Subacute sclerosing panencephalitis is typically characterized by alterations in the fusion protein cytoplasmic domain of the persisting measles virus

Anita Schmid, Pius Spielhofer, Roberto Cattaneo, Knut Baczko, Volker Ter Meulen, Martin A. Billeter

Research output: Contribution to journalArticle

98 Citations (Scopus)

Abstract

Our recent extensive analysis of three cases of subacute sclerosing panencephalitis (SSPE) revealed intriguing genetic defects in the persisting measles virus (MV): the fusion (F) genes encoded truncated cytoplasmic F protein domains (Cattaneo et al., Virology 173, 415-425, 1989). Now this MV genomic region has been investigated in eight additional SSPE cases by PCR amplification, replacement cloning into a vector containing the F gene of a lytic MV, in vitro expression, and sequencing. In all cases at least part of the clones showed mutations leading to F protein truncations, elongation, or nonconservative amino acid replacements. It is proposed that alteration of the F protein cytoplasmic domain may play a critical role in the development of SSPE.

Original languageEnglish (US)
Pages (from-to)910-915
Number of pages6
JournalVirology
Volume188
Issue number2
DOIs
StatePublished - 1992
Externally publishedYes

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Subacute Sclerosing Panencephalitis
Measles virus
Virology
Gene Fusion
Organism Cloning
Clone Cells
Amino Acids
Polymerase Chain Reaction
Mutation
Genes
Protein Domains
Proteins

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

Cite this

Subacute sclerosing panencephalitis is typically characterized by alterations in the fusion protein cytoplasmic domain of the persisting measles virus. / Schmid, Anita; Spielhofer, Pius; Cattaneo, Roberto; Baczko, Knut; Ter Meulen, Volker; Billeter, Martin A.

In: Virology, Vol. 188, No. 2, 1992, p. 910-915.

Research output: Contribution to journalArticle

Schmid, Anita ; Spielhofer, Pius ; Cattaneo, Roberto ; Baczko, Knut ; Ter Meulen, Volker ; Billeter, Martin A. / Subacute sclerosing panencephalitis is typically characterized by alterations in the fusion protein cytoplasmic domain of the persisting measles virus. In: Virology. 1992 ; Vol. 188, No. 2. pp. 910-915.
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