scholarly journals Characterization of a second cleavage site and demonstration of activity in trans by the papain-like proteinase of the murine coronavirus mouse hepatitis virus strain A59.

1997 ◽  
Vol 71 (2) ◽  
pp. 900-909 ◽  
Author(s):  
P J Bonilla ◽  
S A Hughes ◽  
S R Weiss
Keyword(s):  
Virus Strain ◽  
Cleavage Site ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
In Trans ◽  
Murine Coronavirus

scholarly journals The murine coronavirus mouse hepatitis virus strain A59 from persistently infected murine cells exhibits an extended host range.

1997 ◽  
Vol 71 (12) ◽  
pp. 9499-9507 ◽  
Author(s):  
J H Schickli ◽  
B D Zelus ◽  
D E Wentworth ◽  
S G Sawicki ◽  
K V Holmes
Keyword(s):  
Host Range ◽  
Virus Strain ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Persistently Infected ◽  
Murine Coronavirus

scholarly journals Characterization of brain-infiltrating mononuclear cells during infection with mouse hepatitis virus strain JHM

1991 ◽  
Vol 32 (3) ◽  
pp. 199-207 ◽  
Author(s):  
Jo S.P. Williamson ◽  
Karin C. Sykes ◽  
Stephen A. Stohlman
Keyword(s):  
Virus Strain ◽  
Mononuclear Cells ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus

Hepatitis Mutants of Mouse Hepatitis Virus Strain A59

1995 ◽  
pp. 577-582 ◽  
Author(s):  
S. T. Hingley ◽  
J. L. Gombold ◽  
E. Lavi ◽  
S. R. Weiss
Keyword(s):  
Virus Strain ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus

scholarly journals Characterization of the Coronavirus Mouse Hepatitis Virus Strain A59 Small Membrane Protein E

2000 ◽  
Vol 74 (5) ◽  
pp. 2333-2342 ◽  
Author(s):  
Martin J. B. Raamsman ◽  
Jacomine Krijnse Locker ◽  
Alphons de Hooge ◽  
Antoine A. F. de Vries ◽  
Gareth Griffiths ◽  
...  
Keyword(s):  
Virus Strain ◽  
Hepatitis Virus ◽  
Expression System ◽  
Mouse Hepatitis Virus ◽  
Viral Envelope ◽  
Membrane Structures ◽  
Electron Microscopic ◽  
E Protein ◽  
Infected Cells ◽  
Virus Expression

ABSTRACT The small envelope (E) protein has recently been shown to play an essential role in the assembly of coronaviruses. Expression studies revealed that for formation of the viral envelope, actually only the E protein and the membrane (M) protein are required. Since little is known about this generally low-abundance virion component, we have characterized the E protein of mouse hepatitis virus strain A59 (MHV-A59), an 83-residue polypeptide. Using an antiserum to the hydrophilic carboxy terminus of this otherwise hydrophobic protein, we found that the E protein was synthesized in infected cells with similar kinetics as the other viral structural proteins. The protein appeared to be quite stable both during infection and when expressed individually using a vaccinia virus expression system. Consistent with the lack of a predicted cleavage site, the protein was found to become integrated in membranes without involvement of a cleaved signal peptide, nor were any other modifications of the polypeptide observed. Immunofluorescence analysis of cells expressing the E protein demonstrated that the hydrophilic tail is exposed on the cytoplasmic side. Accordingly, this domain of the protein could not be detected on the outside of virions but appeared to be inside, where it was protected from proteolytic degradation. The results lead to a topological model in which the polypeptide is buried within the membrane, spanning the lipid bilayer once, possibly twice, and exposing only its carboxy-terminal domain. Finally, electron microscopic studies demonstrated that expression of the E protein in cells induced the formation of characteristic membrane structures also observed in MHV-A59-infected cells, apparently consisting of masses of tubular, smooth, convoluted membranes. As judged by their colabeling with antibodies to E and to Rab-1, a marker for the intermediate compartment and endoplasmic reticulum, the E protein accumulates in and induces curvature into these pre-Golgi membranes where coronaviruses have been shown earlier to assemble by budding.

scholarly journals Enhanced Virulence Mediated by the Murine Coronavirus, Mouse Hepatitis Virus Strain JHM, Is Associated with a Glycine at Residue 310 of the Spike Glycoprotein

2003 ◽  
Vol 77 (19) ◽  
pp. 10260-10269 ◽  
Author(s):  
Evelena Ontiveros ◽  
Taeg S. Kim ◽  
Thomas M. Gallagher ◽  
Stanley Perlman
Keyword(s):  
Virus Strain ◽  
Hepatitis Virus ◽  
Neurological Diseases ◽  
Mouse Hepatitis Virus ◽  
Neutralizing Antibody ◽  
Lateral Spread ◽  
S Protein ◽  
Acute Encephalitis ◽  
The Central Nervous System

ABSTRACT The coronavirus, mouse hepatitis virus strain JHM, causes acute and chronic neurological diseases in rodents. Here we demonstrate that two closely related virus variants, both of which cause acute encephalitis in susceptible strains of mice, cause markedly different diseases if mice are protected with a suboptimal amount of an anti-JHM neutralizing antibody. One strain, JHM.SD, caused acute encephalitis, while infection with JHM.IA resulted in no acute disease. Using recombinant virus technology, we found that the differences between the two viruses mapped to the spike (S) glycoprotein and that the two S proteins differed at four amino acids. By engineering viruses that differed by only one amino acid, we identified a serine-to-glycine change at position 310 of the S protein (S310G) that recapitulated the more neurovirulent phenotype. The increased neurovirulence mediated by the virus encoding glycine at position S310 was not associated with a different tropism within the central nervous system (CNS) but was associated with increased lateral spread in the CNS, leading to significantly higher brain viral titers. In vitro studies revealed that S310G was associated with decreased S1-S2 stability and with enhanced ability to mediate infection of cells lacking the primary receptor for JHM (“receptor-independent spread”). These enhanced fusogenic properties of viruses encoding a glycine at position 310 of the S protein may contribute to spread within the CNS, a tissue in which expression of conventional JHM receptors is low.

scholarly journals Mouse Hepatitis Virus Strain JHM Infects a Human Hepatocellular Carcinoma Cell Line

Virology ◽  
1999 ◽  
Vol 264 (2) ◽  
pp. 398-409 ◽  
Author(s):  
Peter J. Koetters ◽  
Loubna Hassanieh ◽  
Stephen A. Stohlman ◽  
Thomas Gallagher ◽  
Michael M.C. Lai
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Line ◽  
Virus Strain ◽  
Carcinoma Cell ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Carcinoma Cell Line ◽  
Hepatocellular Carcinoma Cell Line ◽  
Human Hepatocellular Carcinoma Cell ◽  
Hepatocellular Carcinoma Cell

scholarly journals Intranasally administered alpha/beta interferon prevents extension of mouse hepatitis virus, strain JHM, into the brains of BALB/cByJ mice

1987 ◽  
Vol 8 (5-6) ◽  
pp. 239-245 ◽  
Author(s):  
Abigail L. Smith ◽  
Stephen W. Barthold ◽  
Deborah S. Beck
Keyword(s):  
Virus Strain ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Beta Interferon ◽  
Alpha Beta
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