Basic VirologyFind the latest information on the basic research on SARS-CoV-2 and other coronaviruses. Information is organized into subcategories:
Proteins & Translation
- Articles to be updated shortly.
Virus Assembly, Protein Processing and Structure
- Cryo-EM structure of SARS-CoV-2 ORF3a in lipid nanodiscs.
- Coupling of N7-methyltransferase and 3'-5' exoribonuclease with SARS-CoV-2 polymerase reveals mechanisms for capping and proofreading.
- Palmitoylation of SARS-CoV-2 S protein is essential for viral infectivity.
- Structural basis of coronavirus E protein interactions with human PALS1 PDZ domain.
- Structural basis for SARS-CoV-2 envelope protein recognition of human cell junction protein PALS1.
- Crystal structure of SARS-CoV-2 Orf9b in complex with human TOM70 suggests unusual virus-host interactions.
- 2'-O methylation of RNA cap in SARS-CoV-2 captured by serial crystallography.
- Structural insight into SARS-CoV-2 neutralizing antibodies and modulation of syncytia.
- Cryo-electron microscopy structures of the N501Y SARS-CoV-2 spike protein in complex with ACE2 and 2 potent neutralizing antibodies.
- Effect of natural mutations of SARS-CoV-2 on spike structure, conformation and antigenicity.
- A metal ion orients mRNA to ensure accurate 2'-O ribosyl methylation of the first nucleotide of the SARS-CoV-2 genome.
- Remdesivir is a delayed translocation inhibitor of SARS-CoV-2 replication.
- *Research Tool In vivo structural characterization of the SARS-CoV-2 RNA genome identifies host proteins vulnerable to repurposed drugs.
- The E3 Ubiquitin Ligase RNF5 Facilitates SARS-CoV-2 Membrane Protein-Mediated Virion Release.
- Structure of the SARS-CoV-2 RNA-dependent RNA polymerase in the presence of favipiravir-RTP.
- Insights into the secondary structural ensembles of the full SARS-CoV-2 RNA genome in infected cells.
- The effect of the D614G substitution on the structure of the spike glycoprotein of SARS-CoV-2.
- Energetic and structural features of SARS-CoV-2 N-protein co-assemblies with nucleic acids.
- Structural insight reveals SARS-CoV-2 ORF7a as an immunomodulating factor for human CD14+ monocytes.
- Structural Basis for Accommodation of Emerging B.1.351 and B.1.1.7 Variants by Two Potent SARS-CoV-2 Neutralizing Antibodies.
- Cryo-EM structures of the SARS-CoV-2 endoribonuclease Nsp15 reveal insight into nuclease specificity and dynamics.
- Stabilizing the closed SARS-CoV-2 spike trimer.
- Antibody neutralization of SARS-CoV-2 through ACE2 receptor mimicry.
- *Research Tool Comprehensive in vivo secondary structure of the SARS-CoV-2 genome reveals novel regulatory motifs and mechanisms.
- BRD2 inhibition blocks SARS-CoV-2 infection in vitro by reducing transcription of the host cell receptor ACE2.
Evolution & Phylogenetics
- *New* Identification of a High-Frequency Intrahost SARS-CoV-2 Spike Variant with Enhanced Cytopathic and Fusogenic Effects.
- Emergence and spread of a SARS-CoV-2 lineage A variant (A.23.1) with altered spike protein in Uganda.
- Recurrent emergence of SARS-CoV-2 spike deletion H69/V70 and its role in the Alpha variant B.1.1.7.
- Epidemiology and genetic diversity of SARS-CoV-2 lineages circulating in Africa.
- Identification of a novel lineage bat SARS-related coronaviruses that use bat ACE2 receptor.
- Rapid Emergence and Epidemiologic Characteristics of the SARS-CoV-2 B.1.526 Variant - New York City, New York, January 1-April 5, 2021.
- Phylogenomics and population genomics of SARS-CoV-2 in Mexico reveals variants of interest (VOI) and a mutation in the Nucleocapsid protein associated with symptomatic versus asymptomatic carriers.
- Rapidly emerging SARS-CoV-2 B.1.1.7 sub-lineage in the United States of America with spike protein D178H and membrane protein V70L mutations.
- SARS-CoV-2 B.1.617 emergence and sensitivity to vaccine-elicited antibodies.
- *Research Tool Transmission, infectivity, and neutralization of a spike L452R SARS-CoV-2 variant.
- Saudi Arabian SARS-CoV-2 genomes implicate a mutant Nucleocapsid protein in modulating host interactions and increased viral load in COVID-19 patients.
- *Research Tool SARS-CoV-2 gene content and COVID-19 mutation impact by comparing 44 Sarbecovirus genomes.
- A new SARS-CoV-2 variant poorly detected by RT-PCR on nasopharyngeal samples, with high lethality.
- Intra-host evolution provides for continuous emergence of SARS-CoV-2 variants.
- SARS-CoV-2 variant B.1.617 is resistant to Bamlanivimab and evades antibodies induced by infection and vaccination.
- Introduction of ORF3a-Q57H SARS-CoV-2 Variant Causing Fourth Epidemic Wave of COVID-19, Hong Kong, China.
- Novel SARS-CoV-2 Variant Derived from Clade 19B, France.
- Characteristics of SARS-CoV-2 variants of concern B.1.1.7, B.1.351 or P.1: data from seven EU/EEA countries, weeks 38/2020 to 10/2021.
- Comparative Analysis of Emerging B.1.1.7+E484K SARS-CoV-2 isolates from Pennsylvania.
- SARS-CoV-2 evolution in an immunocompromised host reveals shared neutralization escape mechanisms.
- A novel variant of interest of SARS-CoV-2 with multiple spike mutations is identified from travel surveillance in Africa.
- Preliminary report on SARS-CoV-2 Spike mutation T478K.
- Genomic surveillance of SARS-CoV-2 tracks early interstate transmission of P.1 lineage and diversification within P.2 clade in Brazil.
- The ongoing evolution of variants of concern and interest of SARS-CoV-2 in Brazil revealed by convergent indels in the amino (N)-terminal domain of the Spike protein.
- Transmission, infectivity, and antibody neutralization of an emerging SARS-CoV-2 variant in California carrying a L452R spike protein mutation.
- SARS-CoV-2 within-host diversity and transmission.
- The emergence and ongoing convergent evolution of the N501Y lineages coincides with a major global shift in the SARS-CoV-2 selective landscape.
- Emergence of a SARS-CoV-2 variant of concern with mutations in spike glycoprotein.
- Genomics and epidemiology of a novel SARS-CoV-2 lineage in Manaus, Brazil.
- Acquisition of the L452R mutation in the ACE2-binding interface of Spike protein triggers recent massive expansion of SARS-Cov-2 variants.
- A SARS-CoV-2 lineage A variant (A.23.1) with altered spike has emerged and is dominating the current Uganda epidemic.
- Comparative Genomics and Integrated Network Approach Unveiled Undirected Phylogeny Patterns, Co-mutational Hot Spots, Functional Cross Talk, and Regulatory Interactions in SARS-CoV-2.
- A Novel SARS-CoV-2 Variant of Concern, B.1.526, Identified in New York.
- Identification of novel bat coronaviruses sheds light on the evolutionary origins of SARS-CoV-2 and related viruses.
- Genomic epidemiology identifies emergence and rapid transmission of SARS-CoV-2 B.1.1.7 in the United States.
- Sixteen novel lineages of SARS-CoV-2 in South Africa.
- Evidence for SARS-CoV-2 related coronaviruses circulating in bats and pangolins in Southeast Asia.
- Emergence in late 2020 of multiple lineages of SARS-CoV-2 Spike protein variants affecting amino acid position 677.
- Molecular Evolution of Human Coronavirus 229E in Hong Kong and a Fatal COVID-19 Case Involving Coinfection with a Novel Human Coronavirus 229E Genogroup.
- SARS-CoV-2 lineage B.1.526 emerging in the New York region detected by software utility created to query the spike mutational landscape.
- A human coronavirus evolves antigenically to escape antibody immunity.
- Distinct Patterns of Emergence of SARS-CoV-2 Spike Variants including N501Y in Clinical Samples in Columbus Ohio.
- Increased infections, but not viral burden, with a new SARS-CoV-2 variant.
- Temporal dynamics of SARS-CoV-2 mutation accumulation within and across infected hosts.
- Emergence and Evolution of a Prevalent New SARS-CoV-2 Variant in the United States.
- Recombination events are concentrated in the spike protein region of Betacoronaviruses.
- Evaluating the Effects of SARS-CoV-2 Spike Mutation D614G on Transmissibility and Pathogenicity.
- Evolutionary and structural analysis of SARS-CoV-2 specific evasion of host immunity.
Host Immune Response
- CCR2-dependent monocyte-derived cells restrict SARS-CoV-2 infection.
- TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines.
- A molecular single-cell lung atlas of lethal COVID-19.
- *Research Tool Global analysis of protein-RNA interactions in SARS-CoV-2-infected cells reveals key regulators of infection.
- Longitudinal analysis reveals that delayed bystander CD8+ T cell activation and early immune pathology distinguish severe COVID-19 from mild disease.
- Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant.
- Distinct immunological signatures discriminate severe COVID-19 from non-SARS-CoV-2-driven critical pneumonia.
- *Research Tool The SARS-CoV-2 RNA interactome.
- Peripheral and lung resident memory T cell responses against SARS-CoV-2.
- Diverse Functional Autoantibodies in Patients with COVID-19.
- High titers and low fucosylation of early human anti-SARS-CoV-2 IgG promote inflammation by alveolar macrophages.
- RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human lung cells.
- Divergent and self-reactive immune responses in the CNS of COVID-19 patients with neurological symptoms.
- Delayed production of neutralizing antibodies correlates with fatal COVID-19.
- *Research Tool Functional landscape of SARS-CoV-2 cellular restriction.
- Single-cell analyses reveal SARS-CoV-2 interference with intrinsic immune response in the human gut.
- *Research Tool Multilevel proteomics reveals host perturbations by SARS-CoV-2 and SARS-CoV.
- Rapid decay of host basal mRNAs during SARS-CoV-2 infection perturbs host antiviral mRNA biogenesis and export.
- *Research Tool COVID-19 immune features revealed by a large-scale single-cell transcriptome atlas.
- *Research Tool Discovery and functional interrogation of SARS-CoV-2 RNA-host protein interactions.
- Pediatric nasal epithelial cells are less permissive to SARS-CoV-2 replication compared to adult cells.
- *Research Tool Multi-cohort analysis of host immune response identifies conserved protective and detrimental modules associated with severity across viruses.
- Longitudinal profiling of respiratory and systemic immune responses reveals myeloid cell-driven lung inflammation in severe COVID-19.
- The spatial landscape of lung pathology during COVID-19 progression.
- COVID-19-neutralizing antibodies predict disease severity and survival.
- Diverse Functional Autoantibodies in Patients with COVID-19.
- SARS-CoV-2 recruits a haem metabolite to evade antibody immunity.
- Outcome of SARS-CoV-2 infection is linked to MAIT cell activation and cytotoxicity.
- IgA autoantibodies target pulmonary surfactant in patients with severe COVID-19.
- Circuits between infected macrophages and T cells in SARS-CoV-2 pneumonia.
- MDA5 Governs the Innate Immune Response to SARS-CoV-2 in Lung Epithelial Cells.
- SARS-CoV-2 Infection Severity Is Linked to Superior Humoral Immunity Against the Spike.
- A longitudinal study of SARS-CoV-2-infected patients reveals a high correlation between neutralizing antibodies and COVID-19 severity.
- A diagnostic host response biosignature for COVID-19 from RNA profiling of nasal swabs and blood.
- Severely ill COVID-19 patients display impaired exhaustion features in SARS-CoV-2-reactive CD8+ T cells.
- New-Onset IgG Autoantibodies in Hospitalized Patients with COVID-19.
- SARS-CoV-2 infection elicits a rapid neutralizing antibody response that correlates with disease severity.
- Global absence and targeting of protective immune states in severe COVID-19.
- Neutralizing antibody titres in SARS-CoV-2 infections.
- Kinetics of antibody responses dictate COVID-19 outcome.
- The functions of SARS-CoV-2 neutralizing and infection-enhancing antibodies in vitro and in mice and nonhuman primates.
- Neurological Manifestations of COVID-19 Feature T Cell Exhaustion and Dedifferentiated Monocytes in Cerebrospinal Fluid.
- Induction of alarmin S100A8/A9 mediates activation of aberrant neutrophils in the pathogenesis of COVID-19.
- Impact of B.1.1.7 variant mutations on antibody recognition of linear SARS-CoV-2 epitopes.
- Untuned antiviral immunity in COVID-19 revealed by temporal type I/III interferon patterns and flu comparison.
Animal Models & Epizootic Infections
- Articles to be updated shortly.
Viral Entry & Receptors
- TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2.
- Binding and molecular basis of the bat coronavirus RaTG13 virus to ACE2 in humans and other species.
- SARS-CoV-2 spike P681R mutation enhances and accelerates viral fusion.
- B.1.1.7 and B.1.351 SARS-CoV-2 variants display enhanced Spike-mediated fusion.
- SARS-CoV-2 Spreads through Cell-to-Cell Transmission.
- Spike mutation T403R allows bat coronavirus RaTG13 to use human ACE2.
- SARS-CoV-2 infects human adult donor eyes and hESC-derived ocular epithelium.
- Membrane lectins enhance SARS-CoV-2 infection and influence the neutralizing activity of different classes of antibodies.
- Ultrastructural insight into SARS-CoV-2 attachment, entry and budding in human airway epithelium.
- Coagulation factors directly cleave SARS-CoV-2 spike and enhance viral entry.
- Characterisation of B.1.1.7 and Pangolin coronavirus spike provides insights on the evolutionary trajectory of SARS-CoV-2.
- Identification of ACE2 mutations that modulate SARS-CoV-2 spike binding across multiple mammalian species.
- Sialic acid-Dependent Binding and Viral Entry of SARS-CoV-2.
- Genome-wide CRISPR screening identifies TMEM106B as a proviral host factor for SARS-CoV-2.
- The SARS-CoV-2 Y453F mink variant displays a pronounced increase in ACE-2 affinity but does not challenge antibody neutralization.
- Differential gene expression by RNA-Seq in Sigma-2 Receptor/TMEM97 knockout cells reveals its role in complement activation and SARS-CoV-2 viral uptake.
- Critical ACE2 Determinants of SARS-CoV-2 and Group 2B Coronavirus Infection and Replication.
- *Research Tool The B1.351 and P.1 variants extend SARS-CoV-2 host range to mice.
- Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell.
- *Research Tool SARS-CoV-2 comprehensive receptor profiling: mechanistic insight to drive new therapeutic strategies.
- Soluble ACE2-mediated cell entry of SARS-CoV-2 via interaction with proteins related to the renin-angiotensin system.
- SARS-CoV-2 causes severe epithelial inflammation and barrier dysfunction.
- *Research Tool Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics.
- Functional and genetic analysis of viral receptor ACE2 orthologs reveals a broad potential host range of SARS-CoV-2.
- A common TMPRSS2 variant protects against severe COVID-19.
- Circulating SARS-CoV-2 spike N439K variants maintain fitness while evading antibody-mediated immunity.
- The Spike D614G mutation increases SARS-CoV-2 infection of multiple human cell types.
- SARS-CoV-2 spike D614G change enhances replication and transmission.
- SARS-CoV-2 infects and replicates in cells of the human endocrine and exocrine pancreas.
- The basis of a more contagious 501Y.V1 variant of SARS-COV-2.
- SARS-CoV-2 and SARS-CoV spike-mediated cell-cell fusion differ in the requirements for receptor expression and proteolytic activation.
- Biomechanical Characterization of SARS-CoV-2 Spike RBD and Human ACE2 Protein-Protein Interaction.
- Impact of South African 501.V2 Variant on SARS-CoV-2 Spike Infectivity and Neutralization: A Structure-based Computational Assessment.
- Cryo-EM Structure of the N501Y SARS-CoV-2 Spike Protein in Complex with a Potent Neutralizing Antibody.
- ApoE-Isoform-Dependent SARS-CoV-2 Neurotropism and Cellular Response.
- The SARS-CoV-2 Spike protein has a broad tropism for mammalian ACE2 proteins.
- Cross-species recognition of SARS-CoV-2 to bat ACE2.
- *Research Tool Genetic Screens Identify Host Factors for SARS-CoV-2 and Common Cold Coronaviruses.
- SARS-CoV-2 spike downregulates tetherin to enhance viral spread.
- SARS-CoV-2 RBD in vitro evolution follows contagious mutation spread, yet generates an able infection inhibitor.
- The SARS-CoV-2 spike protein disrupts the cooperative function of human cardiac pericytes - endothelial cells through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease.
- Spike glycoprotein and host cell determinants of SARS-CoV-2 entry and cytopathic effects.
- *Research Tool SARS-CoV-2 Requires Cholesterol for Viral Entry and Pathological Syncytia Formation.
- Recombinant ACE2 Expression Is Required for SARS-CoV-2 To Infect Primary Human Endothelial Cells and Induce Inflammatory and Procoagulative Responses.
- D614G Spike Mutation Increases SARS CoV-2 Susceptibility to Neutralization.
Viral Replication/Non-Structural Proteins/Enzymes