R. P. Galao

This paper shows the P681H mutation in the SARS-CoV-2 alpha variant's Spike protein enables resistance to type I interferon and IFITM proteins, enhancing viral entry and transmission.

This paper identifies the extended di-KH and CUBAN domains in KHNYN as critical for its antiviral activity and interaction with ZAP, showing that the CUBAN domain regulates trafficking and abundance.

This study shows the P681H mutation in the SARS-CoV-2 alpha variant's Spike protein confers resistance to Type I interferon, enhancing viral replication by evading innate immune responses.

This study identifies TRIM25 and ZAP as key factors in type I interferon-mediated inhibition of Ebola virus replication by targeting the viral ribonucleoprotein complex.