01851nas a2200337   4500000000100000000000100001008004100002260001500043100001900058700001900077700002000096700001600116700001900132700001800151700001900169700002400188700002500212700001800237700001800255700002600273700002000299700003000319700002000349700002000369700001700389700001900406700002100425245008800446856006400534520091500598       2021                            d  c2021-05-031 aMart M. Lamers1 aTim I. Breugem1 aAnna Z. Mykytyn1 aYiquan Wang1 aNathalie Groen1 aKèvin Knoops1 aDebby Schipper1 aJelte van der Vaart1 aCharlotte D. Koopman1 aJingshu Zhang1 aDouglas C. Wu1 aPetra B. van den Doel1 aTheo Bestebroer1 aCorine H. GeurtsvanKessel1 aPeter J. Peters1 aMauro J. Muraro1 aHans Clevers1 aNicholas C. Wu1 aBart L. Haagmans00aHuman organoid systems reveal in vitro correlates of fitness for SARS-CoV-2 B.1.1.7  uhttps://www.biorxiv.org/content/10.1101/2021.05.03.441080v13 aA 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 Summary British SARS-CoV-2 variant (clade B.1.1.7) infects organoids for extended time and has a higher fitness in vitro.