| Autor: |
Ferran Tarrés-Freixas, Benjamin Trinité, Anna Pons-Grífols, Miguel Romero-Durana, Eva Riveira-Muñoz, Carlos Ávila-Nieto, Mónica Pérez, Edurne Garcia-Vidal, Daniel Perez-Zsolt, Jordana Muñoz-Basagoiti, Dàlia Raïch-Regué, Nuria Izquierdo-Useros, Cristina Andrés, Andrés Antón, Tomàs Pumarola, Ignacio Blanco, Marc Noguera-Julián, Victor Guallar, Rosalba Lepore, Alfonso Valencia, Victor Urrea, Júlia Vergara-Alert, Bonaventura Clotet, Ester Ballana, Jorge Carrillo, Joaquim Segalés, Julià Blanco |
| Jazyk: |
angličtina |
| Rok vydání: |
2022 |
| Předmět: |
|
| Zdroj: |
Frontiers in Microbiology, Vol 13 (2022) |
| Druh dokumentu: |
article |
| ISSN: |
1664-302X |
| DOI: |
10.3389/fmicb.2022.840757 |
| Popis: |
The emerging SARS-CoV-2 variants of concern (VOCs) may display enhanced transmissibility, more severity and/or immune evasion; however, the pathogenesis of these new VOCs in experimental SARS-CoV-2 models or the potential infection of other animal species is not completely understood. Here we infected K18-hACE2 transgenic mice with B.1, B.1.351/Beta, B.1.617.2/Delta and BA.1.1/Omicron isolates and demonstrated heterogeneous infectivity and pathogenesis. B.1.351/Beta variant was the most pathogenic, while BA.1.1/Omicron led to lower viral RNA in the absence of major visible clinical signs. In parallel, we infected wildtype (WT) mice and confirmed that, contrary to B.1 and B.1.617.2/Delta, B.1.351/Beta and BA.1.1/Omicron can infect them. Infection in WT mice coursed without major clinical signs and viral RNA was transient and undetectable in the lungs by day 7 post-infection. In silico modeling supported these findings by predicting B.1.351/Beta receptor binding domain (RBD) mutations result in an increased affinity for both human and murine ACE2 receptors, while BA.1/Omicron RBD mutations only show increased affinity for murine ACE2. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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