A highly conserved cryptic epitope in the receptor-binding domains of SARS-CoV-2 and SARS-CoV.
A multibasic cleavage site in the Spike protein of SARS-CoV-2 is essential for infection of human lung cells.
A new coronavirus associated with human respiratory disease in China.
Adaptation of SARS-CoV-2 in BALB/c mice for testing vaccine efficacy.
Analysis of the SARS-CoV-2 spike protein glycan shield reveals implications for immune recognition.
Biomechanical characterization of SARS-CoV-2 spike RBD and human ACE2 protein-protein interaction.
Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV.
Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation.
D614G Mutation Alters SARS-CoV-2 Spike Conformation and Enhances Protease Cleavage at the S1/S2 Junction.
Deducing the N- and O- glycosylation profile of the spike protein of novel coronavirus SARS-CoV-2.
Early transmissibility assessment of the N501Y mutant strains of SARS-CoV-2 in the United Kingdom, October to November 2020.
Emergence of a SARS-CoV-2 variant of concern with mutations in spike glycoprotein.
Evolutionary and structural analyses of SARS-CoV-2 D614G spike protein mutation now documented worldwide.
Furin cleavage of the SARS-CoV-2 spike is modulated by O-glycosylation.
Hydroxychloroquine-mediated inhibition of SARS-CoV-2 entry is attenuated by TMPRSS2.
In situ structural analysis of SARS-CoV-2 spike reveals flexibility mediated by three hinges.
Increased transmissibility and global spread of SARS-CoV-2 variants of concern as at June 2021.
Integrin mediates cell entry of the SARS-CoV-2 virus independent of cellular receptor ACE2.
Molecular Architecture of the SARS-CoV-2 Virus.
Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity.
Neuropilin-1 is a host factor for SARS-CoV-2 infection.
Proteolytic activation of SARS-CoV-2 spike protein.
Recognition and inhibition of SARS-CoV-2 by humoral innate immunity pattern recognition molecules.
Recurrent emergence of SARS-CoV-2 spike deletion H69/V70 and its role in the Alpha variant B.1.1.7.
S-acylation controls SARS-CoV-2 membrane lipid organization and enhances infectivity.
SARS-CoV-2 D614G variant exhibits efficient replication ex vivo and transmission in vivo.
SARS-CoV-2 Vaccines Based on the Spike Glycoprotein and Implications of New Viral Variants.
SARS-CoV-2 can recruit a heme metabolite to evade antibody immunity.
SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor.
SARS-CoV-2 immune evasion by the B.1.427/B.1.429 variant of concern.
SARS-CoV-2 spike D614G change enhances replication and transmission.
SARS-CoV-2 spike L452R variant evades cellular immunity and increases infectivity.
SARS-CoV-2 variants preferentially emerge at intrinsically disordered protein sites helping immune evasion.
Sequences in the cytoplasmic tail of SARS-CoV-2 Spike facilitate expression at the cell surface and syncytia formation.
Site-specific glycan analysis of the SARS-CoV-2 spike.
Spike mutation D614G alters SARS-CoV-2 fitness.
Structural basis for the recognition of the SARS-CoV-2 by full-length human ACE2.
Structural basis of receptor recognition by SARS-CoV-2.
Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor.
Structure, function, and antigenicity of the SARS-CoV-2 spike glycoprotein.
Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation.
TMPRSS2 and furin are both essential for proteolytic activation of SARS-CoV-2 in human airway cells.
TMPRSS2 expression dictates the entry route used by SARS-CoV-2 to infect host cells.
The Impact of Mutations in SARS-CoV-2 Spike on Viral Infectivity and Antigenicity.
The Integrin Binding Peptide, ATN-161, as a Novel Therapy for SARS-CoV-2 Infection.
The SARS-CoV-2 Envelope and Membrane proteins modulate maturation and retention of the Spike protein, allowing assembly of virus-like particles.
Tracking Changes in SARS-CoV-2 Spike: Evidence that D614G Increases Infectivity of the COVID-19 Virus.
Comparative host-coronavirus protein interaction networks reveal pan-viral disease mechanisms.
Cryo-EM structure of SARS-CoV-2 ORF3a in lipid nanodiscs.
ORF3a of the COVID-19 virus SARS-CoV-2 blocks HOPS complex-mediated assembly of the SNARE complex required for autolysosome formation.
SARS-CoV-2 ORF3a induces RETREG1/FAM134B-dependent reticulophagy and triggers sequential ER stress and inflammatory responses during SARS-CoV-2 infection.
beta-Coronaviruses Use Lysosomes for Egress Instead of the Biosynthetic Secretory Pathway.
A Mouse-Adapted SARS-CoV-2 Induces Acute Lung Injury and Mortality in Standard Laboratory Mice.
A deletion in SARS-CoV-2 ORF7 identified in COVID-19 outbreak in Uruguay.
A household case evidences shorter shedding of SARS-CoV-2 in naturally infected cats compared to their human owners.
A mouse-adapted model of SARS-CoV-2 to test COVID-19 countermeasures.
A plasmid DNA-launched SARS-CoV-2 reverse genetics system and coronavirus toolkit for COVID-19 research.
An 81-Nucleotide Deletion in SARS-CoV-2 ORF7a Identified from Sentinel Surveillance in Arizona (January to March 2020).
An Observational Laboratory-Based Assessment of SARS-CoV-2 Molecular Diagnostics in Benin, Western Africa.
Associations of Early COVID-19 Cases in San Francisco with Domestic and International Travel.
Berberine and Obatoclax Inhibit SARS-Cov-2 Replication in Primary Human Nasal Epithelial Cells In Vitro.
Case Study: Prolonged Infectious SARS-CoV-2 Shedding from an Asymptomatic Immunocompromised Individual with Cancer.
Cold-Adapted Live Attenuated SARS-Cov-2 Vaccine Completely Protects Human ACE2 Transgenic Mice from SARS-Cov-2 Infection.
Complete Genome Sequence of a SARS-CoV-2 Strain Isolated in Northern Germany.
Development of an inactivated vaccine candidate for SARS-CoV-2.
Discovery of SARS-CoV-2 antiviral drugs through large-scale compound repurposing.
Earliest detection to date of SARS-CoV-2 in Florida: Identification together with influenza virus on the main entry door of a university building, February 2020.
Early Diffusion of SARS-CoV-2 Infection in the Inner Area of the Italian Sardinia Island.
Emergence of a Severe Acute Respiratory Syndrome Coronavirus 2 Virus Variant With Novel Genomic Architecture in Hong Kong.
From People to Panthera: Natural SARS-CoV-2 Infection in Tigers and Lions at the Bronx Zoo.
Genomic variation and epidemiology of SARS-CoV-2 importation and early circulation in Israel.
In-Frame 12-Nucleotide Deletion within Open Reading Frame 3a in a SARS-CoV-2 Strain Isolated from a Patient Hospitalized with COVID-19.
Investigation of a COVID-19 outbreak in Germany resulting from a single travel-associated primary case: a case series.
Isolation of infectious SARS-CoV-2 from urine of a COVID-19 patient.
Molecular Evolution of Human Coronavirus 229E in Hong Kong and a Fatal COVID-19 Case Involving Coinfection with a Novel Human Coronavirus 229E Genogroup.
Molecular characterization of SARS-CoV-2 from the first case of COVID-19 in Italy.
Nosocomial outbreak of COVID-19 pneumonia in Wuhan, China.
ORF10-Cullin-2-ZYG11B complex is not required for SARS-CoV-2 infection.
Possible Bat Origin of Severe Acute Respiratory Syndrome Coronavirus 2.
Rapid incorporation of Favipiravir by the fast and permissive viral RNA polymerase complex results in SARS-CoV-2 lethal mutagenesis.
SARS-CoV-2 Phylogenetic Analysis, Lazio Region, Italy, February-March 2020.
SARS-CoV-2 Positivity on or After 9 Days Among Quarantined Student Contacts of Confirmed Cases.
SARS-CoV-2 genomic surveillance in Taiwan revealed novel ORF8-deletion mutant and clade possibly associated with infections in Middle East.
Severe Acute Respiratory Syndrome Coronavirus 2 from Patient with Coronavirus Disease, United States.
Subgenomic RNA identification in SARS-CoV-2 genomic sequencing data.
Territorywide Study of Early Coronavirus Disease Outbreak, Hong Kong, China.
The SARS-CoV-2 ORF10 is not essential in vitro or in vivo in humans.
Viable SARS-CoV-2 in the air of a hospital room with COVID-19 patients.
A molecular pore spans the double membrane of the coronavirus replication organelle.
Activation and evasion of type I interferon responses by SARS-CoV-2.
An atomistic model of the coronavirus replication-transcription complex as a hexamer assembled around nsp15.
Cryo-EM Structure of an Extended SARS-CoV-2 Replication and Transcription Complex Reveals an Intermediate State in Cap Synthesis.
Cryo-EM structures of the SARS-CoV-2 endoribonuclease Nsp15 reveal insight into nuclease specificity and dynamics.
Crystal structure of SARS-CoV-2 main protease provides a basis for design of improved alpha-ketoamide inhibitors.
Dynamic competition between SARS-CoV-2 NSP1 and mRNA on the human ribosome inhibits translation initiation.
Evasion of Type I Interferon by SARS-CoV-2.
How the Replication and Transcription Complex Functions in Jumping Transcription of SARS-CoV-2.
Human NLRP1 is a sensor of pathogenic coronavirus 3CL proteases in lung epithelial cells.
ISG15-dependent activation of the sensor MDA5 is antagonized by the SARS-CoV-2 papain-like protease to evade host innate immunity.
Molecular Basis for ADP-ribose Binding to the Mac1 Domain of SARS-CoV-2 Nsp3.
Papain-like protease regulates SARS-CoV-2 viral spread and innate immunity.
SARS-CoV-2 Disrupts Splicing, Translation, and Protein Trafficking to Suppress Host Defenses.
SARS-CoV-2 Nsp1 binds the ribosomal mRNA channel to inhibit translation.
Structural Basis for RNA Replication by the SARS-CoV-2 Polymerase.
Structural basis for inhibition of the RNA-dependent RNA polymerase from SARS-CoV-2 by remdesivir.
Structural basis for translational shutdown and immune evasion by the Nsp1 protein of SARS-CoV-2.
Structure of Mpro from COVID-19 virus and discovery of its inhibitors.
Structure of replicating SARS-CoV-2 polymerase.
Structure of the RNA-dependent RNA polymerase from COVID-19 virus.
Structure-based design of antiviral drug candidates targeting the SARS-CoV-2 main protease.
The SARS-CoV-2 subgenome landscape and its novel regulatory features.
The mechanism of RNA capping by SARS-CoV-2.
Tipiracil binds to uridine site and inhibits Nsp15 endoribonuclease NendoU from SARS-CoV-2.
Cell surface SARS-CoV-2 nucleocapsid protein modulates innate and adaptive immunity.
Coronaviruses exploit a host cysteine-aspartic protease for replication.
Crystal structure of SARS-CoV-2 nucleocapsid protein RNA binding domain reveals potential unique drug targeting sites.
Nucleocapsid mutations in SARS-CoV-2 augment replication and pathogenesis.
SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation.
Structural basis of RNA recognition by the SARS-CoV-2 nucleocapsid phosphoprotein.
Targeting the coronavirus nucleocapsid protein through GSK-3 inhibition.
Decoupling SARS-CoV-2 ORF6 localization and interferon antagonism.
Molecular mechanism of SARS-CoVs Orf6 targeting the Rae1-Nup98 complex to compete with mRNA nuclear export.
Overexpression of SARS-CoV-2 protein ORF6 dislocates RAE1 and NUP98 from the nuclear pore complex.
SARS-CoV-2 ORF6 Disrupts Bidirectional Nucleocytoplasmic Transport through Interactions with Rae1 and Nup98.
SARS-CoV-2 Orf6 hijacks Nup98 to block STAT nuclear import and antagonize interferon signaling.
Improved binding of SARS-CoV-2 Envelope protein to tight junction-associated PALS1 could play a key role in COVID-19 pathogenesis.
SARS-CoV-2 envelope protein topology in eukaryotic membranes.
Structure and drug binding of the SARS-CoV-2 envelope protein transmembrane domain in lipid bilayers.
A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster.
Characterization of accessory genes in coronavirus genomes.
Characterizations of SARS-CoV-2 mutational profile, spike protein stability and viral transmission.
ORF8 and ORF3b antibodies are accurate serological markers of early and late SARS-CoV-2 infection.
SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNgamma-Induced Antiviral Gene Expression in Human Lung Epithelial Cells.
SARS-CoV-2 accessory protein ORF8 is secreted extracellularly as a glycoprotein homodimer.
Structure of SARS-CoV-2 ORF8, a rapidly evolving immune evasion protein.
The ORF8 protein of SARS-CoV-2 mediates immune evasion through down-regulating MHC-Iota.
Title: ORF8 contributes to cytokine storm during SARS-CoV-2 infection by activating IL-17 pathway.
Viral Mimicry of Interleukin-17A by SARS-CoV-2 ORF8.
Functional landscape of SARS-CoV-2 cellular restriction.
Structural insight reveals SARS-CoV-2 ORF7a as an immunomodulating factor for human CD14+ monocytes.
Ubiquitination of SARS-CoV-2 ORF7a promotes antagonism of interferon response.