Variant watch: What more we know of Omicron today

The researchers studied the mechanism of infection of the latest variant of concern by looking at how it infected lab-grown lung cells.

The mutations in the Omicron variant of Covid-19 make it better at cheating prior immunity, but possibly also compromise its ability to replicate and cause disease, found a study uploaded on Saturday by researchers at Cambridge University.

The study is the second in two days to suggest the Omicron variant does not replicate as efficiently in the lung tissues as its ancestors.(Reuters)

The researchers studied the mechanism of infection of the latest variant of concern by looking at how it infected lab-grown lung cells. Omicron’s entry into the cells was significantly impaired, they found, and it did not lead to fusion of cells that leads to the formation of giant infected cells called syncitia.

Entry into cell determines infectivity, while the formation of the giant cells most notably gave the Delta variant an ability to lead to substantially more severe disease, the authors explained.

“What does this all mean? Efficient infection of lung cells could correlate with severity of lung disease. Syncitia or fused cells are often seen in respiratory tissues taken following severe disease. Delta was very good at both, in contrast to Omicron. Further work is needed,” Ravindra Gupta, professor of clinical microbiology at Cambridge’s department of medicine, said in a tweet on Saturday.

The study is the second in two days to suggest the Omicron variant does not replicate as efficiently in the lung tissues as its ancestors. The first was by researchers at University of Hong Kong, who found a 10-fold drop in how the variant multiplied in the lungs, although its replication in the bronchus, the passage that leads air into the lungs, was significantly higher.

The Hong Kong study offered observations that seem to explain why the variant may be more fast-spreading. If there is more of the virus in a part of the airway such as the bronchus, it will be more readily spewed out by an infected person.

On the other hand, if its ability to infect the lungs is impaired, it may not lead to as severe a disease as the other variants. Both studies appear to reach this inference, although the researchers involved in both have warned against drawing concrete conclusions since more studies are needed.

The Cambridge study notes some new observations that might explain why the replication is impeded. The first is a change in the all-important spike protein, the protruding part of the virus that latches on to human cells before cleaving and initiating entry into the target cell.

In Omicron, it appears, the “cleavage efficiency is lower than for wild type Wuhan-1 D614G and Delta”, the Cambridge study said. Wuhan-1 D614G refers to the variant that swept across the world during the first wave that began in January 2020.

The second reason appears to be an inherent loss in what is known as fusogenecity, or the characteristic of a cell (infected, in this case), to fuse with another.

“In summary this work suggests that Omicron does appear to have become more immune evasive, but that properties associated with disease progression *may* be attenuated to some extent,” Gupta added in another tweet, in which he also stressed: “The significant growth of Omicron nevertheless represents a major public health challenge.”

The virulence of Omicron is at present the most significant unknown that scientists are scrambling to understand. The variant has already demonstrated that it posses the two other traits that could make the pandemic flare again. It is significantly more transmissible and resistant than any prior configuration of the Sars-Cov-2 virus.