# Microbiota-Mediated Bidirectional Interactions Between Alcohol Misuse and Post-COVID-19 Syndrome

> **NIH NIH R01** · RUSH UNIVERSITY MEDICAL CENTER · 2023 · $207,052

## Abstract

PROJECT SUMMARY
Recent data show that 10-30% of coronavirus disease 2019 (COVID-19) patients do not fully recover and suffer
from a wide range of symptoms that persist after the SARS-CoV-2 infection has been cleared (so-called post-
COVID-19 syndrome or Long Hauler). Severe COVID-19 and associated risk factors appear to increase the risk
of developing post-COVID-19 syndrome and yet a substantial number of patients without known risk factors also
develop post-COVID-19 syndrome. Thus, additional risk factors leading to post-COVID-19 syndrome must exist.
One potential risk factor is excessive alcohol consumption. (1) Alcohol is the most frequently used drug in the
United States, and alcohol use increases during public health crises, especially in socioeconomic disadvantaged
communities. (2) Alcohol results in inappropriate immune responses to pathogens. (3) Alcohol disrupts intestinal
and lung barrier integrity which can further promote inflammation. We recently showed that increased serum
Zonulin (a marker of disrupted intestinal barrier integrity) and increased endotoxin (LBP) are associated with
inflammation during COVID-19 and can predict disease severity and mortality. Accordingly, we hypothesize
that: (a) there is a bidirectional interaction between alcohol misuse and SARS-CoV-2 infection leading to
increased risk of post-COVID-19 syndrome in patients with alcohol use disorder (AUD) and more severe AUD
in COVID-19 patients; and (b) the underlying mechanism of these interactions is microbiota dysbiosis and/or
disruption of intestinal barrier integrity, promoting inflammation and dysregulated immune-responses to the virus.
To test our hypotheses, we will leverage our NIAAA supported COVID-19 supplement at Rush University Medical
Center (RUMC), which is actively following more than 7,000 SARS-CoV-2 positive patients and 2,000 SARS-
CoV-2 negative patients over 12 months using structured questionnaires. All patients are screened for alcohol
use/misuse. Furthermore, we will recruit a subset of patients to provide biological samples to test our mechanistic
hypothesis evaluating the link between AUD, post-COVID-19 syndrome, and gut-derived inflammation. In Aim
1, we will test the hypothesis that AUD increases the risk and severity of post-COVID-19 syndrome by
promoting gut-derived inflammation. (1a) We will determine if increased alcohol use/misuse is associated
with risk and severity of post-COVID-19 syndrome. (1b) We will elucidate the role of gut-derived inflammation in
AUD promotion of the post-COVID-19 syndrome by interrogating stool microbiota composition/function, systemic
markers of intestinal barrier integrity, inflammation, and immune activation. In Aim 2, we will test the
hypothesis that COVID-19 increases the risk and severity of AUD and alcohol-induced intestinal barrier
disruption. (2a) we will determine whether post-COVID-19 syndrome is associated with increased risk of AUD.
(2b) We will determine if COVID-19 decreases resilience of in...

## Key facts

- **NIH application ID:** 10690068
- **Project number:** 5R01AA029859-03
- **Recipient organization:** RUSH UNIVERSITY MEDICAL CENTER
- **Principal Investigator:** Mohamed Abdel Mohsen
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $207,052
- **Award type:** 5
- **Project period:** 2021-09-22 → 2025-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10690068

## Citation

> US National Institutes of Health, RePORTER application 10690068, Microbiota-Mediated Bidirectional Interactions Between Alcohol Misuse and Post-COVID-19 Syndrome (5R01AA029859-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10690068. Licensed CC0.

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