The fight against COVID-19 got a big boost this week, with the Pfizer Inc.-BioNTech SE vaccine showing much better-than-expected effectiveness in preventing disease in its first readout and Eli Lilly &Co.’s therapeutic antibody getting an Emergency Use Authorization from the U.S. Food and Drug Administration. Other vaccines and treatments are likely to follow with similarly positive data. So far so good.
But exactly how jubilant should we be? Answering this question depends in large measure on how quickly the virus mutates and finds a way to bypass vaccines and other approved therapies. How quickly it mutates, in turn, depends on our ability to slow the spread through responsible mitigation measures.
Some background. Viruses mutate all the time. During the course of a single infection, a person can have coronaviruses with slight differences. If a vaccine or an antibody isn’t 100% effective in eradicating an infection, then even if it prevents disease it could still allow resistant clones to form. These clones could then spread to other people and undermine the efficacy of the vaccine or treatment.
This isn’t theoretical. Denmark, one of the world’s biggest producers of mink skins, is in the process of culling its entire 17 million mink population after the virus found its way into herds at hundreds of the country’s farms. By virtue of their sheer numbers, the mink provided the virus with an opportunity to spread rapidly and mutate. Then, in exactly the same way that the virus first entered into the human population in China, it jumped back into humans. One variant of the Danish virus has the potential to be resistant to the very vaccines and therapies that we have just been celebrating.
But we don’t need mink farms to generate mutations. A recent study from Emma Thomson, professor at the MRC-University of Glasgow Centre for Virus Research, and associates found a mutation that can bypass infection-fighting antibodies produced by some people. What this means is that there is one more reason to be concerned about the rapid spread of the coronavirus among humans: The more people get infected, the more likely it is for new versions of the virus to evolve. If the number of infections remains at current levels — or if it continues to rise — there is a risk that new mutations start to spread. Some of these new versions may even be able to reinfect people who had been infected before, a phenomenon that until now has been quite rare.
Almost all vaccines in development target the current version of the virus, meaning that they should be effective in preventing the disease in a vast majority of people. However, if we allow the virus to spread, we risk further mutations, and, consequently, less effective vaccines.
Should we put the Champagne back on ice? Definitely not. We can take comfort in that we have seen how effective a vaccine can be, at least based on early prevention of disease, and how quickly we can make one. And the beauty of the Pfizer-BioNTech vaccine and another in development by Moderna Inc. is that they can be adapted to deal with new variants that develop. The same applies to Johnson &Johnson and AstraZeneca Plc’s vaccines, with some caveats.
The Danish experience suggests it’s critically important to stop the evolution of the virus before we even start vaccinating people. That means bringing to bear all mitigation tools, from testing and tracing to social distancing and masks. And we may need to keep up these practices after a vaccine has been deployed until we can be sure inoculations eliminate virus transmission. On top of all this, countries should keep a better eye on their animal populations so as to avoid another Danish mink situation. The more responsible we are with our behavior, the better the chance for a successful vaccine.
Sam Fazeli is senior pharmaceuticals analyst for Bloomberg Intelligence and director of research for EMEA.
