Two omicron variants replicate more efficiently in gut tissue models, experiments reveal
A research team from the School of Public Health at the LKS Faculty of Medicine, the University of Hong Kong (HKUMed), has discovered that emerging omicron sublineages of SARS-CoV-2 use distinct biological strategies to spread and cause disease. Specifically, the XBB.1.5 and EG.5.1 variants are better adapted for respiratory spread and may pose a heightened risk of severe respiratory disease,…
A team of scientists from the University of Hong Kong's School of Public Health has uncovered intriguing insights into how certain omicron sublineages of the SARS-CoV-2 virus replicate more effectively in intestinal tissues compared to respiratory tissues. The researchers focused on the XBB.1.5 and EG.5.1 variants, which are adept at spreading through the respiratory system and may carry a higher risk of severe respiratory disease.
In contrast, the BA.2.86 and JN.1 variants tend to thrive in the intestines, potentially opening up new avenues for transmission.
The study sought to clarify whether differences in transmission and disease severity among these omicron variants stem from the virus's intrinsic properties or from existing immunity acquired through vaccination or previous infections. To investigate, the researchers employed controlled laboratory experiments utilizing models that mirror human tissues, such as bronchial and lung tissues, airway organoids, and intestinal models including proximal intestinal enteroids and colon cells.
The results revealed that XBB.1.5 and EG.5.1, among other omicron sublineages, replicated efficiently in human respiratory tissues, indicating a strong capacity for infecting and multiplying within the airways and lungs. This suggests these variants are well-suited for person-to-person transmission and could heighten the risk of severe lung disease.
Among the examined variants, EG.5.1 exhibited a notable ability to enter human cells via two distinct pathways, facilitating infection in a variety of tissues, particularly the alveolar epithelial cells deep within the lungs. This enhanced lung replication underscores the variant's potential to cause more serious illnesses.
Interestingly, the study found that BA.2.86 and JN.1, while replicating less efficiently in respiratory tissues, demonstrated significantly higher replication levels in proximal intestinal enteroids compared to colon cells. This suggests that these variants may be better adapted to infect and grow in certain regions of the intestine.
Moreover, JN.1 showed a stronger ability to infect and grow in gut tissues while causing relatively low levels of inflammation, which may allow the virus to persist in the gut without triggering obvious symptoms. This persistence could enhance the likelihood of transmission via fecal contamination, although the study emphasizes that these laboratory findings do not establish fecal transmission or increased clinical severity.
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