Format

Send to

Choose Destination
Trends Mol Med. 2018 Apr;24(4):379-394. doi: 10.1016/j.molmed.2018.02.007. Epub 2018 Mar 15.

Human Endogenous Retroviruses in Neurological Diseases.

Author information

1
Department of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
2
Section of infections of the Nervous System, National Institute of Neurological Diseases and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD, USA.
3
Service de Neurologie, Groupe Hospitalier Henri Mondor, Assistance Publique Hopitaux de Paris (APHP), Université Paris Est, Créteil, France.
4
Department of Virology, University of Sassari, Sassari, Italy.
5
Institute for Advanced Biosciences (IAB), University of Grenoble-Alpes, La Tronche, France; Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1209, La Tronche, France.
6
Centre for Neuroscience and Trauma, Blizard Institute, Queen Mary University, London, UK; The Albion Centre, Prince of Wales Hospital, Sydney, Australia.
7
Centre for Neuroscience and Trauma, Blizard Institute, Queen Mary University, London, UK.
8
Department of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany. Electronic address: hans-peter.hartung@uni-duesseldorf.de.
9
Geneuro, Plan les Ouates, Geneva, Switzerland; University of Lyon, Lyon, France.

Abstract

The causes of multiple sclerosis and amyotrophic lateral sclerosis have long remained elusive. A new category of pathogenic components, normally dormant within human genomes, has been identified: human endogenous retroviruses (HERVs). These represent ∼8% of the human genome, and environmental factors have reproducibly been shown to trigger their expression. The resulting production of envelope (Env) proteins from HERV-W and HERV-K appears to engage pathophysiological pathways leading to the pathognomonic features of MS and ALS, respectively. Pathogenic HERV elements may thus provide a missing link in understanding these complex diseases. Moreover, their neutralization may represent a promising strategy to establish novel and more powerful therapeutic approaches.

PMID:
29551251
DOI:
10.1016/j.molmed.2018.02.007
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center