C. M. Swanson

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

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.

TRIM25 and ZAP target the Ebola virus ribonucleoprotein complex to mediate interferon-induced restriction

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.

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.

The Zinc Finger Antiviral Protein restricts SARS-CoV-2

This paper identifies ZAP as an IFN-induced antiviral effector that restricts SARS-CoV-2 by targeting CpG dinucleotides, though SARS-CoV-2 may be adapted to low CpG environments.

KHNYN is essential for ZAP-mediated restriction of HIV-1 containing clustered CpG dinucleotides

The paper identifies KHNYN as a novel ZAP cofactor essential for restricting HIV-1 with clustered CpG dinucleotides.