venous blood collected at the time of admission and repeatedly up to one year. Telomere length was measured using real‐time quantitative PCR, while telomerase activity and CDKN2A expression were measured by reverse transcriptase (RT)–qPCR. Our results show that acute malaria infection affects cellular aging as reflected by elevated levels of CDKN2A expression, lower telomerase activity, and substantial telomere shortening during the first three months postinfection. After that CDKN2A expression declined, telomerase activity increased and telomere length was gradually restored over one year, reflecting that cellular aging was reversed. These findings demonstrate that malaria infection affects cellular aging and the underlying cellular mechanism by which pathogens can affect host cellular aging and longevity need to be elucidated. Our results urge the need to investigate whether repeated malaria infections have more pronounced and long‐lasting effects on cellular aging and lifespan (similarly to what was observed in birds) in populations living in malaria endemic areas.

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“…Similarly, no changes in rates of telomere shortening were found when HIV-infected individuals were switched from an ART regimen of darunavir/ritonavir supplemented with nonnucleoside reverse transcriptase inhibitor (NNRTI) to darunavir/ritonavir without NNRTI (Solomon et al 2014 ). Telomere shortening occurred after seroconversion, but no further shortening was observed with prolonged infection (Leung et al 2017 ), possibly suggesting accentuated aging as measured by telomere length.…”

Section: Molecular Markers Associated With Hiv and Agingmentioning

confidence: 99%

Aging and Apolipoprotein E in HIV Infection

Geffin

McCarthy

2018

J. Neurovirol.Has correction 2018-11-19 Has erratum 2018-11-19

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With the implementation of increasingly effective antiretroviral therapy (ART) over the past three decades, individuals infected with HIV live a much longer life. HIV infection is no longer a terminal but rather a chronic disease. However, the lifespan of infected individuals remains shorter than that of their uninfected peers. Even with ART, HIV infection may potentiate “premature” aging. Organ-associated disease and systemic syndromes that occur in treated HIV-infection are like that of older, uninfected individuals. Brain aging may manifest as structural changes or neurocognitive impairment that are beyond the chronological age. The spectrum of neurological, cognitive, and motor deficiencies, currently described as HIV-associated neurocognitive disorders (HAND), may reflect earlier onset of mechanisms common to HIV infection and aging (accelerated aging). HAND could also reflect the neurological impact of HIV infection superimposed on comorbidities linked to age and chronic inflammation, leading to a higher prevalence of neurocognitive impairment across the age span (accentuated aging). In addition, apolipoprotein E (ApoE), one of the most influential host risk factors for developing Alzheimer’s disease, has been implicated in the development of HAND. But studies differ as to whether ApoE is relevant, and whether age and ApoE interact to impair brain function in the HIV-infected patient. What is clear is that HIV-infected individuals are living longer with HIV, and therefore factors related to aging and health need to be examined in the context of current, effective ART. This review addresses the recent evidence for the influence of aging and ApoE on HIV-associated neurocognitive impairment.Electronic supplementary materialThe online version of this article (10.1007/s13365-018-0660-2) contains supplementary material, which is available to authorized users.

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Longitudinal study of surrogate aging measures during human immunodeficiency virus seroconversion

Cited by 27 publications

References 52 publications

Rapid Decrease in Peripheral Blood Mononucleated Cell Telomere Length After HIV Seroconversion, but Not HCV Seroconversion

Rapid Decrease in Peripheral Blood Mononucleated Cell Telomere Length After HIV Seroconversion, but Not HCV Seroconversion

Cellular aging dynamics after acute malaria infection: A 12-month longitudinal study

Aging and Apolipoprotein E in HIV Infection

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