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https://www.selleckchem.com/ We find that this temporal flexibility contributes substantially to public health goals. Older essential workers are typically targeted first. However, depending on the objective, younger essential workers are prioritized to control spread or seniors to directly control mortality. When the objective is minimizing deaths, relative to an untargeted approach, prioritization averts deaths on a range between 20,000 (when nonpharmaceutical interventions are strong) and 300,000 (when these interventions are weak). We illustrate how optimal prioritization is sensitive to several factors, most notably, vaccine effectiveness and supply, rate of transmission, and the magnitude of initial infections.Coronaviruses are adept at evading host antiviral pathways induced by viral double-stranded RNA, including interferon (IFN) signaling, oligoadenylate synthetase-ribonuclease L (OAS-RNase L), and protein kinase R (PKR). While dysregulated or inadequate IFN responses have been associated with severe coronavirus infection, the extent to which the recently emerged SARS-CoV-2 activates or antagonizes these pathways is relatively unknown. We found that SARS-CoV-2 infects patient-derived nasal epithelial cells, present at the initial site of infection; induced pluripotent stem cell-derived alveolar type 2 cells (iAT2), the major cell type infected in the lung; and cardiomyocytes (iCM), consistent with cardiovascular consequences of COVID-19 disease. Robust activation of IFN or OAS-RNase L is not observed in these cell types, whereas PKR activation is evident in iAT2 and iCM. In SARS-CoV-2-infected Calu-3 and A549ACE2 lung-derived cell lines, IFN induction remains relatively weak; however, activation of OAS-RNase L and PKR is observed. This is in contrast to Middle East respiratory syndrome (MERS)-CoV, which effectively inhibits IFN signaling and OAS-RNase L and PKR pathways, but is similar to mutant MERS-CoV lacking innate immune antagonists. Remarkably, OAS-RN

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