The role of SARS-CoV-2 accessory proteins in immune evasion

Many questions on the SARS-CoV-2 pathogenesis remain to answer. The SARS-CoV-2 genome encodes some accessory proteins that are essential for infection. Notably, accessory proteins of SARS-CoV-2 play significant roles in affecting immune escape and viral pathogenesis. Therefore SARS-CoV-2 accessory proteins could be considered putative drug targets. IFN-I and IFN-III responses are the primary mechanisms of innate antiviral immunity in infection clearance. Previous research has shown that SARS-CoV-2 suppresses IFN-beta by infecting host cells via ORF3a, ORF3b, ORF6, ORF7a, ORF7b, ORF8, and ORF9b. Furthermore, ORF3a, ORF7a, and ORF7b have a role in blocking IFN alpha signaling, and ORF8 represses IFN beta signaling. The ORF3a, ORF7a, and ORF7b disrupt the STAT1/2 phosphorylation. ORF3a, ORF6, ORF7a, and ORF7b could prevent the ISRE promoter ac-tivity. The main SARS-CoV-2 accessory proteins involved in immune evasion are discussed here for compre-hensive learning on viral entry, replication, and transmission in vaccines and antiviral development.

Automated summary

The accessory proteins of SARS-CoV-2 play significant roles in immune evasion and viral pathogenesis, making them potential targets for drug development. The IFN-I and IFN-III responses are essential for clearing the infection. Several SARS-CoV-2 accessory proteins, such as ORF3a, ORF7a, and ORF7b, inhibit the host's IFN-beta response.