Variant BA.2 is sensitive to some monoclonal antibodies used to treat COVID-19, such as AstraZeneca’s Evusheld. However, the antibodies to Etesevimab and Bamlanivmab, used as a sole treatment, were unable to neutralize the Omicron variant (BA.2) at normal levels in these laboratory tests. And other antibody treatments don’t work for Omicron either.
Yoshihiro Kawaoka, a virologist at the UW School of Veterinary Medicine and the University of Tokyo, and his team carried out the study and found these results. The BA.2 Omicron variant is related to the more common BA.1 Omicron virus, and some evidence suggests that BA.2 may spread more rapidly than the already highly contagious BA.1 variant.
“The bottom line is that we have antibodies that seem to be more effective against BA. 2 than BA.1 or BA.1.1. That’s good news, but we don’t know if what we found. “We’ve also tested for resistance compounds,” said Kawaoka, who has previously tested how the BA.1 variant responds to treatments. clinically available viruses and all of them are highly effective.”
Kawaoka and his team published their findings in New England Journal of Medicine on March 9th.
In laboratory experiments using non-human primate cells, Kawaoka’s team tested seven monoclonal antibodies, three antibody combinations, and three antiviral therapies against variant BA.2. Most clinically approved antibody therapies are combinations of several antibodies.
The intravenous drug remdesivir and the active ingredients in the two anti-COVID-19 pills, Paxlovid and Merck’s molnupiravir, are somewhat effective against BA.1 because they fight COVID-19 initially.
The most effective antibody treatment against the BA.2 variant is Evusheld, which is approved in the United States to help prevent the development of COVID-19 infection in individuals. The antibodies of Regeneron and GlaxoSmithKline were more effective against BA.2 than the BA.1 Omicron variant, although they were not as potent as BA.2 against earlier variants of the virus.
Existing COVID-19 therapies are less effective against newer variants than therapies against the original virus strain because they were designed and tested against earlier versions of the virus. Researchers and drug companies can design and test treatments against new variants, but that process can take months or years.
The original work was partially supported by the National Institutes of Health (issues HHSN272201400008C and 75N93021C00014). This study was also supported by the Japan Research Program on Emerging and Recurrent Infectious Diseases (fund JP20fk0108412, JP21fk0108615 and JP21fk0108104), Project to promote drug discovery support (grant JP20nk0101632), Chapter Japan Infectious Disease Research and Infrastructure Program (funded JP21wm0125002) and Grants for Emerging and Recurrent Infectious Diseases from the Ministry of Health, Labor and Welfare, Japan (funded 20HA2007).