Scientists from the Department of Microbiology at the University of Hong Kong (HK) have found that the Omicron variant of SARS-CoV-2 replicates less efficiently and causes fewer diseases than other variants of COVID19.
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Professor Kwok-Yung Yuen led the research team that reported its findings in a peer-reviewed paper published in Nature.
Several cell and mouse models were used to study Omicron’s replication efficiency and pathogenicity. Scientists found that the live Omicron virus replicated less efficiently than the original strain of SARS-CoV-2 (wild type) and the variants Alpha, Beta, and Delta, when laboratory experiments were conducted on human lungs and intestinal epithelial cells.
The human body’s internal and external surfaces—including the respiratory tract and intestines—are covered by epithelial cells. The functions of these tissues include filtration, protection, secretion, and sensory reception.
Researchers found that the Omicron virus multiplied less efficiently than the original COVID19 strain in human lung epithelial cells by more than three times. However, the Alpha, Beta, and Delta variants replicated at a similar or higher level than that of the original virus.
Our findings suggested that the mutating SARS-CoV-2 tries to escape from the control of our immune system which has been activated by vaccines or natural infection. But in doing so, the virus has to pay a price by becoming less efficient in multiplying.”
Kwok-Yung Yuen, Professor, Department of Microbiology, The University of Hong Kong
“We hope that the virus would continue to follow this trajectory of evolution to become a mild common cold corona virus. After growing this Omicron virus on 25 November, we rushed to understand whether this new variant is kinder or nastier than the previous variants,” Yuen added.
Dr Hin Chu, Dr Jasper Fuk-woo Chan, and Dr Huiping Shuai of the Department of Microbiology and Li Ka Shing Faculty of Medicine, HKU were among the other leaders of the research team.
Furthermore, researchers discovered Omicron does not effectively utilize a cell membrane protein called trans-membrane serine protease 2 (TMPRSS2) that facilitates viral entry in certain cells.
In human epithelial cell lines, mutations in the spike protein of Omicron may impair the virus’ ability to use the TMPRSS2 pathway, hindering its entry and replication.
Compared to wild type and Delta mouse models, Omicron replication was reduced in both the upper and lower respiratory tracts. Based on analysis of lung tissue, infection with the Omicron variant resulted in decreased inflammation and damage to the lungs in comparison to infection with the wild type and Delta. Compared to other variants of concern, it was also linked with reduced body weight loss and increased animal survival.
Study findings suggest that the current global vaccination strategy has forced COVID19 on an evolutionary trajectory that makes it less likely to replicate, providing an advantage in immune escape. This means that vaccination with additional boosters may further attenuate the virus.
Shuai, H., et al. (2022) Attenuated replication and pathogenicity of SARS-CoV-2 B.1.1.529 Omicron. Nature. doi.org/10.1038/s41586-022-04442-5.