# Mitochondrial function, immune aging, and frailty among people with and without HIV

> **NIH NIH P30** · JOHNS HOPKINS UNIVERSITY · 2022 · $409,375

## Abstract

This administrative supplement to the the Johns Hopkins Older Americans Independence Center
(OAIC) is designed to capitalize on the Center's expertise on intersecting biological pathways that
drive early onset of physical frailty in a subset of individuals living with HIV through the study of
mitochondrial decline as articulated in this proposal. Among people with HIV (PWH), frailty
predicts mortality, comorbidities, and hospitalization, and is an important indicator of quality of life.
The underlying mechanisms for frailty development are likely multifaceted, due in part to features
of biological aging such as mitochondrial decline and chronic inflammation. A major driver of the
aging process in PWH is mitochondrial damage, resulting from chronic HIV infection, chronic
inflammation, and the effects of some antiretroviral therapies. However, the role of changes in
mitochondrial function in the etiology of frailty among PWH remains unclear. Furthermore, each
immune cell type may develop different metabolic adaptations in response to stress. The interplay
between mitochondrial function and immune activation and senescence in the etiology of frailty
development remains unclear. We propose to evaluate the association of immune cell type-
specific mitochondrial function measurements, including mitochondrial content, membrane
potential, and superoxide, with HIV infection and frailty by leveraging longitudinal data,
specimens, and infrastructure from two established HIV cohorts: 1) the AIDS Linked to the
IntraVenous Experience cohort; and 2) the Multicenter AIDS Cohort Study. These cohorts
uniquely include PWH and comparable HIV uninfected adults. We propose the following aims to
accomplish these goals: (1) to characterize immune cell activation and senescence and cell type-
specific mitochondrial function, stratified by HIV infection status; and (2) to assess the association
between cell type-specific mitochondrial function and frailty during longitudinal follow-up among
people with and without HIV. We will apply a novel machine learning approach to characterize
the complex and high-dimensional biomarker data in immune aging and mitochondrial function to
achieve these aims. With expertise and resources from the OAIC, we will provide data on the
longitudinal change of cell type-specific mitochondrial function profiles before and after frailty
development, which will allow us to observe variations in mitochondrial function among people
with and without HIV. These aims will provide new understanding of the interplay between HIV
infection, immune aging, and mitochondrial function in the etiology of frailty.

## Key facts

- **NIH application ID:** 10614117
- **Project number:** 3P30AG021334-20S1
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Karen J. Bandeen-Roche
- **Activity code:** P30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $409,375
- **Award type:** 3
- **Project period:** 2003-06-01 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10614117

## Citation

> US National Institutes of Health, RePORTER application 10614117, Mitochondrial function, immune aging, and frailty among people with and without HIV (3P30AG021334-20S1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10614117. Licensed CC0.

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