In 2020, as the COVID-19 pandemic raged and other effective drugs were elusive, monoclonal antibodies emerged as a lifesaving treatment. But now, 3 years later, all the approvals for COVID-19–fighting antibodies have been rescinded in the United States, as mutations of the SARS-CoV-2 virus have left the drugs—which target parts of the original virus—ineffective.
The antibodies that initially saved lives all glommed on to the tip of spike, the protein SARS-CoV-2 uses to attach to angiotensin-converting enzyme 2 , a receptor on the surface of human cells. For the first 2 years of the pandemic, spike changed modestly enough for the mAbs to continue to work.
Other groups are pursuing the same strategy. Researchers at the Fred Hutchinson Cancer Center reported in a March bioRxiv preprint that they, too, have A separate approach takes aim at the human protein, ACE2, that SARS-CoV-2 and its relatives bind to on the cell surface. Last week, Bieniasz and his colleagues reported. They injected mice with copies of a soluble version of the human ACE2 receptor. Thirty-five days later, they screened the animals’ blood serum for antibodies that targeted ACE2 and blocked SARS-CoV-2 from binding to it.