Susan R. Weiss

Intracellular processing of the N-terminal ORF 1a proteins of the coronavirus MHV-A59 requires multiple proteolytic events.

Mouse hepatitis virus A59 increases steady-state levels of MHC mRNAs in primary glial cell cultures and in the murine central nervous system.

Mouse hepatitis virus ORF 2a is expressed in the cytosol of infected mouse fibroblasts.

Induction of MHC class I antigens on glial cells is dependent on persistent mouse hepatitis virus infection.

Molecular cloning of the gene encoding the putative polymerase of mouse hepatitis coronavirus, strain A59.

A general method for the induction and screening of antisera for cDNA-encoded polypeptides: antibodies specific for a coronavirus putative polymerase-encoding gene.

Detection of a murine coronavirus nonstructural protein encoded in a downstream open reading frame.

Coronavirus mouse hepatitis virus (MHV)-A59 causes a persistent, productive infection in primary glial cell cultures.

In vitro synthesis of two polypeptides from a nonstructural gene of coronavirus mouse hepatitis virus strain A59.

Coronaviruses SD and SK share extensive nucleotide homology with murine coronavirus MHV-A59, more than that shared between human and murine coronaviruses.

Mouse hepatitis virus A59-induced demyelination can occur in the absence of CD8+ T cells.

Identification and characterization of a 65-kDa protein processed from the gene 1 polyprotein of the murine coronavirus MHV-A59.

Mouse hepatitis virus strain A59 RNA polymerase gene ORF 1a: heterogeneity among MHV strains.

The ns 4 gene of mouse hepatitis virus (MHV), strain A 59 contains two ORFs and thus differs from ns 4 of the JHM and S strains.

Syncytia formation induced by coronavirus infection is associated with fragmentation and rearrangement of the Golgi apparatus.

Efficient autoproteolytic processing of the MHV-A59 3C-like proteinase from the flanking hydrophobic domains requires membranes.

Altered pathogenesis of a mutant of the murine coronavirus MHV-A59 is associated with a Q159L amino acid substitution in the spike protein.

The spike protein of murine coronavirus mouse hepatitis virus strain A59 is not cleaved in primary glial cells and primary hepatocytes.

Roles in cell-to-cell fusion of two conserved hydrophobic regions in the murine coronavirus spike protein.

Targeted recombination within the spike gene of murine coronavirus mouse hepatitis virus-A59: Q159 is a determinant of hepatotropism.

Cellular reservoirs for coronavirus infection of the brain in beta2-microglobulin knockout mice.

Expression of murine coronavirus recombinant papain-like proteinase: efficient cleavage is dependent on the lengths of both the substrate and the proteinase polypeptides.

Pathogenesis of chimeric MHV4/MHV-A59 recombinant viruses: the murine coronavirus spike protein is a major determinant of neurovirulence.

Amino acid substitutions within the leucine zipper domain of the murine coronavirus spike protein cause defects in oligomerization and the ability to induce cell-to-cell fusion.

Further requirements for cleavage by the murine coronavirus 3C-like proteinase: identification of a cleavage site within ORF1b.

Demyelination determinants map to the spike glycoprotein gene of coronavirus mouse hepatitis virus.

Murine coronavirus spike protein determines the ability of the virus to replicate in the liver and cause hepatitis.

Multiple regions of the murine coronavirus spike glycoprotein influence neurovirulence.

Further in vitro characterization of mouse hepatitis virus papain-like proteinase 1: cleavage sequence requirements within pp1a.

Murine coronavirus spike glycoprotein mediates degree of viral spread, inflammation, and virus-induced immunopathology in the central nervous system.

Systematic assembly of a full-length infectious cDNA of mouse hepatitis virus strain A59.

Perforin-mediated CTL cytolysis counteracts direct cell-cell spread of Listeria monocytogenes.

Enhanced green fluorescent protein expression may be used to monitor murine coronavirus spread in vitro and in the mouse central nervous system.

The virulence of mouse hepatitis virus strain A59 is not dependent on efficient spike protein cleavage and cell-to-cell fusion.

Conformational changes in the spike glycoprotein of murine coronavirus are induced at 37 degrees C either by soluble murine CEACAM1 receptors or by pH 8.

The N-terminal domain of the murine coronavirus spike glycoprotein determines the CEACAM1 receptor specificity of the virus strain.

Murine coronavirus-induced hepatitis: JHM genetic background eliminates A59 spike-determined hepatotropism.

Amino acid substitutions within the heptad repeat domain 1 of murine coronavirus spike protein restrict viral antigen spread in the central nervous system.

The glycosylation status of the murine hepatitis coronavirus M protein affects the interferogenic capacity of the virus in vitro and its ability to replicate in the liver but not the brain.

Effects of an epitope-specific CD8+ T-cell response on murine coronavirus central nervous system disease: protection from virus replication and antigen spread and selection of epitope escape mutants.

SARS: lessons learned from other coronaviruses.

Coronavirus replication and pathogenesis: Implications for the recent outbreak of severe acute respiratory syndrome (SARS), and the challenge for vaccine development.

Increased epitope-specific CD8+ T cells prevent murine coronavirus spread to the spinal cord and subsequent demyelination.

Single-amino-acid substitutions in open reading frame (ORF) 1b-nsp14 and ORF 2a proteins of the coronavirus mouse hepatitis virus are attenuating in mice.

Identification of murine CD8 T cell epitopes in codon-optimized SARS-associated coronavirus spike protein.

Murine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein.

Expression and purification of SARS coronavirus proteins using SUMO-fusions.

Contributions of the viral genetic background and a single amino acid substitution in an immunodominant CD8+ T-cell epitope to murine coronavirus neurovirulence.

Enhanced expression and purification of membrane proteins by SUMO fusion in Escherichia coli.

Expression of hemagglutinin esterase protein from recombinant mouse hepatitis virus enhances neurovirulence.

Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus.

Endosomal proteolysis by cathepsins is necessary for murine coronavirus mouse hepatitis virus type 2 spike-mediated entry.

Both spike and background genes contribute to murine coronavirus neurovirulence.

CD8+ T-cell priming during a central nervous system infection with mouse hepatitis virus.

Murine hepatitis virus strain 1 produces a clinically relevant model of severe acute respiratory syndrome in A/J mice.

Replicase genes of murine coronavirus strains A59 and JHM are interchangeable: differences in pathogenesis map to the 3' one-third of the genome.

Inhibition of the alpha/beta interferon response by mouse hepatitis virus at multiple levels.

The spike glycoprotein of murine coronavirus MHV-JHM mediates receptor-independent infection and spread in the central nervous systems of Ceacam1a-/- Mice.

The SARS-CoV ferret model in an infection-challenge study.

Chemokine expression during mouse-hepatitis-virus-induced encephalitis: contributions of the spike and background genes.

Demyelinating and nondemyelinating strains of mouse hepatitis virus differ in their neural cell tropism.

Priming of CD8+ T cells during central nervous system infection with a murine coronavirus is strain dependent.

Murine coronavirus mouse hepatitis virus is recognized by MDA5 and induces type I interferon in brain macrophages/microglia.

Organ-specific attenuation of murine hepatitis virus strain A59 by replacement of catalytic residues in the putative viral cyclic phosphodiesterase ns2.

The murine coronavirus nucleocapsid gene is a determinant of virulence.

Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response.

Murine coronavirus delays expression of a subset of interferon-stimulated genes.

Pathogenesis of murine coronavirus in the central nervous system.

Genetic determinants of mouse hepatitis virus strain 1 pneumovirulence.

Murine coronavirus receptors are differentially expressed in the central nervous system and play virus strain-dependent roles in neuronal spread.

Murine coronavirus neuropathogenesis: determinants of virulence.

Pathogenesis of neurotropic murine coronavirus is multifactorial.

Characteristics of opioid prescriptions in 2009.

Cell-type-specific type I interferon antagonism influences organ tropism of murine coronavirus.

The role of interferon antagonist, non-structural proteins in the pathogenesis and emergence of arboviruses.

Coronavirus pathogenesis.

A novel full-length isoform of murine pregnancy-specific glycoprotein 16 (psg16) is expressed in the brain but does not mediate murine coronavirus (MHV) entry.

Antagonism of the interferon-induced OAS-RNase L pathway by murine coronavirus ns2 protein is required for virus replication and liver pathology.

Novel inhibitors of severe acute respiratory syndrome coronavirus entry that act by three distinct mechanisms.

Cell-type-specific activation of the oligoadenylate synthetase-RNase L pathway by a murine coronavirus.

Homologous 2',5'-phosphodiesterases from disparate RNA viruses antagonize antiviral innate immunity.

Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.

Cell-type-specific effects of RNase L on viral induction of beta interferon.

Evaluation of SSYA10-001 as a replication inhibitor of severe acute respiratory syndrome, mouse hepatitis, and Middle East respiratory syndrome coronaviruses.

Viral phosphodiesterases that antagonize double-stranded RNA signaling to RNase L by degrading 2-5A.

Murine AKAP7 has a 2',5'-phosphodiesterase domain that can complement an inactive murine coronavirus ns2 gene.

Coronavirus-induced demyelination of neural pathways triggers neurogenic bladder overactivity in a mouse model of multiple sclerosis.

The nsp1, nsp13, and M proteins contribute to the hepatotropism of murine coronavirus JHM.WU.

Structural basis for 2'-5'-oligoadenylate binding and enzyme activity of a viral RNase L antagonist.

MDA5 Is Critical to Host Defense during Infection with Murine Coronavirus.

RNase L is a negative regulator of cell migration.

Activation of RNase L by Murine Coronavirus in Myeloid Cells Is Dependent on Basal Oas Gene Expression and Independent of Virus-Induced Interferon.

Crystal structure of the mouse hepatitis virus ns2 phosphodiesterase domain that antagonizes RNase L activation.

Primary Role for Toll-Like Receptor-Driven Tumor Necrosis Factor Rather than Cytosolic Immune Detection in Restricting Coxiella burnetii Phase II Replication within Mouse Macrophages.

Activation of RNase L is dependent on OAS3 expression during infection with diverse human viruses.

Middle East Respiratory Syndrome Coronavirus NS4b Protein Inhibits Host RNase L Activation.

Antagonism of RNase L Is Required for Murine Coronavirus Replication in Kupffer Cells and Liver Sinusoidal Endothelial Cells but Not in Hepatocytes.

Lineage A Betacoronavirus NS2 Proteins and the Homologous Torovirus Berne pp1a Carboxy-Terminal Domain Are Phosphodiesterases That Antagonize Activation of RNase L.

Neurovirulent Murine Coronavirus JHM.SD Uses Cellular Zinc Metalloproteases for Virus Entry and Cell-Cell Fusion.

Early endonuclease-mediated evasion of RNA sensing ensures efficient coronavirus replication.

Ribonuclease L mediates the cell-lethal phenotype of double-stranded RNA editing enzyme ADAR1 deficiency in a human cell line.

Role of the inflammasome-related cytokines Il-1 and Il-18 during infection with murine coronavirus.

Replication defective viral genomes exploit a cellular pro-survival mechanism to establish paramyxovirus persistence.

Origins and pathogenesis of Middle East respiratory syndrome-associated coronavirus: recent advances.

Murine Hepatitis Virus nsp14 Exoribonuclease Activity Is Required for Resistance to Innate Immunity.

A novel mechanism of RNase L inhibition: Theiler's virus L* protein prevents 2-5A from binding to RNase L.

Third Tofo Advanced Study Week on Emerging and Re-emerging Viruses, 2018.

Real-time 2-5A kinetics suggest that interferons β and λ evade global arrest of translation by RNase L.

OAS-RNase L innate immune pathway mediates the cytotoxicity of a DNA-demethylating drug.

Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection.

Zika Virus Production Is Resistant to RNase L Antiviral Activity.

Activation of RNase L in Egyptian Rousette Bat-Derived RoNi/7 Cells Is Dependent Primarily on OAS3 and Independent of MAVS Signaling.

No credible evidence supporting claims of the laboratory engineering of SARS-CoV-2.

Forty years with coronaviruses.

Broad Anti-coronavirus Activity of Food and Drug Administration-Approved Drugs against SARS-CoV-2 and SARS-CoV .

A phenolic small molecule inhibitor of RNase L prevents cell death from ADAR1 deficiency.

Physiologic RNA targets and refined sequence specificity of coronavirus EndoU.

SARS-CoV-2 Genomic Variation in Space and Time in Hospitalized Patients in Philadelphia.

Molecular determinants and mechanism for antibody cocktail preventing SARS-CoV-2 escape.

Copan eNAT Transport System To Address Challenges in COVID-19 Diagnostics in Regions with Limited Testing Access.

Activation of STING Signaling Pathway Effectively Blocks Human Coronavirus Infection.

Femtomolar SARS-CoV-2 Antigen Detection Using the Microbubbling Digital Assay with Smartphone Readout Enables Antigen Burden Quantitation and Dynamics Tracking.

SARS-CoV-2 induces double-stranded RNA-mediated innate immune responses in respiratory epithelial-derived cells and cardiomyocytes.

Discrimination of SARS-CoV-2 infected patient samples by detection dogs: A proof of concept study.

Zika virus employs the host antiviral RNase L protein to support replication factory assembly.

Detection of SARS-CoV-2 RNA using RT-LAMP and molecular beacons.

Author Correction: Molecular determinants and mechanism for antibody cocktail preventing SARS-CoV-2 escape.

Femtomolar SARS-CoV-2 Antigen Detection Using the Microbubbling Digital Assay with Smartphone Readout Enables Antigen Burden Quantitation and Tracking.

Multiplexed detection of SARS-CoV-2 genomic and subgenomic RNA using hybridization.

The origins of SARS-CoV-2: A critical review.

Single- and Two-Stage, Closed-Tube, Point-of-Care, Molecular Detection of SARS-CoV-2.

Adenovirus prevents dsRNA formation by promoting efficient splicing of viral RNA.

Subcellular Detection of SARS-CoV-2 RNA in Human Tissue Reveals Distinct Localization in Alveolar Type 2 Pneumocytes and Alveolar Macrophages.

Detection and Interspecies Comparison of SARS-CoV-2 Delta Variant (AY.3) in Feces from a Domestic Cat and Human Samples.

SARS-CoV-2 Delta Variant (AY.3) in the Feces of a Domestic Cat.

MERS-CoV endoribonuclease and accessory proteins jointly evade host innate immunity during infection of lung and nasal epithelial cells.

SARS-CoV-2 diverges from other betacoronaviruses in only partially activating the IRE1α/XBP1 ER stress pathway in human lung-derived cells.

Targeted Mutations in the Fusion Peptide Region of La Crosse Virus Attenuate Neuroinvasion and Confer Protection against Encephalitis.

SARS-CoV-2 disrupts host epigenetic regulation via histone mimicry.

Infection of primary nasal epithelial cells differentiates among lethal and seasonal human coronaviruses.

Inborn errors of OAS-RNase L in SARS-CoV-2-related multisystem inflammatory syndrome in children.

Publisher Correction: SARS-CoV-2 disrupts host epigenetic regulation via histone mimicry.

Author Correction: SARS-CoV-2 disrupts host epigenetic regulation via histone mimicry.

Infection of primary nasal epithelial cells differentiates among lethal and seasonal human coronaviruses.

Detection of blood-brain barrier disruption in brains of patients with COVID-19, but no evidence of brain penetration by SARS-CoV-2.

Comparison of SARS-CoV-2 variants in primary human nasal cultures indicates Delta as most cytopathic and Omicron as fastest replicating.