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Persistent and lytic infections with SSPE virus: a comparison of the synthesis of virus-specific polypeptides

Insights

Measles virus protein synthesis differs between lytic and persistent infections. Messenger RNA from both infection types directs the synthesis of all viral proteins, including M protein, in cell-free systems.

Area of Science:

  • Virology
  • Molecular Biology
  • Neuroscience

Background:

  • Subacute sclerosing panencephalitis (SSPE) is a chronic, fatal neurological disease caused by measles virus.
  • Persistent measles virus infections in cell cultures mimic aspects of SSPE, offering a model for studying viral replication in the central nervous system.

Purpose of the Study:

  • To compare measles virus protein and messenger RNA synthesis in persistently infected cells versus lytic infections.
  • To investigate the role of messenger RNA in directing viral protein synthesis during different infection phases.

Main Methods:

  • Comparison of measles virus polypeptide and messenger RNA synthesis in persistently infected and lytically infected cell cultures.
  • Cell-free translation systems to analyze messenger RNA coding capacity.
  • Polyadenylation analysis of viral messenger RNAs.
  • Immunological analysis of viral proteins.

Main Results:

  • H, N, and possibly F proteins were synthesized in both lytic and persistent infections.
  • M protein synthesis was detected only in lytic infections, but its corresponding messenger RNA was present in both.
  • Cell-free translation of messenger RNA from both infection types produced all structural polypeptides, including M, and three non-structural polypeptides.
  • Viral messenger RNAs were polyadenylated, and haemagglutinin-related polypeptides showed structural changes after persistent infection.

Conclusions:

  • Persistent measles virus infection alters viral protein synthesis, but messenger RNA remains capable of directing the synthesis of all viral proteins.
  • Structural changes in viral proteins, particularly haemagglutinin, may occur during persistent infections and contribute to SSPE pathogenesis.

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