Previous Article | Next Article ![]()
Journal of Virology, March 2001, p. 2452-2457, Vol. 75, No. 5
Departments of
Microbiology1 and Pathology and
Laboratory Medicine,2 University of
Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6076, and Department of Microbiology, Philadelphia College of
Osteopathic Medicine, Philadelphia, Pennsylvania
19131-16943
Received 7 August 2000/Accepted 5 December 2000
Recombinant mouse hepatitis viruses (MHV) differing only in the
spike gene, containing A59, MHV-4, and MHV-2 spike genes in the
background of the A59 genome, were compared for their ability to
replicate in the liver and induce hepatitis in weanling C57BL/6 mice
infected with 500 PFU of each virus by intrahepatic injection. Penn98-1, expressing the MHV-2 spike gene, replicated to high titer in
the liver, similar to MHV-2, and induced severe hepatitis with
extensive hepatocellular necrosis. SA59R13, expressing the A59 spike gene, replicated to a somewhat lower titer and induced moderate to severe hepatitis with zonal necrosis, similar to MHV-A59. S4R21, expressing the MHV-4 spike gene, replicated to a
minimal extent and induced few if any pathological changes, similar to MHV-4. Thus, the extent of replication and the degree of hepatitis in
the liver induced by these recombinant viruses were determined largely
by the spike protein.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.5.2452-2457.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Murine Coronavirus Spike Protein Determines the
Ability of the Virus To Replicate in the Liver and Cause
Hepatitis
*
Corresponding author. Mailing address: Department of
Microbiology, University of Pennsylvania School of Medicine, 36th
Street and Hamilton Walk, Philadelphia, PA 19104-6076. Phone: (215)
898-8013. Fax: (215) 573-4858. E-mail:
weisssr{at}mail.med.upenn.edu.
This article has been cited by other articles:
| J. Bacteriol. | Mol. Cell. Biol. | Microbiol. Mol. Biol. Rev. |
|---|
| Clin. Vaccine Immunol. | ALL ASM JOURNALS |
|---|