Delayed discharge is associated with higher complement C3 levels and a longer nucleic acid-negative conversion time in patients with COVID-19.

To determine factors associated with delayed discharge of hospitalized patients with coronavirus disease (COVID-19). This retrospective cohort study included 47 patients with COVID-19 admitted to three hospitals in Quanzhou City, Fujian Province, China, between January 21, 2020 and March 6, 2020. Univariate and multivariate logistic regression analyses were conducted to identify factors associated with delayed discharge. The median length of hospital stay was 22 days. Patients in the delayed discharge group (length of hospital stay ≥ 21 days, n = 27) were more likely to have diarrhea, anorexia, decreased white blood cell counts, increased complement C3 and C-reactive protein levels, air bronchograms, undergo thymalfasin treatment, and take significantly longer to convert to a severe acute respiratory syndrome coronavirus (SARS-CoV-2) RNA-negative status than those in the control group (length of hospital stay, < 21 days; n = 20). In multivariate logistic regression analysis, the time to SARS-CoV-2 RNA-negative conversion (odds ratio [OR]: 1.48, 95% confidence interval [CI] 1.09-2.04, P = 0.01) and complement C3 levels (OR 1.14 95% CI 1.02-1.27, P = 0.03) were the only risk factors independently associated with delayed discharge from the hospital. Dynamic monitoring of complement C3 and SARS-CoV-2 RNA levels is useful for predicting delayed discharge of patients.

A Retrospective Study of the Epidemiologic and Clinical Characteristics of COVID-19 Among Hospitalized Patients in Quanzhou, China.

Coronavirus disease 2019 (COVID-19) has spread throughout China. However, information about COVID-19 in cities and regions outside Wuhan is limited and the indicators that predict the length of hospital stay for patients with COVID-19 are unclear. Therefore, we collected clinical data from 47 patients with COVID-19 in Quanzhou City. The median age was 38 years [interquartile range (IQR): 31-50 years], and 24 (51%) were male. There were 8 mild, 36 moderate, and 3 severe/critical cases. The median interval from exposure to disease onset was 13 days (IQR: 8-18 days). The incidence of severe/critical cases was 33% (3/10) in patients with hypertension. Common symptoms included fever (83%), cough (77%), fatigue (40%), a sore, dry throat (28%), and diarrhea (21%). One patient (2%) developed respiratory distress syndrome on day 13 of inpatient treatment. Six patients had leukopenia, 17 had elevated C-reactive protein (CRP), and 8 had lymphocytopenia and elevated lactate dehydrogenase (LDH). The median length of hospitalization was 22 days (IQR: 16-30 days). Dynamic monitoring of LDH, CRP, and neutrophil-lymphocyte ratio predicted whether length of hospitalization would exceed 21 days. Most patients presented with mild and moderate disease. Patients with hypertension were more likely to become severe or critical. Dynamic monitoring of LDH, CRP, and neutrophil-lymphocyte ratio levels can help predict delayed discharge from the hospital.

Angiotensin-converting enzyme 2 (ACE2) mediates influenza H7N9 virus-induced acute lung injury.

Since March 2013, the emergence of an avian-origin influenza A (H7N9) virus has raised concern in China. Although most infections resulted in respiratory illness, some severe cases resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that further contributes to morbidity. To date, no effective drugs that improve the clinical outcome of influenza A (H7N9) virus-infected patients have been identified. Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal disease, and acute lung injury. In the current study, we report that ACE2 could mediate the severe acute lung injury induced by influenza A (H7N9) virus infection in an experimental mouse model. Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor (AT1). The current findings demonstrate that ACE2 plays a critical role in influenza A (H7N9) virus-induced acute lung injury, and suggest that might be a useful potential therapeutic target for future influenza A (H7N9) outbreaks.