Bacterial survival on inanimate surfaces: a field study.

OBJECTIVE: Environmental surfaces may serve as potential reservoirs for nosocomial pathogens and facilitate transmissions via contact depending on its tenacity. This study provides data on survival kinetics of the most important nosocomial bacteria on a panel of commonly used surfaces. Type strains of S. aureus, K. pneumoniae, P. aeruginosa, A. baumannii, S. marcescens, E. faecium, E. coli, and E. cloacae were suspended in 0.9% NaCl solution at a McFarland of 1 and got then plated via cotton swabs either on glass, polyvinyl chloride, stainless steel, or aluminum. Surfaces were stored at regular ambient temperature and humidity to simulate routine daycare conditions. Sampling was performed by contact plates for a time period of four weeks. RESULTS: The longest survival was observed for A. baumannii and E. faecium on all materials (at least four weeks). S. aureus remained viable for at least one week. Gram negative species other than A. baumannii were usually inactivated in less than two days. Nosocomial transmission of the above mentioned bacteria may easily occur if no appropriate infection control measures are applied on a regular daily basis. This might be of particular importance when dealing with outbreaks of A. baumannii and E. faecium.

Genome-wide CRISPR screen reveals host genes that regulate SARS-CoV-2 infection

Identification of host genes essential for SARS-CoV-2 infection may reveal novel therapeutic targets and inform our understanding of COVID-19 pathogenesis. Here we performed a genome-wide CRISPR screen with SARS-CoV-2 and identified known SARS-CoV-2 host factors including the receptor ACE2 and protease Cathepsin L. We additionally discovered novel pro-viral genes and pathways including the SWI/SNF chromatin remodeling complex and key components of the TGF-{beta} signaling pathway. Small molecule inhibitors of these pathways prevented SARS-CoV-2-induced cell death. We also revealed that the alarmin HMGB1 is critical for SARS-CoV-2 replication. In contrast, loss of the histone H3.3 chaperone complex sensitized cells to virus-induced death. Together this study reveals potential therapeutic targets for SARS-CoV-2 and highlights host genes that may regulate COVID-19 pathogenesis.