Key result
DAXX restricts SARS-CoV-2 replication by up to 62-fold in human cells, an antiviral effect that is independent of the SUMOylation pathway and partially counteracted by the viral PLpro.
Why the study?
Interferon restricts SARS-CoV-2 replication in cell culture, but only a handful of Interferon Stimulated Genes with antiviral activity against SARS-CoV-2 have been identified.
DAXX is a potent restriction factor for SARS-CoV-2 that targets viral transcription and is counteracted by the viral papain-like protease (PLpro).
Interferon restricts SARS-CoV-2 replication in cell culture, but only a handful of Interferon Stimulated Genes with antiviral activity against SARS-CoV-2 have been identified. Here, we describe a functional CRISPR/Cas9 screen aiming at identifying SARS-CoV-2 restriction factors. We identified DAXX, a scaffold protein residing in PML nuclear bodies known to limit the replication of DNA viruses and retroviruses, as a potent inhibitor of SARS-CoV-2 and SARS-CoV replication in human cells. Basal expression of DAXX was sufficient to limit the replication of SARS-CoV-2, and DAXX over-expression further restricted infection. In contrast with most of its previously described antiviral activities, DAXX-mediated restriction of SARS-CoV-2 was independent of the SUMOylation pathway. SARS-CoV-2 infection triggered the re-localization of DAXX to cytoplasmic sites and promoted its degradation. Mechanistically, this process was mediated by the viral papain-like protease (PLpro) and the proteasome. Together, these results demonstrate that DAXX restricts SARS-CoV-2, which in turn has evolved a mechanism to counteract its action.
No takes yet. Share an insight, caveat, or question.
Kain et al. (2021) studied SARS-CoV-2 infection. DAXX knockout and overexpression vs. Wild-type or control cells was evaluated on SARS-CoV-2 replication (viral RNA levels and infectious viral particles). DAXX restricts SARS-CoV-2 replication by up to 62-fold in human cells, an antiviral effect that is independent of the SUMOylation pathway and partially counteracted by the viral PLpro.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: