Review
Version 2
This version is not peer-reviewed
Human Endogenous Retrovirus as Therapeutic Targets in Neurologic Disease
Version 1
: Received: 8 April 2021 / Approved: 9 April 2021 / Online: 9 April 2021 (13:30:49 CEST)
Version 2 : Received: 9 April 2021 / Approved: 12 April 2021 / Online: 12 April 2021 (12:17:32 CEST)
Version 2 : Received: 9 April 2021 / Approved: 12 April 2021 / Online: 12 April 2021 (12:17:32 CEST)
A peer-reviewed article of this Preprint also exists.
Giménez-Orenga, K.; Oltra, E. Human Endogenous Retrovirus as Therapeutic Targets in Neurologic Disease. Pharmaceuticals 2021, 14, 495. Giménez-Orenga, K.; Oltra, E. Human Endogenous Retrovirus as Therapeutic Targets in Neurologic Disease. Pharmaceuticals 2021, 14, 495.
Abstract
Human endogenous retroviruses (HERVs) are ancient retroviral DNA sequences established into germline. They contain regulatory elements and encoded proteins few of which may provide benefits to hosts when co-opted as cellular genes. Their tight regulation is mainly achieved by epigenetic mechanisms which can be altered by environmental factors, e.g. viral infections, leading to HERV activation. Aberrant expression of HERVs associates with neurological disease, such as multiple sclerosis (MS) or amyotrophic lateral sclerosis (ALS), inflammatory processes and neurodegeneration. This review summarizes recent advances on the epigenetic mechanisms controlling HERV expression and the pathogenic effects triggered by HERV derepression. The article ends describing new promising therapies targeting HERV elements, one of which, temelimab, has completed phase II trials with encouraging results in treating MS. The information gathered here may turn helpful in the design of new strategies to unveil epigenetic failures behind HERV-triggered disease, opening new possibilities for druggable targets and/or for extending the use of temelimab to treat other associated diseases.
Keywords
amyotrophic lateral sclerosis; epigenetics; HERV-K; HERV-W; monoclonal antibody; multiple sclerosis; neurodegeneration; temelimab.
Subject
Medicine and Pharmacology, Pathology and Pathobiology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Comments (1)
We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.
Leave a public commentSend a private comment to the author(s)
* All users must log in before leaving a comment
Commenter: Elisa Oltra
Commenter's Conflict of Interests: Author
Dr. Hervé Perron has manifested his will to be removed as coauthor by written mail to the corresponding author.
Instead his name has been added to Acknowledgements.