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Biased hypermutation and other genetic changes in defective measles viruses in human brain infections

R Cattaneo1, A Schmid, D Eschle

  • 1Institute for Molecular Biology I, University of Zürich, Switzerland.

Cell
|October 21, 1988
PubMed

Insights

Persistent measles virus (MV) infections in the brain show significant mutations. These genetic changes, particularly in the matrix gene, may enhance viral propagation in brain cells.

Area of Science:

  • Virology
  • Neuroscience
  • Genetics

Background:

  • Subacute sclerosing panencephalitis (SSPE) and measles inclusion body encephalitis (MIBE) are severe neurological complications of persistent measles virus (MV) infection.
  • Understanding the genetic alterations of MV during these chronic infections is crucial for elucidating disease pathogenesis.

Purpose of the Study:

  • To investigate the mutational landscape of MV genes in persistent infections.
  • To determine if observed mutations confer a selective advantage for viral propagation in the central nervous system.

Main Methods:

  • Cloning of full-length MV gene transcripts from brain autopsies of SSPE and MIBE patients.
  • DNA sequencing to identify nucleotide mutations and their impact on amino acid sequences.
  • In vitro translation assays to confirm alterations in gene reading frames.

Main Results:

  • Approximately 2% of MV nucleotides were mutated during persistent infection, with 35% affecting amino acid sequences.
  • Mutations altered reading frames in two fusion genes, confirmed by in vitro translation.
  • A distinct mutation cluster in the MIBE matrix gene showed 50% U-to-C substitutions, suggesting a biased copying event.

Conclusions:

  • Accumulated mutations in persistent MV infections, especially within brain tissue, can lead to significant genetic divergence.
  • Specific mutation patterns, like the MIBE matrix gene alteration, may represent adaptive changes favoring viral persistence and propagation in the brain.
  • These findings suggest a role for viral genetic evolution in the pathogenesis of severe MV-associated neurological diseases.

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