| Autor: |
Antia A; Department of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA., Alvarado DM; Inflammatory Bowel Diseases Center, Division of Gastroenterology, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA., Zeng Q; Department of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA., Casorla-Perez LA; Inflammatory Bowel Diseases Center, Division of Gastroenterology, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA., Davis DL; Inflammatory Bowel Diseases Center, Division of Gastroenterology, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA., Sonnek NM; Inflammatory Bowel Diseases Center, Division of Gastroenterology, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA., Ciorba MA; Inflammatory Bowel Diseases Center, Division of Gastroenterology, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA., Ding S; Department of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA. |
| Abstrakt: |
The Omicron variant of SARS-CoV-2, characterized by multiple subvariants including BA.1, XBB.1.5, EG.5, and JN.1, became the predominant strain in early 2022. Studies indicate that Omicron replicates less efficiently in lung tissue compared to the ancestral strain. However, the infectivity of Omicron in the gastrointestinal tract is not fully defined, despite the fact that 70% of COVID-19 patients experience digestive disease symptoms. Here, using primary human colonoids, we found that, regardless of individual variability, Omicron infects colon cells similarly or less effectively than the ancestral strain or the Delta variant. The variant induced limited type III interferon expression and showed no significant impact on epithelial integrity. Further experiments revealed inefficient cell-to-cell spread and spike protein cleavage in the Omicron spike protein, possibly contributing to its lower infectious particle levels. The findings highlight the variant-specific replication differences in human colonoids, providing insights into the enteric tropism of Omicron and its relevance to long COVID symptoms. |
