Sheng-Han Wang

TL;DR: Host proteases that proteolytically activate the SARS-CoV-2 spike protein, critical for its fusion after binding to angiotensin-converting enzyme 2 (ACE2), as antiviral targets are focused on.

TL;DR: The results suggest that S variants emerge or are selected under the immune pressure generated by the host or by administration of hepatitis B immune globulin and hepatitis B vaccination.

TL;DR: It is demonstrated that the androgens pathway can increase the transcription of HBV through direct binding to the androgen‐responsive element sites in viral enhancer I, which may explain a higher HBV titer in male carriers and an increased risk of HCC.

TL;DR: By using a cell-population genetic definition, this approach identified three coding changes (CCNG1, P62, and an indel/fusion gene) as tumor driver mutations, functionally distinct from mutations that accumulated earlier, many of which are involved in inflammation/immunity or cell anchoring.

TL;DR: The comprehensive understanding of the sex disparity in HBV virology and pathogenesis will be helpful to provide newly biomarkers for clinical diagnosis and develop novel drugs to manage HBV‐related HCC patients.