Coronavirus Spike Proteins in Viral Entry and Pathogenesis
By T. Gallagher, Michael J. Buchmeier. Virology, 2001
651 citations recorded by the source corpus.
u t p r r b e m Coronaviruses comprise a large and diverse family of enveloped, positive-stranded RNA viruses. The Coronaviridae exhibit broad host range, infecting many mammalian and avian species and causing upper respiratory, gastrointestinal, hepatic, and central nervous system diseases. In humans and fowl, coronaviruses primarily cause upper respiratory tract infections, while porcine and bovine coronaviruses establish enteric infections that result in severe economic loss. Coronaviruses of laboratory mice are, for historical reasons, designated as mouse hepatitis viruses (MHVs), but among these only a subset are strictly hepatotropic. Enteric strains are commonly found in rodent colonies and neurotropic strains are exploited to study central nervous system infection and demyelinating disease (Perlman et al., 2000). The extraordinary variations in host range and tissue tropism among coronaviruses are in large part attributable to variations in the spike glycoprotein. The S protein is a large, type I membrane glycoprotein that contains distinct functional domains near the amino (S1) and carboxy (S2) termini. These spikes function to define viral tropism by their receptor specificity and perhaps also by their membrane fusion activity during virus entry into cells. Recently their natural variation has attracted the attention of researchers interested in determinants of viral host range, virus entry, and virus–receptor interactions and their relationship to tropism. Evidence supporting a role for spike protein projections as agents of organ tropism and pathogenesis began with comparative studies of different naturally occurring MHV strains. In essence, nucleotide sequencing revealed that alterations in virus virulence were most closely associated with differences in the spike gene. These correlative findings were recently reinforced using the new technology of targeted RNA recombination, a
Subfields: Animal Science and Zoology, Infectious Diseases
View Paper: https://www.semanticscholar.org/paper/93d5b6f973c9098927bdd7974ea73e3fee239e7f
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Animal Science and Zoology
In Infectious Diseases
Citations in the corpus
- Receptor and viral determinants of SARS-coronavirus adaptation to human ACE2 (2005, positive): “The coronavirus spike (S) protein mediates infection of receptor-bearing cells (Gallagher and Buchmeier, 2001; Holmes, 2003; Hofmann and Pohlmann, 2004).”
- Coronavirus Pathogenesis and the Emerging Pathogen Severe Acute Respiratory Syndrome Coronavirus (2005, positive): “It is likely that this ability is related to the less stable association of S1 and S2, such that the conformational changes in spike that lead to fusion are more easily triggered, and this in turn is at least partially responsible for its very high neurovirulence (103, 161).”
- Potent binding of 2019 novel coronavirus spike protein by a SARS coronavirus-specific human monoclonal antibody (2020, neutral): “ory epithelial cells by interacting with cell surface receptor angiotensin-converting enzyme 2 (ACE2) [8].”
- Coronavirus Structural Proteins and Virus Assembly (2008, positive): “S protein binds the host cell receptor and mediates virus-to-cell and cell-to-cell fusion (57).”
- Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus (2003, neutral): “jpg" NDATA ITEM> ]> Spike (S) proteins of coronaviruses, including the coronavirus that causes severe acute respiratory syndrome (SARS), associate with cellular receptors to mediate infection of their target cell”
- TMPRSS2 and ADAM17 Cleave ACE2 Differentially and Only Proteolysis by TMPRSS2 Augments Entry Driven by the Severe Acute Respiratory Syndrome Coronavirus Spike Protein (2013, positive): “Cleavage of the S protein by host cell proteases is essential for viral infectivity (15), and the responsible enzymes constitute potential targets for intervention.”
- Identification of residues in the receptor-binding domain (RBD) of the spike protein of human coronavirus NL63 that are critical for the RBD-ACE2 receptor interaction. (2008, positive): “The S1 domain of coronaviruses is responsible for binding to the cellular receptor, whilst the S2 domain is mainly involved in membrane fusion during viral entry into the host cell (Bonavia et al., 2003; Gallagher & Buchmeier, 2001 ).”
- Coronavirus Pathogenesis (2011, positive): “1 (Fazakerley et al., 1992), are associated with single site mutations or deletions within the HVR (Dalziel et al., 1986; Gallagher and Buchmeier, 2001; Phillips and Weiss, 2001) and the spike of the neuroattenuated A59 strain contains a large deletion (52 amino acids) within the HVR.”
- The Molecular Biology of Coronaviruses (2006, positive): “This results in a hair-trigger spike so highly fusogenic that it can mediate fusion between infected cells and cells lacking receptors, thereby leading to more extensive neuropathogenesis than occurs with other MHV strains (Gallagher and Buchmeier, 2001; Gallagher et al., 1992; Krueger et al., 2001;”
- Further Evidence for Bats as the Evolutionary Source of Middle East Respiratory Syndrome Coronavirus (2017, neutral): “Recombination in the spike gene is particularly significant because the derived protein is responsible for host receptor recognition and membrane fusion (16) and thus is central in determining host specificity.”
- Circulation of genetically distinct contemporary human coronavirus OC43 strains (2005, positive): “Host immunity escape mechanisms, variation in host range and tissue tropism of coronaviruses are largely attributed to variations in the spike glycoprotein (Gallagher and Buchmeier, 2001).”