Although the highly effective measles vaccine has dramatically reduced the incidence of measles, measles, and outbreaks continue to occur in individuals who received the measles vaccine because of immunization failure. In this study, patients who have definite records of immunization were enrolled based on measles surveillance in Shanghai, China, from 2009 to 2017, and genomic characteristics regarding viruses retrieved from these cases provided insights into immunization failure. A total of 147 complete genomes of measles virus (MV) were obtained from the laboratory-confirmed cases through Illumina MiSeq. Epidemiological, and genetic characteristics of the MV were focused on information about age, gender, immunization record, variation, and evolution of the whole genome. Furthermore, systematic genomics using phylogeny and selection pressure approaches were analyzed. Our analysis based on the whole genome of 147 isolates revealed 4 clusters: 2 for the genotype H1 (clusters named H1-A, including 73 isolates; H1-B, including 72 isolates) and the other 2 for D8 and B3, respectively. Estimated nucleotide substitution rates of genotype H1 MV derived using genome and individual genes are lower than other genotypes. Our study contributes to global measles epidemiology and proves that whole-genome sequencing was a useful tool for more refined genomic characterization. The conclusion indicates that vaccination may have an effect on virus evolution. However, no major impact was found on the antigenicity in Shanghai isolates.

Objectives An accurate prognostic score to predict mortality for adults with COVID-19 infection is needed to understand who would benefit most from hospitalizations and more intensive support and care. We aimed to develop and validate a two-step score system for patient triage, and to identify patients at a relatively low level of mortality risk using easy-to-collect individual information. Design Multicenter retrospective observational cohort study. Setting Four health centers from Virginia Commonwealth University, Georgetown University, the University of Florida, and the University of California, Los Angeles. Patients Coronavirus Disease 2019-confirmed and hospitalized adult patients. Measurements and Main Results We included 1,673 participants from Virginia Commonwealth University (VCU) as the derivation cohort. Risk factors for in-hospital death were identified using a multivariable logistic model with variable selection procedures after repeated missing data imputation. A two-step risk score was developed to identify patients at lower, moderate, and higher mortality risk. The first step selected increasing age, more than one pre-existing comorbidities, heart rate >100 beats/min, respiratory rate ≥30 breaths/min, and SpO 2 <93% into the predictive model. Besides age and SpO 2 , the second step used blood urea nitrogen, absolute neutrophil count, C-reactive protein, platelet count, and neutrophil-to-lymphocyte ratio as predictors. C-statistics reflected very good discrimination with internal validation at VCU (0.83, 95% CI 0.79–0.88) and external validation at the other three health systems (range, 0.79–0.85). A one-step model was also derived for comparison. Overall, the two-step risk score had better performance than the one-step score. Conclusions The two-step scoring system used widely available, point-of-care data for triage of COVID-19 patients and is a potentially time- and cost-saving tool in practice.

More than 200 cases of lipoprotein glomerulopathy (LPG) have been reported since it was first discovered 30 years ago. Although relatively rare, LPG is clinically an important cause of nephrotic syndrome and end-stage renal disease. Mutations in the APOE gene are the leading cause of LPG. APOE mutations are an important determinant of lipid profiles and cardiovascular health in the population and can precipitate dysbetalipoproteinemia and glomerulopathy. Apolipoprotein E-related glomerular disorders include APOE 2 homozygote glomerulopathy and LPG with heterozygous APOE mutations. In recent years, there has been a rapid increase in the number of LPG case reports and some progress in research into the mechanism and animal models of LPG. We consequently need to update recent epidemiological studies and the molecular mechanisms of LPG. This endeavor may help us not only to diagnose and treat LPG in a more personized manner but also to better understand the potential relationship between lipids and the kidney.