Human organoid systems reveal in vitro correlates of fitness for SARS-CoV-2 B.1.1.7
Lamers, M. M.; Breugem, T. I.; Mykytyn, A. Z.; Wang, Y.; Groen, N.; Knoops, K.; Schipper, D.; van der Vaart, J.; Koopman, C. D.; Zhang, J.; Wu, D. C.; van den Doel, P. B.; Bestebroer, T.; GeurtsvanKessel, C. C.; Peters, P. J.; Muraro, M. J.; Clevers, H.; Wu, N. C.; Haagmans, B. L.
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A new phase of the COVID-19 pandemic has started as several SARS-CoV-2 variants are rapidly emerging globally, raising concerns for increased transmissibility. As animal models and traditional in vitro systems may fail to model key aspects of the SARS-CoV-2 replication cycle, representative in vitro systems to assess variants phenotypically are urgently needed. We found that the British variant (clade B.1.1.7), compared to an ancestral SARS-CoV-2 clade B virus, produced higher levels of infectious virus late in infection and had a higher replicative fitness in human airway, alveolar and intestinal organoid models. Our findings unveil human organoids as powerful tools to phenotype viral variants and suggest extended shedding as a correlate of fitness for SARS-CoV-2. One-Sentence SummaryBritish SARS-CoV-2 variant (clade B.1.1.7) infects organoids for extended time and has a higher fitness in vitro.
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