This is the second of a three-part series
The best news about the Omicron variant has been that our vaccine booster doses were effective against it. The booster doses took efficacy against hospitalization from 70% to close to 90% and from infection from 40% to 70%.
But there are still more breakthrough cases with three doses than there were with the ancestral strain to two doses. That’s what’s hard to accept. Why can’t we get back to December 2020? Well, we can, in some very real ways. Importantly, we’ve created several new treatments to complement the astounding development of our vaccines. But production issues are presently limiting widespread implementation of those medications. Controlling an epidemic takes combination therapy, which my colleague Mike Cohen and I wrote about at the beginning of our battle with SARS-CoV-2, before we had medical countermeasures. Today we have a combination of effective measures to protect us from the worst outcomes of SARS-CoV-2: behavioral measures and reducing risk of exposure, masks, and the three biomedical interventions of vaccines, some monoclonal antibodies, and antivirals. Vaccines and monoclonals came earliest and were hugely effective. Monoclonals have emerged as effective treatments for early outpatient therapy and as prevention for people with high exposure or at greater risk (e.g., household exposure or immune compromised). When available, some monoclonals provide the backup coverage for breakthrough infections — they are more expensive than vaccines but also highly effective in preventing hospitalizations, deaths, and, more recently, reducing the risk of getting COVID-19 for unvaccinated people. Their disadvantages are the requirement for more frequent administration and higher cost than vaccines. A more recent tool are antiviral medicines. Antiviral research in coronaviruses was an orphan field before SARS-CoV-2. We knew it would take considerable time to figure out what to target in the complicated SARS-CoV-2 virus and what compounds would selectively inhibit the viral genes and not inhibit important proteins in our cells and cause problems. Remdesivir was one potential solution. An off-the-shelf drug initially tested for Ebola that had efficacy against other coronaviruses such as MERS, remdesivir has been useful in hospitalized people and has been available since early in the pandemic. But we couldn’t build on this knowledge and needed a better drug against the viral protein that remdesivir inhibited. So, different targets of the SARS-CoV-2's viral life cycle needed to be evaluated.Dr. Larry Corey is the leader of the COVID-19 Prevention Network (CoVPN) Operations Center, which was formed by the National Institute of Allergy and Infectious Diseases at the US National Institutes of Health to respond to the global pandemic and the Chair of the ACTIV COVID-19 Vaccine Clinical Trials Working Group. He is a Professor of Medicine and Virology at University of Washington and a Professor in the Vaccine and Infectious Disease Division and past President and Director of Fred Hutchinson Cancer Research Center.