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

K. M. Kaye, D. R. Spriggs, R. Bassel-Duby, B. N. Fields, K. L. Tyler

Research output: Contribution to journalArticle

42 Scopus citations

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 biiologic 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 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.

Original languageEnglish (US)
Pages (from-to)90-97
Number of pages8
JournalJournal of virology
Volume59
Issue number1
DOIs
StatePublished - 1986

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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