Alcohol consumption can heighten the risk of SARS-CoV-2 infection and influence how the body responds to the virus. A study conducted by researchers affiliated with the Emory University School of Medicine in the United States and published in a major physiology journal examined this connection in depth. The investigation included individuals with alcohol use disorder alongside a control group without dependence, enabling researchers to compare airway biology across different exposure histories.
Samples were gathered from the respiratory tract of both groups, and laboratory models of airway epithelium were developed. These models mimic the mucosal surfaces lining the larynx, lungs, bronchi, and nasopharynx, providing a controlled setup to observe how chronic alcohol exposure might affect airway tissue. By recreating the behavior of mucosal tissues under realistic conditions, scientists could study biological responses with precision and reduce the variability often seen in living subjects. [citation: Emory University study]
To identify molecular changes associated with alcohol exposure, researchers used RNA sequencing to map gene expression patterns within the epithelial models. This method showed how long-term alcohol use can reshape cellular pathways that govern airway function, immune signaling, and inflammatory responses. After establishing baseline differences, the team introduced SARS-CoV-2 into the models to observe how infected airway tissues respond in environments shaped by alcohol exposure. Inflammatory responses were quantified, offering a direct view of how alcohol might modify viral infection dynamics and tissue inflammation. [citation: Emory University study]
The results indicated that prior alcohol exposure increases the sensitivity of respiratory tract cells to SARS-CoV-2. This heightened responsiveness could worsen early symptoms and raise the likelihood of infection during the initial phase of disease. Cells derived from individuals with alcohol use disorder exhibited a distinct pro-inflammatory profile that intensified after viral challenge. Specifically, researchers noted elevated levels of inflammatory mediators, including cytokines such as TNFα, IL-1β, and IFNγ, which play central roles in coordinating immune and inflammatory responses. These mediators can amplify signaling loops that drive tissue inflammation and may contribute to more pronounced symptoms in the early stages of infection. [citation: Emory University study]
Additionally, the study identified barrier dysfunction in bronchial epithelial cells linked to chronic alcohol exposure. This impairment weakens the protective membranes that normally help prevent pathogen entry, potentially increasing vulnerability to respiratory infections. When barrier properties are compromised, viruses can access underlying tissues more easily, and the local immune environment may respond in ways that influence disease trajectory. [citation: Emory University study]
Overall, the findings suggest that alcohol consumption can prime airway tissues for a more inflammatory and potentially less protective response to SARS-CoV-2. The implications extend to both susceptibility to infection and the early course of disease. The study emphasizes the importance of considering substance use as a factor in respiratory infection risk and highlights biological pathways that could be targeted for therapeutic strategies aimed at reducing virus-induced inflammation in populations with heightened vulnerability. While this work centers on a specific virus, the broader message resonates with how lifestyle factors can modulate mucosal immunity and the body’s initial defense against respiratory pathogens. Health practitioners and policymakers may find value in integrating substance use considerations into risk assessments and recommendations for preventing infections, especially in communities with higher prevalence of alcohol-related disorders. [citation: Emory University study]
Taken together, the research highlights a complex interaction between alcohol exposure and airway biology that can shape the early phase of SARS-CoV-2 infection. It invites further exploration into how modulating immune signaling and preserving epithelial barrier function might mitigate inflammation and improve outcomes for at-risk groups. By continuing to study these mechanisms, scientists hope to identify practical interventions that support respiratory health in individuals who have used alcohol over extended periods and could be more susceptible to viral insults. [citation: Emory University study]