denotes emergency department, and IQR interquartile range. † Race was determined by the clinical team. ‡ Obesity was defined as a body-mass index (the weight in kilograms divided by the square of the height in meters) of 30 or higher.

Background: Some reports suggest that obesity could be a risk factor for complications in coronavirus disease 2019 (COVID-19) (1). Several mechanisms could explain this. First, adipocytes, which activate the inflammatory cascade, can increase risk for thromboembolism and susceptibility to the cytokine storm described in COVID-19 (2). Second, obesity negatively affects lung mechanics, which could predispose obese persons to more severe respiratory distress and failure (3). Finally, obesity can alter mitochondrial bioenergetics in lung epithelial cells and increase risk for acute lung injury (4). However, some have suggested an obesity paradox in some critical illnesses, including acute respiratory distress syndrome, where patients with obesity may have improved outcomes; whether this phenomenon occurs in patients with COVID-19 is unclear (5). Objective: To study the association between obesity and outcomes among a diverse cohort of 1687 persons hospitalized with confirmed COVID-19 at 2 New York City hospitals. Methods and Findings: This retrospective observational cohort study included consecutive adults with confirmed COVID-19 who were hospitalized between 3 March and 15 May 2020 at an 862-bed quaternary referral center or a 180bed community hospital in New York City. We excluded 46 patients who did not have height or weight data available to calculate body mass index (BMI). Patient data were manually abstracted (1) from the electronic health record through 6 June 2020. We determined BMI on the basis of the most recent height and weight listed in the electronic health record. Height and weight were collected during hospitalization for 95.5% of the cohort; the remaining BMIs were collected during ambulatory encounters within 3 months of hospitalization. We defined BMI categories as underweight (<18.5 kg/m 2), normal (18.5 to 24.9 kg/m 2), overweight (25.0 to 29.9 kg/m 2), mild to moderate obesity (30.0 to 39.9 kg/m 2), and morbid obesity (≥40.0 kg/m 2). To examine the association between BMI and in-hospital mortality, we used a Cox proportional hazards model adjusted for age, sex, race, smoking, diabetes, hypertension, chronic obstructive pulmonary disease, asthma, end-stage renal disease, coronary artery disease, heart failure, and cancer. These characteristics were chosen on the basis of risk factors for severe COVID-19 identified by the Centers for Disease Control and Prevention. We also examined for effect modification by age, sex, and race. To examine the association between BMI and respiratory failure, defined as a need for invasive mechanical ventilation, we used a Fine and Gray model to account for the competing risk for death and adjusted for the same 12 variables used in the model for mortality. We excluded the underweight group from this analysis because of low numbers. Finally, we repeated the adjusted Cox proportional hazards model analysis for mortality among persons with respiratory failure, again excluding the underweight group. To account for missing data (12% for race), we did multiple imputation.

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Background The long-term prevalence and risk factors for post-acute COVID-19 sequelae (PASC) are not well described and may have important implications for unvaccinated populations and policy makers. Objective To assess health status, persistent symptoms, and effort tolerance approximately 1 year after COVID-19 infection Design Retrospective observational cohort study using surveys and clinical data Participants Survey respondents who were survivors of acute COVID-19 infection requiring Emergency Department presentation or hospitalization between March 3 and May 15, 2020. Main Measure(s) Self-reported health status, persistent symptoms, and effort tolerance Key Results The 530 respondents (median time between hospital presentation and survey 332 days [IQR 325–344]) had mean age 59.2±16.3 years, 44.5% were female and 70.8% were non-White. Of these, 41.5% reported worse health compared to a year prior, 44.2% reported persistent symptoms, 36.2% reported limitations in lifting/carrying groceries, 35.5% reported limitations climbing one flight of stairs, 38.1% reported limitations bending/kneeling/stooping, and 22.1% reported limitations walking one block. Even those without high-risk comorbid conditions and those seen only in the Emergency Department (but not hospitalized) experienced significant deterioration in health, persistent symptoms, and limitations in effort tolerance. Women (adjusted relative risk ratio [aRRR] 1.26, 95% CI 1.01–1.56), those requiring mechanical ventilation (aRRR 1.48, 1.02–2.14), and people with HIV (aRRR 1.75, 1.14–2.69) were significantly more likely to report persistent symptoms. Age and other risk factors for more severe COVID-19 illness were not associated with increased risk of PASC. Conclusions PASC may be extraordinarily common 1 year after COVID-19, and these symptoms are sufficiently severe to impact the daily exercise tolerance of patients. PASC symptoms are broadly distributed, are not limited to one specific patient group, and appear to be unrelated to age. These data have implications for vaccine hesitant individuals, policy makers, and physicians managing the emerging longer-term yet unknown impact of the COVID-19 pandemic. Supplementary Information The online version contains supplementary material available at 10.1007/s11606-021-07379-z.

ToxT is an AraC-family transcriptional activator protein that controls the expression of key virulence factors in Vibrio cholerae, the causative agent of cholera. ToxT directly activates the expression of the genes that encode the toxin-coregulated pilus and cholera toxin, and also positively auto-regulates its own expression from the tcp promoter. The crystal structure of ToxT has previously been solved at 1.9 Å resolution (PDB entry 3gbg). In this study, a crystal structure of ToxT at 1.65 Å resolution with a similar overall structure to the previously determined structure is reported. However, there are distinct differences between the two structures, particularly in the region that extends from Asp101 to Glu110. This region, which can influence ToxT activity but was disordered in the previous structure, can be traced entirely in the current structure.