Human endogenous retrovirus and multiple sclerosis: A review and transcriptome findings

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Luiz H Nali1, Guilherme S Olival2, Horácio Montenegro3

  • 1Laboratório de Virologia, Instituto de Medicina Tropical de São Paulo, LIM-52 (LIMHC) Universidade de São Paulo, Rua Dr. Enéas de Carvalho Aguiar, 470, São Paulo 05403-000, Brazil; Post-graduation Program in Health Sciences, Santo Amaro University, Rua Prof. Enéas de Siqueira Neto, 340, São Paulo 04829-300, Brazil.

Multiple Sclerosis and Related Disorders
|December 18, 2021
PubMed

Insights

Human Endogenous Retroviruses (HERVs), particularly HERV-W, are implicated in Multiple Sclerosis (MS) pathogenesis. This study explores the diverse expression of HERVs in MS patients, furthering our understanding of this autoimmune disease.

Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • Multiple Sclerosis (MS) is an autoimmune disorder with complex, multifactorial etiology.
  • Genetic and environmental factors are implicated in MS pathogenesis, with a focus on infectious agents.
  • Human Endogenous Retroviruses (HERVs), remnants of ancient viral infections comprising ~8% of the human genome, are investigated for their role in MS.

Purpose of the Study:

  • To discuss the potential links between HERVs and MS pathogenesis.
  • To present novel data on the diversity of HERV expression in samples from MS patients.
  • To investigate the association of HERV-W with MS.

Main Methods:

  • Review of existing evidence on HERV-W and MS.
  • Analysis of HERV expression diversity in MS patient samples.
  • In vitro and in vivo modeling of HERV env protein effects.

Main Results:

  • Elevated HERV-W expression levels are observed in MS patients.
  • HERV-W proteins are detected within MS lesions (plaques).
  • The HERV-W env protein can induce inflammatory responses.

Conclusions:

  • HERVs, especially HERV-W, are strongly associated with MS pathogenesis.
  • Further research into HERV expression diversity is crucial for understanding MS.
  • HERV-W's role in inflammation supports its link to MS development.

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