R. Frise

Robustness of the ferret model for influenza risk assessment studies: a cross-laboratory exercise

This study evaluates the consistency of ferret transmission experiments across laboratories for two H1N1 influenza viruses, finding concordant results and suggesting a minimum of three to five labs for reliable risk assessment.

Mutations that adapt SARS-CoV-2 to mustelid hosts do not increase fitness in the human airway.

The paper identifies spike mutations that adapt SARS-CoV-2 to mustelid hosts and assesses their impact on human infectivity and antigenicity.

Increased transmission of SARS-CoV-2 lineage B.1.1.7 (VOC 2020212/01) is not accounted for by a replicative advantage in primary airway cells or antibody escape

This study shows that SARS-CoV-2 variant B.1.1.7 does not replicate better in airway cells or escape antibodies, suggesting its increased transmissibility is due to other factors.

The furin cleavage site of SARS-CoV-2 spike protein is a key determinant for transmission due to enhanced replication in airway cells.

This study shows the furin cleavage site in SARS-CoV-2 spike protein enhances replication in airway cells, contributing to transmission efficiency.

Evaluating the fitness of PA/I38T-substituted influenza A viruses with reduced baloxavir susceptibility in a competitive mixtures ferret model

The paper evaluates the fitness of baloxavir-resistant influenza A viruses in ferrets, finding reduced within-host fitness for A/H3N2 I38T and lower between-host fitness for A/H1N1pdm09 I38T compared to wild-type viruses.

Mammalian ANP32A and ANP32B proteins drive alternative avian influenza virus polymerase adaptations

This study identifies alternative PB2 adaptations that enable influenza polymerase to use mammalian ANP32 proteins, with PB2-E627K showing a preference for ANP32B.

Favipiravir-resistant influenza A virus shows potential for transmission

This study shows favipiravir-resistant influenza A virus can transmit in ferrets but may lose its resistance mutation in vivo due to fitness trade-offs.

A rare variant in ANP32B impairs influenza virus replication in human cells

This study identifies a rare variant in ANP32B that impairs influenza virus replication by disrupting FluPol dimer formation and function.