The covid-19 pandemic is once again resurging throughout the U.S. and elsewhere, and while now we have many more tools available against the viral illness than we did last winter—namely, a full armada of preventive vaccines and soon-to-debut treatments—the emergence of the Omicron variant around Thanksgiving tossed a spanner in the works. Even if Omicron hadn’t entered the picture, though, the U.S. would still be facing a rise in covid-19 cases, deaths, and hospitalizations.
Below is a summary of some of the latest research on Omicron and its risks. It’s important to note that many of these studies are still preliminary and may not have undergone peer review yet, so their conclusions should be viewed with added caution. It takes time and a base of evidence to be sure of anything.
Omicron has unnerved scientists because of its unique mix of mutations that appear to make it look and behave differently from the original coronavirus, as well as from earlier variants. It’s theorized that these mutations might allow the virus to be more easily transmitted between people and to better evade the immune systems of people who have been vaccinated or infected in the past. And we’re now starting to see data support those theories.
This week, a preliminary lab study from researchers in Hong Kong found that Omicron can infect and multiply inside the cells of our bronchus (the two tubes that carry air from the windpipe to the lungs) much faster than the Delta variant could—up to 70 times faster. This voracious speed could explain why cases of Omicron in the real world have appeared to spread much more quickly than the standard covid outbreak, even among mostly vaccinated populations.
But there may be a silver lining here: The same study found that Omicron didn’t replicate as fast as Delta in the cells of the lung. That could possibly explain why some data has suggested that Omicron causes milder illness than past variants. But covid-related illness is a complicated process, one that isn’t just about how the virus behaves but also how our immune response responds. Because so many people have been vaccinated or previously infected, it’s still too early to tell whether Omicron is inherently milder or simply being stopped by these trained immune systems before it can cause too much trouble.
Speaking of immunity, there continues to be good and bad news on that front.
A preprint paper on BioRXiv this week, for instance, compared how the Omicron variant responded to antibodies collected from previously infected people and those given various vaccines—not only the two mRNA vaccines from Moderna and Pfizer/BioNTech, but the AstraZeneca vaccine, the Johnson & Johnson shot, as well as vaccines from Russia and China. Across the board, when compared to the original virus and the Alpha variant, levels of neutralizing antibodies (the kind that help prevent infection from happening) declined substantially to Omicron specifically. For both the Johnson & Johnson vaccine and Russia’s Sputnik V, levels dropped to the point where little protection from infection would be expected.
The results line up with other evidence indicating that vaccines aren’t great at preventing infection from Omicron. Recent data from South Africa, where the variant was first discovered, estimated that the effectiveness of the Pfizer vaccine at stopping infection fell from 80% to 33% once Omicron became dominant.
At the same time, antibodies are not the full picture of immunity. Studies released this week have suggested that T cells—another key line of defense against familiar germs—specific to the coronavirus remain robust even in the face of Omicron, as many scientists had expected. These cells are thought to be very important at keeping the infection from causing severe illness. And while scientists are working fast on developing an Omicron-specific vaccine, booster shots based on the original virus do seem to provide a buffer even there. A study from Moderna this week found that levels of neutralizing antibodies climbed back up considerably following a third shot.
Boosters were already worthwhile even before Omicron was in the mix, but they’re looking more prudent by the minute.
One of the many mysteries surrounding Omicron is where it came from. It was first discovered in South Africa in November, but that’s not necessarily where it originated—the country’s impressive genetic surveillance may have just spotted it before anyone else.
Leaving aside geography, there’s also the matter of its lineage. All of the variants of concern to date have had only slight tweaks to their basic structure, but Omicron has upwards of 30 mutations in its spike protein alone. Because scientists are now constantly tracking the evolution of the coronavirus by periodically looking at the genetics of virus samples collected from patients, it would be very strange for a variant to pick up that many mutations right underneath our noses without notice—and yet, that’s exactly what seems to have happened here.
Currently, there are two major theories on how Omicron came to be. One is that the variant emerged in an immunocompromised person, where the infection was able to persist and adapt to a weakened immune system for much longer than usual, allowing some populations of the coronavirus to survive with these mutations and then be transmitted to someone else. The other is that Omicron mutated while in an animal host and then jumped back to humans. A preprint paper by scientists in China this week posits that the ancestor of Omicron jumped from humans to mice, then at some point later, jumped right back to humans, now with a spiffy new genetic get-up.
Based on their lab experiments, the researchers argue that the mutations found in Omicron don’t look much like the mutations we’ve seen from human-hosted viruses before, but they do resemble mutations seen in strains collected from mice-hosted cells. Omicron’s mutations also look somewhat like the mutations that may allow the virus to better infect mouse cells, they say.
“Collectively, our results suggest that the progenitor of Omicron jumped from humans to mice, rapidly accumulated mutations conducive to infecting that host, then jumped back into humans, indicating an inter-species evolutionary trajectory for the Omicron outbreak,” they wrote.
These aren’t the only scientists to theorize an animal origin for Omicron. And it’s certainly plausible—scientists have been worried about this kind of evolution for a while now, once it became apparent that the coronavirus could easily jump from humans to other animals. This is still only preliminary work, and there’s sure to be more research conducted on this. For context, there are still fierce debates over the origins of the pandemic itself two years in, so answers on Omicron’s source may not come easily either.
The arrival of Omicron should serve as a reminder that, as much as we can and have adapted to the virus over time, the germ can learn new tricks of its own.