Key result
SARS-CoV-2 accessory proteins drive crucial virus-host interactions and viral pathogenicity, prompting structural characterization efforts.
Why the study?
Although accessory proteins of SARS-CoV-2 were originally thought non-essential for viral replication, emerging evidence indicates they play crucial roles in virus-host interactions and pathogenicity.
Provides a structural characterization of SARS-CoV-2 accessory proteins, highlighting their role in virus-host interactions and pathogenicity.
Structural data on accessory proteins may inform antiviral targeting; leaves open their in vivo roles and therapeutic relevance.
The coronavirus SARS-CoV-2 is the causative agent for the COVID-19 pandemic. Its proteome is typically separated into three classes of proteins: (1) Structural proteins which facilitate the transport and host cell infiltration of the viral RNA, (2) non-structural proteins which are thought to be essential for the viral life cycle and are all produced from open reading frame 1ab (ORF1ab) on the RNA, and (3) everything else, called accessory proteins. Although it was originally thought that these accessory proteins are non-essential for viral replication, a growing body of evidence suggests that these diverse proteins have crucial roles in virus-host interactions, in particular in the way they interfere with the signalling pathways that modulate the host cell’s response to infection and viral pathogenicity. Here, we summarize efforts to structurally characterize the accessory proteins from SARS-CoV-2.
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Briggs et al. (2023) conducted a review in COVID-19. SARS-CoV-2 accessory proteins was evaluated. SARS-CoV-2 accessory proteins play crucial roles in virus-host interactions and viral pathogenicity, prompting efforts to structurally characterize them.
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