Ursodeoxycholic acid may protect from severe acute respiratory syndrome coronavirus 2 Omicron variant by reducing angiotensin‐converting enzyme 2

compared to the mock group (Figure 3B ; Figure S2C ). Since ACE2 functions as a receptor, interactions with viruses or other stimuli may alter the ACE2 expression by ACE2 shedding or ACE2-expressing cell death during Omicron infection. 36 Besides, in Syrian hamsters, ACE2 expression is relatively low in the lung samples. 37 Confirming the reduction in expression brought on by UDCA may be challenging given the low level of ACE2 expression in the lungs of Syrian hamsters. We found that UDCA treatment lowered lung damage caused by viral infection on 4 dpi (Figure S1 ). Directly infected hamsters showed a relatively higher inflammation score of 2.00 ± 0.41 points at 2 dpi and 1.75 ± 1.19 points at 4 dpi. In the mock group, the score was similarly boosted to 0.67 ± 0.58 points on 4 dpi within the histological investigation on the lung lesions. At both time points, there were no pathological changes in UDCA and Molnupiravir groups. Similarly, whereas no plaque was found in UDCA-treated group, the mock group had significant viral replication on 4 dpi (Figure S3C ). The donor group had the highest viral RNA level and titer at 2 dpi, while the mock group had the highest at 4 dpi. Since 5 or 7 days after infection, the viral load may have been lowered by spontaneous recovery in the donor group. In contrast, viral replication might be started in the early stages of infection by airborne transmission in the mock group. Viral replication of the Omicron variant is higher in the..