This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kaye, K M Articles by Tyler, K L Search for Related Content PubMed PubMed Citation Articles by Kaye, K M Articles by Tyler, K L

 Previous Article  |  Next Article 

J Virol. 1986 July; 59(1): 90-97

Genetic basis for altered pathogenesis of an immune-selected antigenic variant of reovirus type 3 (Dearing).

ABSTRACT

In this paper we provide a step by step comparison of the pathogenesis of murine infection caused by reovirus type 3 (Dearing) and an antigenic variant (K) selected by its resistance to neutralization with a monoclonal antibody (G5) directed against the T3 hemagglutinin. To show that specific changes in the biologic properties of variant K were due to mutation in the S1 double-stranded RNA segment (gene), which encodes the viral hemagglutinin, we generated a reassortant virus ("1 HA K") containing the variant K S1 gene and compared its properties to variant K and to a reassortant ("1 HA 3") containing the T3 (Dearing) S1 gene. These studies, in conjunction with our previous nucleotide sequence analysis of the S1 genes of variant K and T3 (Dearing) [R. Bassel-Duby, A. Jayasuriya, D. Chatterjee, N. Sonenberg, J. V. Maizel, Jr., and B. N. Fields, Nature (London) 315:421-423, 1985; R. Bassel-Duby, D. R. Spriggs, K. L. Tyler, and B. N. Fields, submitted for publication], indicate that a single amino acid change in the T3 hemagglutinin can alter viral growth and tropism within the central nervous system without affecting either its primary replication in the intestine or its pattern of spread to or within the central nervous system.

This article has been cited by other articles:

• Campbell, J. A., Schelling, P., Wetzel, J. D., Johnson, E. M., Forrest, J. C., Wilson, G. A. R., Aurrand-Lions, M., Imhof, B. A., Stehle, T., Dermody, T. S. (2005). Junctional Adhesion Molecule A Serves as a Receptor for Prototype and Field-Isolate Strains of Mammalian Reovirus. J. Virol. 79: 7967-7978 [Abstract] [Full Text]  
• Richardson-Burns, S. M., Tyler, K. L. (2004). Regional Differences in Viral Growth and Central Nervous System Injury Correlate with Apoptosis. J. Virol. 78: 5466-5475 [Abstract] [Full Text]  
• Chappell, J. D., Duong, J. L., Wright, B. W., Dermody, T. S. (2000). Identification of Carbohydrate-Binding Domains in the Attachment Proteins of Type 1 and Type 3 Reoviruses. J. Virol. 74: 8472-8479 [Abstract] [Full Text]  
• Rodgers, S. E., Connolly, J. L., Chappell, J. D., Dermody, T. S. (1998). Reovirus Growth in Cell Culture Does Not Require the Full Complement of Viral Proteins: Identification of a sigma 1s-Null Mutant. J. Virol. 72: 8597-8604 [Abstract] [Full Text]  
• Chappell, J. D., Barton, E. S., Smith, T. H., Baer, G. S., Duong, D. T., Nibert, M. L., Dermody, T. S. (1998). Cleavage Susceptibility of Reovirus Attachment Protein sigma 1 during Proteolytic Disassembly of Virions Is Determined by a Sequence Polymorphism in the sigma 1 Neck. J. Virol. 72: 8205-8213 [Abstract] [Full Text]