Multiple viral mutations rather than host factors cause defective measles virus gene expression in a subacute sclerosing panencephalitis cell line

R. Cattaneo, A. Schmid, M. A. Billeter, R. D. Sheppard, S. A. Udem

Research output: Contribution to journalArticlepeer-review

83 Scopus citations

Abstract

A measles virus (MV) genome originally derived from brain cells of a subacute sclerosing panencephalitis patient expressed in IP-3-Ca cells an unstable MV matrix protein and was unable to produce virus particles. Transfection of this MV genome into other cell lines did not relieve these defects, showing that they are ultimately encoded by viral mutations. However, these defects were partially relieved in a weakly infectious virus which emerged from IP-3-Ca cells and which produced a matrix protein of intermediate stability. The sequences of several cDNAs related to the unstable and intermediately stable matrix proteins showed many differences in comparison with a stable matrix protein sequence and even appreciable heterogeneity among themselves. Nevertheless, partial restoration of matrix protein stability could be ascribed to a single additional amino acid change. From an examination of additional genes, we estimated that, on average, each MV genome in IP-3-Ca cells differs from the others in 30 to 40 of its 16,000 bases. The role of extreme variability of RNA virus genomes in persistent viral infections is discussed in the context of the pathogenesis of subacute sclerosing panencephalitis and of other human diseases of suspected viral etiology.

Original languageEnglish (US)
Pages (from-to)1388-1397
Number of pages10
JournalJournal of virology
Volume62
Issue number4
DOIs
StatePublished - 1988

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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