G. Whittaker

Detection and characterization of novel luchacoviruses, genus Alphacoronavirus, shed in saliva and feces of meso-carnivores in the northeastern United States

This study detects and characterizes novel luchacoviruses in meso-carnivores in the northeastern US, revealing genetic distinctions from known rodent and lagomorph isolates.

Bioinformatic analysis of the spike protein cleavage sites of coronaviruses in the mammalian order Eulipotyphla

The paper analyzes coronavirus spike protein cleavage sites in Eulipotyphla mammals, finding potential spillover risks in certain shrew coronaviruses.

Natural selection differences detected in key protein domains between non-pathogenic and pathogenic Feline Coronavirus phenotypes

This study identifies natural selection differences in key protein domains between non-pathogenic FECV and pathogenic FIPV FCoVs, highlighting sites under positive selection associated with FIP development.

Analysis of the molecular determinants for furin cleavage of the spike protein S1/S2 site in defined strains of the prototype coronavirus murine hepatitis virus (MHV)

The paper analyzes the molecular determinants of furin cleavage of MHV spike protein S1/S2 site, identifying structural requirements and sequence variations affecting cleavage efficiency.

Intrinsic furin-mediated cleavability of the spike S1/S2 site from SARS-CoV-2 variant B.1.1.529 (Omicron)

This study assesses the furin cleavage site of the SARS-CoV-2 Omicron variant, finding increased intrinsic cleavability due to mutations N679K and P681H compared to ancestral and other variants.

Characterization of Hydrophobic Interactions of SARS-CoV-2 and MERS-CoV Spike Protein Fusion Peptides Using Single Molecule Force Measurements

This study uses single molecule force measurements to quantify hydrophobic interactions in SARS-CoV-2 and MERS-CoV FP1 sequences, revealing that a single residue difference significantly affects interaction strength.

A mechanistic understanding of the modes of Ca2+ ion binding to the SARS-CoV-1 fusion peptide and their role in the dynamics of host membrane penetration

This study identifies specific Ca2+ binding residue pairs in SARS-CoV-1 fusion peptide that promote or inhibit membrane insertion through molecular dynamics and biological assays.

In vitro and computational analysis of the putative furin cleavage site (RRARS) in the divergent spike protein of the rodent coronavirus AcCoV-JC34 (sub-genus luchacovirus)

The paper analyzes the spike protein of AcCoV-JC34, identifying a putative furin cleavage site that is not cleaved by furin, suggesting a potential progenitor sequence for viral emergence.

A high throughput screening assay for inhibitors of SARS-CoV-2 pseudotyped particle entry

This paper develops a high throughput screening assay using SARS-CoV-2 pseudotyped particles to identify inhibitors of viral entry, finding 7 active compounds effective against both pseudotyped particles and live virus.

Inhibitors of L-type calcium channels show therapeutic potential for treating SARS-CoV-2 infections by preventing virus entry and spread

This study tests L-type calcium channel blockers for inhibiting SARS-CoV-2 infection in cell culture, finding that felodipine and nifedipine limit virus entry and infection with minimal toxicity.

Spike protein cleavage-activation mediated by the SARS-CoV-2 P681R mutation: a case-study from its first appearance in variant of interest (VOI) A.23.1 identified in Uganda

The paper analyzes the P681R mutation in the SARS-CoV-2 spike protein of variant A.23.1, showing increased furin cleavage and infectivity compared to earlier variants, but only when combined with other spike changes.

Functional evaluation of the P681H mutation on the proteolytic activation the SARS-CoV-2 variant B.1.1.7 (Alpha) spike

This study evaluates the impact of the P681H mutation in the SARS-CoV-2 B.1.1.7 spike on furin cleavage and viral entry, finding no significant effect on these processes.

β-Coronaviruses use lysosomal organelles for cellular egress.

This study shows β-coronaviruses exit cells via lysosomal trafficking, not the secretory pathway, and identifies Arl8b as a regulator of this process.