ObjectiveTo develop evidence of work-related and personal predictors of COVID-19 transmission.Setting and respondentsData are drawn from a population survey of individuals in the USA and UK conducted in June 2020.Background methodsRegression models are estimated for 1467 individuals in which reported evidence of infection depends on work-related factors as well as a variety of personal controls.ResultsThe following themes emerge from the analysis. First, a range of work-related factors are significant sources of variation in COVID-19 infection as indicated by self-reports of medical diagnosis or symptoms. This includes evidence about workplace types, consultation about safety and union membership. The partial effect of transport-related employment in regression models makes the chance of infection over three times more likely while in univariate analyses, transport-related work increases the risk of infection by over 40 times in the USA. Second, there is evidence that some home-related factors are significant predictors of infection, most notably the sharing of accommodation or a kitchen. Third, there is some evidence that behavioural factors and personal traits (including risk preference, extraversion and height) are also important.ConclusionsThe paper concludes that predictors of transmission relate to work, transport, home and personal factors. Transport-related work settings are by far the greatest source of risk and so should be a focus of prevention policies. In addition, surveys of the sort developed in this paper are an important source of information on transmission pathways within the community.

All poxviruses contain a set of proteinaceous structures termed lateral bodies (LB) that deliver viral effector proteins into the host cytosol during virus entry. To date, the spatial proteotype of LBs remains unknown. Using the prototypic poxvirus, vaccinia virus (VACV), we employed a quantitative comparative mass spectrometry strategy to determine the poxvirus LB proteome. We identified a large population of candidate cellular proteins, the majority being mitochondrial, and 15 candidate viral LB proteins. Strikingly, one-third of these are VACV redox proteins whose LB residency could be confirmed using super-resolution microscopy. We show that VACV infection exerts an anti-oxidative effect on host cells and that artificial induction of oxidative stress impacts early and late gene expression as well as virion production. Using targeted repression and/or deletion viruses we found that deletion of individual LB-redox proteins was insufficient for host redox modulation suggesting there may be functional redundancy. In addition to defining the spatial proteotype of VACV LBs, these findings implicate poxvirus redox proteins as potential modulators of host oxidative anti-viral responses and provide a solid starting point for future investigations into the role of LB resident proteins in host immunomodulation.

CRELD1 (Cysteine-Rich with EGF-Like Domains 1) is a risk gene for non-syndromic atrioventricular septal defects in human patients. In a mouse model, Creld1 has been shown to be essential for heart development, particularly in septum and valve formation. However, due to the embryonic lethality of global Creld1 knockout (KO) mice, its cell type-specific function during peri-and postnatal stages remains unknown.Here, we generated conditional Creld1 KO mice lacking Creld1 either in the endocardium (KO Tie2 ) or the myocardium (KO MyHC ). Using a combination of cardiac phenotyping, histology, immunohistochemistry, RNAsequencing, and flow cytometry, we demonstrate that Creld1 function in the endocardium is dispensable for heart development. Lack of myocardial Creld1 causes extracellular matrix remodeling and trabeculation defects by modulation of the Notch1 signaling pathway. Hence, KO MyHC mice die early postnatally due to myocardial hypoplasia.Our results reveal that Creld1 not only controls the formation of septa and valves at an early stage during heart development, but also cardiac maturation and function at a later stage. These findings underline the central role of Creld1 in mammalian heart development and function.