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Updated: Nov 10, 2025

Author Spotlight: Novel Assay for Studying B-Cell Responses in Multiple Sclerosis Research
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Author Spotlight: Novel Assay for Studying B-Cell Responses in Multiple Sclerosis Research

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The Interaction of Human and Epstein-Barr Virus miRNAs with Multiple Sclerosis Risk Loci

Ali Afrasiabi1,2, Nicole L Fewings2, Stephen D Schibeci2

  • 1Systems Biology and Health Data Analytics Lab, The Graduate School of Biomedical Engineering, UNSW Sydney, Sydney, NSW 2052, Australia.

International Journal of Molecular Sciences
|April 3, 2021
PubMed

Insights

Epstein-Barr virus (EBV) infection may influence Multiple Sclerosis (MS) development. This study reveals how EBV impacts microRNAs (miRNAs) in B cells, potentially contributing to MS pathogenesis through interactions with MS risk genes.

Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • The etiology of Multiple Sclerosis (MS) is largely unknown, but Epstein-Barr virus (EBV) infection is a suspected contributing factor.
  • MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and are implicated in various diseases.

Purpose of the Study:

  • To investigate the role of EBV-encoded and host cellular miRNAs in MS pathogenesis.
  • To identify potential interactions between miRNAs and MS risk genes in the context of EBV infection.

Main Methods:

  • Analysis of differentially expressed host miRNAs in EBV-infected B cells (lymphoblastoid cell lines, LCLs).
  • In silico identification of host/EBV miRNA interactions with MS risk loci.
  • In silico estimation of genotype effects of MS risk single nucleotide polymorphisms (SNPs) on miRNA:mRNA interactions.
  • In vitro validation of SNP effects on gene expression in LCLs and B cells.

Main Results:

  • The protective allele of MS risk SNP rs4808760 was found to reduce the expression of hsa-mir-3188-3p.
  • hsa-let-7b-5p showed differential interaction with ZC3HAV1 in LCLs versus B cells.
  • The protective allele of MS risk SNP rs10271373 increased ZC3HAV1 expression in LCLs, suggesting enhanced IFN response and reduced EBV immune evasion.

Conclusions:

  • EBV infection dysregulates the miRNA machinery in B cells, including MS risk-associated miRNAs.
  • These dysregulated miRNAs may contribute to MS pathogenesis by interacting with MS risk genes.
  • Findings provide evidence for a mechanistic link between EBV, miRNA dysregulation, and MS development.
Keywords:
EBNA2EBVGWASMSZC3HAV1miRNA

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