Many lung cells carry a protein called TMPRSS2 on their surface which can inadvertently help passing viruses into the cell. But Dr. Gupta’s team found that this protein doesn’t attach very well to Omicron. As a result, Omicron succeeds in infecting cells in this way worse than Delta. A team at the University of Glasgow independently came to the same conclusion.
Alternatively, coronaviruses can also slip into cells that do not produce TMPRSS2. Higher in the airways cells tend not to carry the protein, which could explain the evidence that Omicron is found there more often than the lungs.
Dr Gupta speculated that Omicron had become an upper respiratory specialist, thriving in the throat and nose. If this is true, the virus might have a better chance of being expelled in tiny drops into the surrounding air and meeting new hosts.
“It all depends on what is going on in the upper respiratory tract so that they can transmit, right? ” he said. “It’s not really what’s going on down in the lungs where serious disease occurs. So you can understand why the virus evolved this way. “
While these studies clearly help explain why Omicron causes milder disease, they don’t yet answer why the variant is so effective in spreading from person to person. The United States recorded more than 580,000 cases as of Thursday alone, the majority of which are believed to be Omicron.
“These studies address the question of what can happen to the lungs but do not really address the issue of transmissibility,” said Sara Cherry, virologist at the Perelman School of Medicine at the University of Pennsylvania.
Dr Diamond said he wanted to wait until more studies were done, especially in humans rather than animals, before endorsing the hypothesis that TMPRSS2 is the key to understanding Omicron. “I think it’s still premature about this,” he said.