# Alcohol metabolism potentiates HIV-induced lung and liver multimorbidity via inter-organ crosstalk

> **NIH NIH K99** · EMORY UNIVERSITY · 2024 · $148,449

## Abstract

PROJECT SUMMARY/ABSTRACT
Human immunodeficiency virus (HIV) / acquired immune deficiency syndrome (AIDS) remains one of the most
critical public health problems in the 21st century, with more than 39 million global infections. Antiretroviral
therapy (ART) significantly suppresses viremia, leading to a decline in AIDS-related mortality. Conversely, there
are emerging concerns of multimorbidity (i.e., co-occurrence of ≥2 chronic diseases) despite ART-induced
longevity. Multimorbidity significantly impacts the health quality of people living with HIV (PLWH) and poses a
substantial financial burden on the healthcare system. While HIV drives multimorbidity, alcohol, consumed by
more than 50% of PLWH, promotes HIV-associated multimorbidity. Alcohol mediates multimorbidity by promoting
organ-organ crosstalk via extracellular vesicles (EVs) and inflammatory mediators. The direct effects of HIV and
alcohol on the lungs and the liver have been demonstrated; however, there is a gap in knowledge about whether
HIV- and alcohol-induced lung and liver injuries are regulated by EV-mediated crosstalk. The objectives of the
studies outlined in this proposal are to investigate the triggering effects of alcohol metabolism and HIV on the
secretion of lung-derived EVs and the role of these EVs in amplifying the release of liver cytokines into circulation
to induce lung injury. To achieve these objectives, during the K99 phase of this award, the PI will determine how
alcohol enhances EV release in HIV-infected alveolar macrophages, AMs (Aim 1). Then, the roles of EVs
secreted by alcohol and HIV-stressed AMs in the depletion of alveolar epithelial cells and barrier dysfunction will
be examined (Aim 2). During the R00 phase, the PI will examine the contribution of EVs to lung-liver crosstalk
driven by HIV infection and EtOH consumption in vivo (Aim 3). Successful completion of these studies will identify
molecular targets that will make it possible to concurrently address both lung and liver multimorbidity among
PLWH who misuse alcohol.
The PI’s focus on alcohol research began during his predoctoral training when he investigated the contribution
of the hepatocyte-hepatic stellate cell axis to alcohol—and HIV-induced liver injury via the NRSA NIAAA F31
funding mechanism. The PI acquired additional expertise with numerous molecular techniques during his
postdoctoral training in the laboratories of Dr. Yeligar and Koval, when exploring the contribution of alcohol and
HIV to AM immune dysfunction and alveolar barrier impairment.
The support from this MOSAIC K99/R00 grant will provide the PI an outstanding opportunity to expand and
consolidate his experimental and laboratory skills, collect critical preliminary data for subsequent grant
applications, present research findings at national meetings, and support his career goal to become an
independent investigator. Thus, this MOSAIC K99/R00 application provides an excellent opportunity to advance
the career of the PI in develop...

## Key facts

- **NIH application ID:** 11085643
- **Project number:** 1K99AA032220-01
- **Recipient organization:** EMORY UNIVERSITY
- **Principal Investigator:** Moses O New-Aaron
- **Activity code:** K99 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $148,449
- **Award type:** 1
- **Project period:** 2024-09-17 → 2026-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11085643

## Citation

> US National Institutes of Health, RePORTER application 11085643, Alcohol metabolism potentiates HIV-induced lung and liver multimorbidity via inter-organ crosstalk (1K99AA032220-01). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/11085643. Licensed CC0.

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