Key Points Question What are the risk factors associated with hospitalization, mechanical ventilation, and death among patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection? Findings In this national cohort study of 88 747 veterans tested for SARS-CoV-2, hospitalization, mechanical ventilation, and mortality were significantly higher in patients with positive SARS-CoV-2 test results than among those with negative test results. Significant risk factors for mortality included older age, high regional coronavirus disease 2019 burden, higher Charlson Comorbidity Index score, fever, dyspnea, and abnormal results in many routine laboratory tests; however, obesity, Black race, Hispanic ethnicity, chronic obstructive pulmonary disease, hypertension, and smoking were not associated with mortality. Meaning In this study, most deaths from SARS-CoV-2 occurred in patients with age of 50 years or older, male sex, and greater comorbidity burden.

Background and Aims. Whether patients with cirrhosis have increased risk of SARS-CoV-2 infection and the extent to which infection and cirrhosis increase the risk of adverse patient outcomes remain unclear. Approach and Results: We identified 88,747 patients tested for SARS-CoV-2 between 3/1/20-5/14/20 in the Veterans Affairs (VA) national healthcare system, including 75,315 with no cirrhosis-SARS-CoV-2 negative (C0-S0), 9826 with no cirrhosis-SARS-CoV-2 positive (C0-S1); 3301 with cirrhosis-SARS-CoV-2 negative (C1-S0); and 305 with cirrhosis-SARS-CoV-2 positive (C1-S1). Patients were followed through 6/22/20. Hospitalization, mechanical ventilation and death were modeled in time-to-event analyses using Cox proportional hazards regression. Patients with cirrhosis were less likely to test positive than patients without cirrhosis (8.5% vs. 11.5%, adjusted odds ratio 0.83, 95% CI 0.69-0.99). Thirty-day mortality and ventilation rates increased progressively from C0-S0 (2.3% and 1.6%), to C1-S0 (5.2% and 3.6%), to C0-S1 (10.6% and 6.5%), to C1-S1(17.1% and 13.0%). Among patients with cirrhosis, those who tested positive for SARS-CoV-2 were 4.1 times more likely to undergo mechanical ventilation (adjusted hazard ratio [aHR] 4.12, 95% CI 2.79-6.10) and 3.5 times more likely to die (aHR 3.54, 95% CI 2.55-4.90) than those who tested negative. Among patients with SARS-CoV-2 infection, those with cirrhosis were more likely to be hospitalized (aHR 1.37, 95% CI 1.12-1.66), undergo ventilation (aHR 1.61, 95% CI 1.05-2.46) or die (aHR 1.65, 95% CI 1.18-2.30) than patients without cirrhosis. Among patients with cirrhosis and SARS-CoV-2 infection, the most important predictors of mortality were advanced age, cirrhosis decompensation and high MELD score. Conclusions: SARS-CoV-2 infection was associated with a 3.5-fold increase in mortality in patients with cirrhosis. Cirrhosis was associated with a 1.7-fold increase in mortality in patients with SARS-CoV-2 infection.

: Bacterial vaginosis, characterized by the replacement of the Lactobacillus-dominant microbiota with anaerobic bacteria and facultative Gram-negative rods, has been associated with adverse reproductive health outcomes including HIV acquisition. With the advent of newer molecular techniques, the vaginal microbiota can be investigated in more detail and the association with HIV examined more thoroughly. This review examines recent evidence suggesting that vaginal dysbiosis with increased microbial diversity, specific vaginal bacterial communities, and the presence and concentrations of some individual bacterial species, may increase HIV susceptibility. Potential mechanisms through which vaginal microbiota could impact HIV susceptibility are discussed. On the basis of the available data, this review finds that there is a modest, but growing, body of evidence linking vaginal microbiota to HIV susceptibility in women. The evidence could be strengthened through two main pathways. First, laboratory studies such as ex-vivo or animal experiments are needed to move from plausible mechanisms towards proven mechanisms that explain an effect of the vaginal microbiota on HIV susceptibility. Second, experimental evidence could directly test the hypothesis that sustaining optimal microbiota reduces HIV risk, though there are important obstacles to conducting such studies. Finally, this review examines strong evidence from a recent publication suggesting that deviations from an optimal vaginal microbiome, and particularly the presence of some bacterial communities with high relative abundance of Gardnerella vaginalis, reduces the efficacy of vaginal tenofovir-based microbicides.