Reevaluation of immune activation in the era of cART and an aging HIV-infected population

Armas, Lesley R. de; Pallikkuth, Suresh; George, Valérie; Rinaldi, Stefano; Pahwa, Rajendra; Arheart, Kristopher L.; Pahwa, Savita

doi:10.1172/jci.insight.95726

Cited by 37 publications

(53 citation statements)

References 60 publications

(60 reference statements)

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“…Interestingly the young HIV + showed maximum variance from HIV − and more rapid decay in titer after peak at 28 days postvaccination. In statistical analysis somewhat surprisingly effect of age rather than HIV dominated the impaired immune response observed in old persons (age > 60 years), whereas HIV clearly had a strong effect on immunity at younger ages ( 99 , 100 ).…”

Section: Introductionmentioning

confidence: 87%

“…To examine the role of age and HIV infection further, we are engaged in a large ongoing study ( 99 , 100 ) in virologically suppressed HIV + and HIV − adults grouped by age as young (<40 years), middle aged (40–59 years), and old (≥60 years). Following seasonal trivalent influenza vaccine (TIV), magnitude of Ab titers against each vaccine strain were found to be lower in old age compared to others, regardless of HIV status.…”

Section: Introductionmentioning

confidence: 99%

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T Follicular Helper Cells and B Cell Dysfunction in Aging and HIV-1 Infection

et al. 2017

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T follicular helper (Tfh) cells are a subset of CD4 T cells that provide critical signals to antigen-primed B cells in germinal centers to undergo proliferation, isotype switching, and somatic hypermutation to generate long-lived plasma cells and memory B cells during an immune response. The quantity and quality of Tfh cells therefore must be tightly controlled to prevent immune dysfunction in the form of autoimmunity and, on the other hand, immune deficiency. Both Tfh and B cell perturbations appear during HIV infection resulting in impaired antibody responses to vaccines such as seasonal trivalent influenza vaccine, also seen in biologic aging. Although many of the HIV-associated defects improve with antiretroviral therapy (ART), excess immune activation and antigen-specific B and T cell responses including Tfh function are still impaired in virologically controlled HIV-infected persons on ART. Interestingly, HIV infected individuals experience increased risk of age-associated pathologies. This review will discuss Tfh and B cell dysfunction in HIV infection and highlight the impact of chronic HIV infection and aging on Tfh–B cell interactions.

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Section: Introductionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

T Follicular Helper Cells and B Cell Dysfunction in Aging and HIV-1 Infection

et al. 2017

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“…Serum antibody responses postvaccination showed the best responses (frequency and magnitude) in young uninfected participants, whereas a high proportion of old uninfected participants, as well as PWH of all age groups, were vaccine nonresponders (VNR). 49 Defects of B cells 50 and monocyte/macrophages 51 and association of inflammation and immune activation with VNR status 52 were also described. Interestingly, there was also a profound deficiency of influenza-specific and total peripheral T follicular helper (pTfh) cells in VNR and their pTfh cells exhibited markers of immune activation.…”

Section: Immune Dysregulation: Inflammation Activation Vaccine Respmentioning

confidence: 99%

Harvard HIV and Aging Workshop: Perspectives and Priorities from Claude D. Pepper Centers and Centers for AIDS Research

Montano

Bhasin

D’Aquila

et al. 2019

AIDS Research and Human Retroviruses

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People aging with HIV (PAWH) infection experience greater impairments in physical and cognitive function, in addition to higher rates of peripheral comorbid conditions (e.g., renal failure, diabetes, bone fracture, hypertension, cardiovascular disease, polypharmacy, and multimorbidity). While multifactorial drivers, including HIV infection itself, antiretroviral therapy-related toxicities, disparities in care, and biobehavioral factors, likely contribute, there remains an overarching question as to what are the relevant age-related mechanisms and models that could inform interventions that promote health span and life span in PAWH? This workshop was convened to hear from experts on the biology of aging and HIV researchers studying PAWH to focus on advancing investigations at the interface of HIV and Aging. In this study, we summarize the discussions from the Harvard Center for AIDS Research and Boston Claude D. Pepper cosponsored workshop on HIV and Aging, which took place in October 2018.

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“…The mechanism explaining CD4 + T cell loss during HIV infection is still debated (4,5). Persistent immune activation plays a critical role in the induction of this CD4 + T cell decline (6)(7)(8). A major mechanism results from damage of the mucosal barrier and lymphoid tissues of the gastrointestinal (GI) tract that follows acute infection.…”

Section: Introductionmentioning

confidence: 99%