# Cell-Type Specific Mechanisms of HIV Cardiomyopathy

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 2024 · $699,504

## Abstract

Project Summary
By 2030, 73% of people with HIV will be ≥ 50 years of age and 78% will have cardiovascular disease. People
with HIV have a 50% increased risk of acute myocardial infarction, a 61% higher risk of heart failure with
reduced ejection fraction and > 4 fold higher rates of sudden cardiac death compared to the general
population. In addition to traditional risk factors, HIV-associated features such as chronic inflammation and
immune dysregulation in the setting of treated HIV infection are strong predictors of cardiovascular disease.
However, studies elucidating the pathogenesis of heart failure in HIV have been largely descriptive and have
thus provided limited insight into the underlying mechanisms of these disease processes. Thus, we propose to
address the pathogenesis of heart failure in people with HIV through investigating the impact of HIV, immune
activation and antiretroviral therapies on the broad range of cell types comprising the human heart. Overall,
the proposed studies will illuminate underlying mechanisms of HIV cardiomyopathy, which may be translated to
the creation of cell-type specific therapies for HIV-related cardiac diseases.

## Key facts

- **NIH application ID:** 10741763
- **Project number:** 5R01HL158315-03
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO
- **Principal Investigator:** Neil C Chi
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $699,504
- **Award type:** 5
- **Project period:** 2021-12-06 → 2025-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10741763

## Citation

> US National Institutes of Health, RePORTER application 10741763, Cell-Type Specific Mechanisms of HIV Cardiomyopathy (5R01HL158315-03). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10741763. Licensed CC0.

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