Omicron (B.1.1.529), is a heavily mutated and highly contagious SARS-CoV-2 variant, thus antiviral therapies are crucial to protect the most vulnerable individuals from severe COVID-19.

Few antiviral small-molecule drugs are under investigation or already approved for the treatment of COVID-19. Like Remdesivir comes as the first antiviral drug to be approved for the treatment of COVID-19. Approval of Molnupiravir and PF-07321332 is likely to overcome the problems associated with an intravenous agent. 

Other antiviral drug candidates for SARS-CoV-2 are the protease inhibitors, camostat, nafamostat, and aprotinin, which inhibit cleavage and activation of the viral spike (S) protein by host cell proteases thus restricting SARS-CoV-2 entry into host cells.

Antibody therapies have shown a reduced activity against the Omicron variant, Thus a study tested the effects of EIDD-1931, ribavirin, remdesivir, favipiravir, PF-07321332, nafamostat, camostat, and aprotinin on the replication of two SARS-CoV-2 Omicron (B.1.1.529) isolates and one Delta (B.1.167.2) isolate.

Omicron viruses showed less effectiveness than Delta viruses in antagonizing the interferon response in human cells, which may be the reason behind the lower pathogenicity of the Omicron variant observed in patients.

Antiviral testing showed a similar sensitivity of Omicron and Delta isolates to EIDD-1931, PF-07321332, remdesivir, favipiravir, ribavirin, nafamostat, camostat, and aprotinin, which proves that mutations in the Omicron variant do not cause significant changes in the drug sensitivity profiles of the viruses.

This study shows that Omicron viruses remain sensitive to a broad range of anti-SARS-CoV-2 drugs and drug candidates with a broad range of mechanisms of action. Also, Omicron viruses antagonize the host cell interferon response less effectively, thus causing less severe disease.

SOURCE- Cell Res, 2022. https://doi.org/10.1038/s41422-022-00619-9