Author: Yifei Lang; Wentao Li; Zeshi Li; Danielle Koerhuis; Arthur C.S. van den Burg; Erik Rozemuller; Berend-Jan Bosch; Frank J.M. van Kuppeveld; Geert-Jan P.H. Boons; Eric G. Huizinga; Hilde M. van der Schaar; Raoul J. de Groot
Title: Coronavirus hemagglutinin-esterase and spike proteins co-evolve for functional balance and optimal virion avidity Document date: 2020_4_5
ID: 0c7tf0np_5
Snippet: The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.04.03.003699 doi: bioRxiv preprint function selects for mutations in S1 A that reduce S receptor-binding affinity and virion avidity. of the S1 A -Fc fusion protein, the biosynthesis and intracellular transport of native trimeric spikes was 242 seemingly affected to lesser extent. At least, the uptake of S-Arg 197 Cys into VSV pseudotypes wa.....
Document: The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.04.03.003699 doi: bioRxiv preprint function selects for mutations in S1 A that reduce S receptor-binding affinity and virion avidity. of the S1 A -Fc fusion protein, the biosynthesis and intracellular transport of native trimeric spikes was 242 seemingly affected to lesser extent. At least, the uptake of S-Arg 197 Cys into VSV pseudotypes was not 243 noticeably impaired as compared to that of wildtype S (sFig. 3E). Still, the mutation did alter the 244 infectivity of the pseudotyped particles making them less dependent on exogenous HE-Fc (sFig. 3F) 245 presumably by reducing the avidity of S trimers through local S1 A misfolding and consequential 246 disruption of the RBS in one or more monomers. (iv) Perhaps most surprisingly, quasispecies 247 developed in which loss of HE lectin function was compensated at the level of the viral population 248 with minority low affinity variants, constituting less than 6% of the swarm, not only sustaining the 249 replication of high affinity variants but actually allowing the latter to flourish and amplify to become 250 the majority phenotype.
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