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Hemagglutinin-specific neutralization of subacute sclerosing panencephalitis viruses

Miguel Ángel Muñoz-Alía1, Claude P Muller2,3, Stephen J Russell1,4

  • 1Department of Molecular Medicine, Mayo Clinic, Rochester, Minnesota, United States of America.

Plos One
|February 22, 2018
PubMed

Insights

Subacute sclerosing panencephalitis (SSPE) is a lethal measles complication. This study found SSPE viruses have altered measles virus hemagglutinin (MeV-H) but antigenic drift doesn't explain SSPE's cause.

Area of Science:

  • Virology
  • Immunology
  • Neurology

Background:

  • Subacute sclerosing panencephalitis (SSPE) is a fatal neurological complication of measles virus (MeV) infection.
  • SSPE pathogenesis is poorly understood, with the hypothesis that measles virus antigenic drift plays a role.
  • The MeV hemagglutinin protein (MeV-H) is crucial for viral entry and a target for neutralizing antibodies.

Purpose of the Study:

  • To investigate the role of antigenic drift in MeV-H in the pathogenesis of SSPE.
  • To analyze antigenic alterations in MeV-H from SSPE patients and compare them to circulating MeV genotypes.
  • To identify potential new antigenic sites on MeV-H.

Main Methods:

  • Obtained cDNA of the MeV-H gene from brain autopsy tissue of three SSPE patients with varying disease durations.
  • Generated recombinant MeVs with substituted MeV-H genes using a reverse genetic system.
  • Performed virus neutralization assays with monoclonal antibodies (mAbs) and polyclonal sera, alongside functional and receptor-binding analyses.

Main Results:

  • SSPE-derived MeV-H exhibited altered antigenic profiles, similar to wild-type viruses, and maintained SLAM/nectin-4-dependent function.
  • Specific genotypes (D7, F, H1, D4.2) showed enhanced neutralization or significant antigenic alterations.
  • A novel antigenic site (Φ) on MeV-H was identified between previously defined sites Ia and Ib.

Conclusions:

  • SSPE-causing MeV strains display antigenic properties comparable to currently circulating MeV genotypes.
  • The findings do not support antigenic drift as a primary pathogenetic mechanism in SSPE.
  • The identification of a new antigenic site (Φ) offers insights into MeV-H structure and antibody interactions.

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