Assessing immune aging in HIV-infected patients

Appay, Victor; Sauce, Delphine

doi:10.1080/21505594.2016.1195536

Cited by 50 publications

(41 citation statements)

References 108 publications

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“…HIV leads to massive T cell turnover and immune exhaustion, contracted naive T cell populations, and expanded memory T cell populations (especially those T cells directed toward other chronic viruses, like cytomegalovirus (CMV)). This occurs at a younger age than in those without HIV and is only partially mitigated by ART . It has been known for many years that aging results in a similar phenotype, characterized by accumulation of more terminally differentiated CD8 + T cells in peripheral blood.…”

Section: Diseases Accelerate the Appearance Of Aging Phenotypes In Humentioning

confidence: 99%

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Kohanski

Deeks

Gravekamp

et al. 2016

Annals of the New York Academy of Sciences

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Aging is the major risk factor for both the development of chronic diseases and loss of functional capacity. Geroscience provides links among the biology of aging, the biology of disease, and the physiology of frailty, three fields where enormous progress has been made in the last few decades. While, previously, the focus was on the role of aging in susceptibility to disease and disability, the other side of this relationship, which is the contribution of disease to aging, has been less explored at the molecular/cellular level. Indeed, the role of childhood or early adulthood exposure to chronic disease and/or treatment on accelerating aging phenotypes is well known in epidemiology, but the biological basis is poorly understood. A recent summit co-organized by the National Institutes of Health GeroScience Interest Group and the New York Academy of Sciences explored these relationships, using three chronic diseases as examples: cancer, HIV/AIDS, and diabetes. The epidemiological literature clearly indicates that early exposure to any of these diseases and/or their treatments results in an acceleration of the appearance of aging phenotypes, including loss of functional capacity and accelerated appearance of clinical symptoms of aging-related diseases not obviously related to the earlier event. The discussions at the summit focused on the molecular and cellular relationships between each of these diseases and the recently defined molecular and cellular pillars of aging. Two major conclusions from the meeting include the desire to refine an operational definition of aging and to concomitantly develop biomarkers of aging, in order to move from chronological to physiological age. The discussion also opened a dialogue on the possibility of improving late-life outcomes in patients affected by chronic disease by including age-delaying modalities along with the standard care for the disease in question.

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Section: Diseases Accelerate the Appearance Of Aging Phenotypes In Humentioning

confidence: 99%

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Kohanski

Deeks

Gravekamp

et al. 2016

Annals of the New York Academy of Sciences

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“…Aging of the immune system or immunosenescence is one of the immune alterations observed in persons chronically infected with HIV, and it can persist over time despite efficacious antiretroviral therapy (ART). Blood telomere length (TL) shortening is a hallmark of this immunosenescence status [1].…”

Section: Introductionmentioning

confidence: 99%

Determinants of blood telomere length in antiretroviral treatment‐naïve HIV‐positive participants enrolled in the NEAT 001/ANRS 143 clinical trial

et al. 2019

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Objectives Our aim was to investigate factors associated with baseline blood telomere length in participants enrolled in NEAT 001/ANRS 143, a randomized, open‐label trial comparing ritonavir‐boosted darunavir (DRV/r) plus raltegravir (RAL) with DRV/r plus tenofovir disoproxil fumarate/emtricitabine (TDF/FTC) in antiretroviral therapy (ART)‐naïve HIV‐positive adults. Methods A cross‐sectional study of 201 randomly selected participants who had stored samples available was carried out. We measured telomere length (i.e. the relative telomere length, calculated as the telomere to single copy gene ratio) at baseline with monochrome quantitative multiplex polymerase chain reaction (PCR). We used multivariable predictive linear regression to calculate mean differences and 95% confidence intervals (CIs) for the association between baseline telomere length and baseline characteristics. Results The baseline characteristics of the 201 participants did not differ from those of the 805 participants in the parent trial population: 89% were male, the mean age was 39 years, 83.6% were Caucasian, 93% acquired HIV infection via sexual transmission, the mean estimated time since HIV diagnosis was 2.1 years, the mean HIV‐1 RNA load was 4.7 log10 HIV‐1 RNA copies/mL, the mean nadir and baseline CD4 counts were 301 and 324 cells/μL, respectively, and the mean CD4:CD8 ratio was 0.4. In the univariate analysis, shorter telomere length was associated with older age (per 10 years) (P < 0.001), HIV‐1 RNA ≥ 100 000 copies/mL (P = 0.001), CD4 count < 200 cells/μL (P = 0.037), lower CD4:CD8 ratio (P = 0.018), statin treatment (P = 0.004), and current alcohol consumption (P = 0.035). In the multivariable analysis, older age (P < 0.001) and HIV RNA ≥ 100 000 copies/mL (P = 0.054) were independently associated with shorter telomere length. Conclusions Both age and HIV RNA viral load correlated with shorter blood telomere length in untreated persons living with HIV. These results suggest that HIV infection and age have synergistic and independent impacts upon immunosenescence.

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“…Alcune alterazioni dei comparti dell'immunità innata e adattiva nei pazienti HIV+ ricordano i processi dell'invecchiamento immunitario caratteristici dell'età avanzata. Queste alterazioni definiscono l'età immunologica ed è probabile che partecipino al declino dell'immuno-competenza nella progressione dell'infezione da HIV (14). La prima analogia riscontrata tra il processo di invecchiamento e l'infezione da HIV è l'aumento di linfociti T CD8+ che perdono l'espressione del co-recettore CD28.…”

Section: Aspetti Immunologiciunclassified

“…Nei pazienti HIV+, l'espressione di CD69+ e HLA-DR+ correla con i livelli plasmatici di lipopolisaccaride, indicatore di traslocazione microbica intestinale. Livelli aumentati di citochine e chemochine plasmatiche associate all'attivazione monocitaria (ad esempio CD163 e CXCL10) sono descritti nel paziente anziano e nell'individuo HIV+ (20,14).…”

Section: Aspetti Immunologiciunclassified

Invecchiamento cellulare e infezione da HIV

Dentone¹,

Fenoglio²

2016

JHA

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RiassuntoCon la maggiore disponibilità della terapia antiretrovirale, la popolazione HIV positiva del mondo sta invecchiando. I pazienti trattati con successo sembra possano raggiungere una longevità che si avvicina a quella della popolazione generale. Sebbene l'aspettativa di vita dei soggetti HIV positivi stia aumentando sempre di più, è controverso se il virus stesso dell'HIV acceleri il processo di invecchiamento. L'infiammazione cronica persistente e l'immuno-attivazione osservate tipicamente nella popolazione anziana possono essere ritrovate nei pazienti HIV positivi con un processo di invecchiamento prematuro. Questi aspetti sono correlati all'immuno-senescenza che determina un danno immunologico funzionale ed una ridotta abilità adattativa allo stress metabolico. Anche se i pazienti HIV positivi con la terapia antiretrovirale raggiungono la viremia non rilevabile e un'elevata conta di TCD4+, valori elevati di infiammazione in questi soggetti sono associati alle più importanti complicanze non AIDS-correlate dell'infezione cronica da HIV. Lo scopo di questa review è l'analisi del processo dinamico del rimodellamento immunitario, conosciuto come immuno-senescenza, che avviene nella storia del paziente con infezione da HIV e della sua influenza sulle comorbità a lungo termine. Abstract With the wider availability of antiretroviral therapy, HIV positive population is aging worldwide. Successfully treated individuals could achieve a longevity approaching that of the general population. Although the life expectancy of HIV positive people has increased dramatically, whether HIV itself accelerates the aging process is still controversial. A persistent chronic inflammation and immune activation, typically observed in elderly people, can be present in HIV infected patients who experience a type of premature aging. These aspects are linked to the immune senescence that results in functional impairments of immunity and in reduced ability to adapt to metabolic stress. Even if the HIV positive patients on antiretroviral therapy reach an undetectable viral load and a high CD4 cells count, elevated rates of inflammation in these population are associated with the most important non-AIDS related complication of chronic HIV infection. The purpose of this review is to focus on the dynamic process of immune remodelling, known as immune senescence, which occurs during HIV infection, and how it affects long-term comorbidities.Introduzione L'introduzione della terapia antiretrovirale altamente efficace (HAART) ha migliorato significativamente gli aspetti immunologici e virologici del paziente HIV positivo (HIV+), modificandone anche lo stato patologico e la mortalità (1). Recenti dati riguardanti la mortalità dei soggetti HIV positivi indicano che pazienti con conta dei linfociti T CD4+ superiore a 350 cellule/mmc e soppressione virologica, in assenza di altri fattori di rischio, presentano un'aspettativa di vita simile a quella della popolazione generale (2). In Europa e negli Stati Uniti è aumentata notevolmente la proporzion...

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Assessing immune aging in HIV-infected patients

Cited by 50 publications

References 108 publications

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

Determinants of blood telomere length in antiretroviral treatment‐naïve HIV‐positive participants enrolled in the NEAT 001/ANRS 143 clinical trial

Invecchiamento cellulare e infezione da HIV

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