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Subacute Sclerosing Panencephalitis: How Measles Virus Adapts to the Brain

Roberto Cattaneo1, Kalpana Yadav1, Rory D de Vries2

  • 11Department of Molecular Medicine, Mayo Clinic, Rochester, Minnesota, USA;

Annual Review of Virology
|April 28, 2026
PubMed

Insights

Measles virus (MeV) uses specific receptors to infect immune and epithelial cells. In rare brain infections causing SSPE, mutated MeV utilizes surrogate receptors for cell spread and evolution.

Area of Science:

  • Virology
  • Immunology
  • Neuroscience

Background:

  • Measles virus (MeV) utilizes distinct cellular receptors, SLAMF1 on immune cells and nectin-4 on epithelial cells, for infection.
  • MeV infection of immune cells leads to systemic disease and immunosuppression, while epithelial cell infection facilitates transmission.
  • Rarely, MeV infects the brain, causing subacute sclerosing panencephalitis (SSPE) through spread in cells lacking typical receptors.

Purpose of the Study:

  • To investigate the mechanisms of MeV spread in the brain during SSPE.
  • To understand the role of mutated MeV fusion apparatus and surrogate receptors in neuropathogenesis.
  • To explore the potential implications of MeV genome evolution in CIUs for other RNA viruses.

Main Methods:

  • Analysis of MeV mutations in the membrane fusion apparatus in SSPE brain samples.
  • Investigation of host proteins acting as surrogate receptors for MeV entry.
  • Characterization of collective infectious units (CIUs) and their role in MeV evolution.

Main Results:

  • Multiple mutations in the MeV membrane fusion apparatus are selected in SSPE brains.
  • These mutations enable triggering by host surrogate receptors, facilitating cell-to-cell spread.
  • Mutations promote MeV genome evolution and the formation of adaptable collective infectious units (CIUs).

Conclusions:

  • MeV adaptation in the brain involves selection of mutations enabling surrogate receptor use and enhanced cell-to-cell spread.
  • Collective infectious units (CIUs) represent a mechanism for MeV genome evolution and adaptation in neuropathogenesis.
  • The findings may inform understanding of neuropathogenesis for other nonsegmented negative-strand RNA viruses.

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