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Epstein-Barr Virus Load Correlates with Multiple Sclerosis-Associated Retrovirus Envelope Expression

Silvia Pérez-Pérez1, María Inmaculada Domínguez-Mozo1, María Ángel García-Martínez1

  • 1Environmental Factors in Degenerative Diseases Research Group, Hospital Clínico San Carlos, IdISSC, 28040 Madrid, Spain.

Biomedicines
|February 25, 2022
PubMed

Insights

Epstein-Barr virus (EBV) load variations correlate with human endogenous retrovirus W family (HERV-W) gene expression in multiple sclerosis (MS) patients. This suggests EBV may activate HERV-W, potentially contributing to MS development.

Area of Science:

  • Neuroimmunology
  • Virology
  • Retroviral Research

Background:

  • Multiple Sclerosis (MS) pathogenesis involves potential etiological factors like human endogenous retrovirus W family (HERV-W) envelope proteins and herpesviruses (Epstein-Barr virus [EBV], human herpesvirus 6A/B [HHV-6A/B]).
  • Previous research suggests a strong association between these viral agents and MS development.

Purpose of the Study:

  • To investigate the relationship between viral loads and antibody titers of EBV and HHV-6A/B and the expression of pHERV-W ENV/syncytin-1 in relapsing-remitting MS (RRMS) patients.
  • To explore the potential transactivation of pHERV-W ENV by EBV.

Main Methods:

  • A 12-month longitudinal study of 98 RRMS patients.
  • Quantification of serum antibody titers against EBV and HHV-6A/B using ELISA.
  • Analysis of viral loads via qPCR.
  • Assessment of pHERV-W ENV/syncytin-1 gene and protein expression in immune cells using qPCR and flow cytometry, respectively.
  • Genotyping of HLA MS-related alleles.

Main Results:

  • A positive correlation was observed between the 12-month variation in pHERV-W ENV gene expression and the variation in EBV viral load.
  • This correlation was particularly evident in patients with high baseline EBV loads.
  • No significant association was found with HHV-6A/B viral loads or antibody titers, or with HLA alleles.

Conclusions:

  • The findings support the hypothesis that EBV may transactivate pHERV-W ENV expression.
  • This interaction could represent a novel mechanism contributing to MS pathogenesis.
  • Further research is warranted to elucidate the precise relationship and its implications for MS.
Keywords:
EBVHERV-WHHV-6A/Bmultiple sclerosissyncytin-1

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