Up-to-date knowledge about the association between multiple sclerosis and the reactivation of human endogenous retrovirus infections
- PMID: 29423611
- DOI: 10.1007/s00415-018-8783-1
Up-to-date knowledge about the association between multiple sclerosis and the reactivation of human endogenous retrovirus infections
Abstract
Background: Although existing studies show that reactivation of the human endogenous retrovirus (HERVs) plays a leading role in multiple sclerosis (MS) progression, the practitioners are yet to establish effective approaches for managing MS without jeopardizing the patients' immune systems.
Aim: To provide up-to-date knowledge on the specific roles played by the reactivation of the HERVs in the pathogenesis of MS.
Materials and methods: A systematic review of 70 peer-reviewed journals accessed via PubMed was conducted. The searches generated more than 600 sources that were evaluated based on three step in and exclusion criteria. The selected sources were critically analyzed vis-à-vis the paper's hypothesis which posits that the HERVs reactivation does not directly cause the MS, but triggers a demyelination process by promoting the pathogenic effects of the retroviruses. The paper further documents the advancements in the therapeutic applications resulting from the immunohistological analysis and pathological studies aimed at minimizing the adverse consequences of the HERVs reactivation.
Results and discussions: Only three out of the 70 reviewed sources did not find provide evidence linking the reactivation of HERV and MS progression. On the other hand, overwhelming pieces of evidence confirm that the reactivations often drive the demyelinating plaques by initiating microglial inflammation. Pathological examinations reveal that the inflammatory monocytes (Ly6ChiCCR2 + CX3CR1lo) trigger the reactivation of the malignant T cells that are responsible for the progression of MS. These findings are promoting new discoveries as far as managing MS is concerned.
Keywords: Human endogenous retrovirus; Multiple sclerosis; Pathogenesis.
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