H. Winstone

The P681H mutation in the Spike glycoprotein escapes IFITM restriction and is necessary for type I interferon resistance in the SARS-CoV-2 alpha variant

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.

A nuclear export signal in KHNYN required for its antiviral activity evolved as ZAP emerged in tetrapods

Regulation of KHNYN antiviral activity by the extended di-KH domain and nucleo-cytoplasmic trafficking

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.

The P681H mutation in the Spike glycoprotein confers Type I interferon resistance in the SARS-CoV-2 alpha (B.1.1.7) variant

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.

TMPRSS2 promotes SARS-CoV-2 evasion from NCOA7-mediated restriction

This study shows that NCOA7 restricts SARS-CoV-2 infection by promoting endosomal acidification, and TMPRSS2 or removal of the furin cleavage site reduces this restriction.

Impact of the B.1.1.7 variant on neutralizing monoclonal antibodies recognizing diverse epitopes on SARS-CoV-2 Spike

This study examines how mutations in the B.1.1.7 variant of SARS-CoV-2 affect neutralization by monoclonal antibodies targeting non-RBD epitopes.

The polybasic cleavage site in the SARS-CoV-2 spike modulates viral sensitivity to Type I IFN and IFITM2

This paper shows that the polybasic cleavage site in SARS-CoV-2 spike protein reduces sensitivity to IFITM2 and type I IFNs, enhancing viral replication and transmission.

IFN-independent cell cycle arrest and SAMHD1 activation following TLR4 activation in macrophages

This study shows TLR4 activation in macrophages induces G0 arrest and SAMHD1 activation independently of IFN, blocking HIV-1 infection through SAMHD1.