The XXXX endogenous retrovirus link between genes and environment in @entity15 and in multifactorial diseases associating neuroinflammation.

@entity1 @entity18341 @entity75 @entity1800 @entity26633 @entity2939 @entity15
Endogenous retroviruses represent about 8% of the @entity1 genome and belong to the superfamily of transposable and retrotransposable genetic elements. Altogether, these mobile genetic elements and their numerous inactivated "junk" sequences represent nearly one half of the @entity1 DNA. Nonetheless, a significant part of this "non-conventional" genome has retained potential activity. Epigenetic control is notably involved in silencing most of these genetic elements but certain environmental factors such as viruses are known to dysregulate their expression in susceptible cells. More particularly, embryonal cells with limited gene methylation are most susceptible to uncontrolled activation of these mobile genetic elements by, e.g., @entity1800 . In particular, certain viruses transactivate promoters from endogenous retroviral family type W (HERV-W). HERV-W RNA was first isolated in circulating viral particles ( @entity15 -associated RetroViral element, MSRV) that have been associated with the evolution and prognosis of @entity15 . HERV-W elements encode a powerful immunopathogenic @entity26633 ( @entity26633 ) that activates a pro-inflammatory and autoimmune cascade through interaction with @entity2939 on immune cells. This @entity26633 protein has repeatedly been detected in @entity75 and may be involved in other diseases. Epigenetic factors controlling @entity18341 protein expression then reveal critical. This review addresses the gene-environment epigenetic interface of such HERV-W elements and its potential involvement in disease.
