Purpose The aim of this article is to study how Covid-19 stress-related factors and changes in social engagement during the pandemic contributed to changes in alcohol use among first-year college students. Methods We used data on 439 first-year students (ages 18–20) at a large public university in North Carolina both before (October 2019 to February 2020) and after (June/July 2020) the start of the Covid-19 pandemic. We evaluated changes in prevalence and days of alcohol use and binge drinking. We estimated the associations between Covid-19 stressors/stress (work reductions, health, distanced learning difficulties, perceived stress) and social engagement (perceived social support from friends, social isolation, and social distancing) after controlling for students’ pre-pandemic alcohol use, social engagement, and demographic characteristics. Results We found that the prevalence of alcohol use and binge drinking in the past 30 days decreased from 54.2% to 46.0% and 35.5% to 24.6%, respectively; days of use did not change significantly. The decreases were primarily associated with reductions in social engagement. Among Covid-19 stressors/stress, only challenges with distance learning were associated with higher alcohol use among those who were already drinking prior to the pandemic. Drinking increased more among those who endorsed using substances to cope, while drinking was not associated with resilient coping. Conclusions Unless new drinking habits are formed during the pandemic, decreases in alcohol use among college students are unlikely to be sustained as social distancing measures are removed. Colleges may want to target interventions to students who have responded to stress with increased alcohol use, partly by addressing difficulties with distance learning.

While current therapeutic strategies for people living with human immunodeficiency virus type 1 (HIV-1) suppress virus replication peripherally, viral proteins such as transactivator of transcription (Tat) enter the central nervous system early upon infection and contribute to chronic inflammatory conditions even alongside antiretroviral treatment. As demand grows for supplemental strategies to combat virus-associated pathology presenting frequently as HIV-associated neurocognitive disorders (HAND), the present study aimed to characterize the potential utility of inhibiting monoacylglycerol lipase (MAGL) activity to increase inhibitory activity at cannabinoid receptor-type 1 receptors through upregulation of 2-arachidonoylglycerol (2-AG) and downregulation of its degradation into proinflammatory metabolite arachidonic acid (AA). The MAGL inhibitor MJN110 significantly reduced intracellular calcium and increased dendritic branching complexity in Tat-treated primary frontal cortex neuron cultures. Chronic MJN110 administration in vivo increased 2-AG levels in the prefrontal cortex (PFC) and striatum across Tat(+) and Tat(–) groups and restored PFC N-arachidonoylethanolamine (AEA) levels in Tat(+) subjects. While Tat expression significantly increased rate of reward-related behavioral task acquisition in a novel discriminative stimulus learning and cognitive flexibility assay, MJN110 altered reversal acquisition specifically in Tat(+) mice to rates indistinguishable from Tat(–) controls. Collectively, our results suggest a neuroprotective role of MAGL inhibition in reducing neuronal hyperexcitability, restoring dendritic arborization complexity, and mitigating neurocognitive alterations driven by viral proteins associated with latent HIV-1 infection.