W. S. Barclay

This study models SARS-CoV-2 Delta and Omicron replication in nasal and lung cells, finding Omicron has higher infectivity but lower production rate than Delta, leading to higher transmission in nasal cells and higher severity in lung cells.

The paper shows avian influenza polymerase uses human ANP32 for cRNA synthesis but requires avian ANP32 for vRNA synthesis, highlighting a difference in ANP32's role in viral replication steps.

This study compares the antigenic properties of SARS-CoV-2 Omicron variants BA.4 and BA.5 with BA.1, BA.2, and vaccine-induced antibodies, finding they are antigenically distinct and show enhanced neutralisation breadth after breakthrough infection.

This study shows Delta and Omicron SARS-CoV-2 variants do not provide cross-protective immunity against reinfection in hamsters.

This study investigates the origins and molecular evolution of SARS-CoV-2 lineage B.1.1.7 (Alpha) in the UK, finding that a chronically-infected immunocompetent individual likely drove its rapid mutation and spread.

This study identifies distinct genetic determinants in the Omicron spike protein for altered cell entry and antigenic properties, showing they are separable and may affect future variant severity and vaccine efficacy.

This study compares the severity of SARS-CoV-2 Omicron-B.1.1.529, Pango B, and Delta variants in a mouse model, finding Omicron causes less severe disease with lower viral load and inflammation.

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

This study shows SARS-CoV-2 B.1.617 variants have enhanced spike cleavage by furin due to the P681R mutation, potentially increasing transmissibility and pathogenicity.

This study shows that UK swimming pool water guidelines can reduce SARS-CoV-2 infectious titre by at least 3 orders of magnitude.

This study uses electron microscopy to examine SARS-CoV-2 infection in human airway epithelium, showing viral entry through the plasma membrane and budding from intracellular compartments.

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.

This study shows that endothelial cells are resistant to SARS-CoV-2 infection due to low ACE2 and TMPRSS2 expression, suggesting vascular dysfunction in COVID-19 arises from inflammatory factors rather than direct viral infection.

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

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.

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

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.

This study shows swine ANP32A supports avian influenza polymerase activity, and human-adapted viruses evolved to use human ANP32 proteins more efficiently.

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

This study examines how egg adaptation of the H3N2 influenza vaccine strain affects antibody responses in children, finding higher seroconversion rates to the adapted strain but differential mucosal IgA responses based on prior serostatus.

The paper identifies M2-N31 inhibitors that show synergistic antiviral effects when combined with existing drugs, offering a strategy to combat rimantadine-resistant influenza.

This study identifies HLA-DR as a receptor for bat influenza A-like H17N10 virus entry into mammalian cells, revealing a novel mechanism distinct from classical influenza A viruses.

This study uses next-generation sequencing to determine the mutation bias caused by favipiravir in influenza virus RNA, showing it primarily acts as a guanine analogue and secondarily as an adenine analogue.