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Measles Virus: Identification in the M Protein Primary Sequence of a Potential Molecular Marker for Subacute
Hasan Kweder1, Michelle Ainouze1, Joanna Brunel1
1CIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France ; Inserm, U1111, 69007 Lyon, France ; Ecole Normale Supérieure de Lyon, 69007 Lyon, France ; Centre International de Recherche en Infectiologie, Université Lyon 1, 69007 Lyon, France ; CNRS, UMR 5308, Lyon, France.
Abstract:
Subacute Sclerosing Panencephalitis (SSPE), a rare lethal disease of children and young adults due to persistence of measles virus (MeV) in the brain, is caused by wild type (wt) MeV. Why MeV vaccine strains never cause SSPE is completely unknown. Hypothesizing that this phenotypic difference could potentially be represented by a molecular marker, we compared glycoprotein and matrix (M) genes from SSPE cases with those from the Moraten vaccine strain, searching for differential structural motifs. We observed that all known SSPE viruses have residues P64, E89, and A209 (PEA) in their M proteins whereas the equivalent residues for vaccine strains are either S64, K89, and T209 (SKT) as in Moraten or PKT. Through the construction of MeV recombinants, we have obtained evidence that the wt MeV-M protein PEA motif, in particular A209, is linked to increased viral spread. Importantly, for the 10 wt genotypes (of 23) that have had their M proteins sequenced, 9 have the PEA motif, the exception being B3, which has PET. Interestingly, cases of SSPE caused by genotype B3 have yet to be reported. In conclusion, our results strongly suggest that the PEA motif is a molecular marker for wt MeV at risk to cause SSPE.
Insights
Wild-type measles virus (MeV) causes SSPE, but vaccine strains do not. Researchers identified a specific M protein motif (PEA) in wild-type MeV linked to increased viral spread and SSPE risk.
Area of Science:
- Virology
- Molecular Biology
- Neuroscience
Background:
- Subacute Sclerosing Panencephalitis (SSPE) is a fatal neurological disease caused by persistent wild-type measles virus (MeV) infection.
- The reason why MeV vaccine strains do not cause SSPE remains unknown, prompting investigation into molecular differences.
Purpose of the Study:
- To identify a potential molecular marker differentiating wild-type MeV strains that cause SSPE from non-pathogenic vaccine strains.
- To investigate the role of specific matrix (M) protein motifs in MeV pathogenesis and viral spread.
Main Methods:
- Comparative analysis of glycoprotein and matrix (M) genes from SSPE-causing MeV and the Moraten vaccine strain.
- Construction of MeV recombinants to assess the functional impact of identified M protein motifs.
- Correlation of M protein genotypes with the occurrence of SSPE in different MeV genotypes.
Main Results:
- A specific M protein motif, PEA (Proline-64, Glutamate-89, Alanine-209), was consistently found in SSPE-associated wild-type MeV strains.
- Vaccine strains exhibited different residues (e.g., Serine-64, Lysine-89, Threonine-209) at these positions.
- Experimental evidence indicated that the PEA motif, particularly Alanine-209, enhances viral spread, a key factor in SSPE pathogenesis.
- Wild-type MeV genotypes lacking the PEA motif (e.g., genotype B3 with PET) have not been associated with reported SSPE cases.
Conclusions:
- The PEA motif in the M protein serves as a potential molecular marker for wild-type MeV strains with a high risk of causing SSPE.
- This finding provides crucial insights into the pathogenesis of SSPE and potential avenues for future research and prevention strategies.
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