Author: Stewart, H; Johansen, KH; McGovern, N; Palmulli, R; Carnell, GW; Heeney, JL; Okkenhaug, K; Firth, AE; Peden, AA; Edgar, JR
Title: SARS-CoV-2 spike downregulates tetherin to enhance viral spread Cord-id: pxr11u9b Document date: 2021_1_6
ID: pxr11u9b
Snippet: The antiviral restriction factor, tetherin, blocks the release of several different families of enveloped viruses, including the Coronaviridae. Tetherin is an interferon-induced protein that forms parallel homodimers between the host cell and viral particles, linking viruses to the surface of infected cells and inhibiting their release. We demonstrate that SARS-CoV-2 downregulates tetherin to aid its release from cells, and investigate potential proteins involved in this process. Loss of tetheri
Document: The antiviral restriction factor, tetherin, blocks the release of several different families of enveloped viruses, including the Coronaviridae. Tetherin is an interferon-induced protein that forms parallel homodimers between the host cell and viral particles, linking viruses to the surface of infected cells and inhibiting their release. We demonstrate that SARS-CoV-2 downregulates tetherin to aid its release from cells, and investigate potential proteins involved in this process. Loss of tetherin from cells caused an increase in SARS-CoV-2 viral titre. We find SARS-CoV-2 spike protein to be responsible for tetherin downregulation, rather than ORF7a as previously described for the 2002–2003 SARS-CoV. We instead find ORF7a to be responsible for Golgi fragmentation, and expression of ORF7a in cells recapitulates Golgi fragmentation observed in SARS-CoV-2 infected cells.
Search related documents:
Co phrase search for related documents- absence presence and luminal domain: 1
- accessory protein and luminal domain: 1, 2
Co phrase search for related documents, hyperlinks ordered by date