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And if the "environmental" factor missing in some of our most deadly neurological diseases was actually in our genome?
While writing in Frontiers in Genetics, researchers at the University of Düsseldorf explain how viruses have found themselves in our DNA – and what places them in the context of unresolved diseases such as multiple sclerosis.
The enemy in the interior
About 8% of our DNA comes from viruses. In particular, retroviruses, not because they are old, but because they reverse the normal process of reading the DNA to be written in the genome of their host.
Retroviruses are old, however: they began to merge with our oldest primordial ancestors, millions of years ago. Over the millennia, most of their remains in our DNA – called human endogenous retroviruses or HERVs – have been silenced by mutations. Others, who had evolved to protect themselves from rival viruses, formed the prototypical immune system and still protect us from infection.
However, HERV may also be the missing causal link in the major "unresolved" neurological diseases.
"HERVs have been implicated in the onset and progression of multiple sclerosis [MS], amyotrophic lateral sclerosis [ALS] and schizophrenia [SCZ]Patrick Kuery, seasoned author, can be reactivated by environmental factors such as inflammation, mutations, drugs or infection with other viruses, so could be a mechanism for establishing a link established epidemiological approach with these disorders. "
Role in MS
Until now, the strongest evidence links HERVs to MS.
"MS is caused by direct autoimmune attacks of myelin – the fat envelope of nerve cells – of the brain and spinal cord," Kuery explains. "But we still do not understand how these attacks are triggered."
Various studies suggest that reactivation of HERV could be such a trigger.
"Retroviruses were badociated with MS for the first time in 1989, but it was only decades later that it was actually HERV.
"Thereafter, it has been shown that RNA levels and HERV proteins – the" reads "of reactivated HERV DNA – are increased in the cerebral and medullary fluid [CSF] affected people, as well as in their post-mortem brain tissue.
"By linking this reactivation of HERV to autoimmune attacks in MS, it has been found that HERV proteins can trigger an immune response against myelin, triggering a disease similar to MS in murine models."
Mechanically, HERV proteins could trigger autoimmunity by "molecular imitation".
"In addition to the direct effects of HERV on myelinating cells, several groups report structural similarities between HERV and the myelin oligodendrocyte glycoprotein – a molecule displayed on the surface of myelin.This similarity could induce the immune system by destroying myelin. when she rides an attack on the HERV. "
Experimental evidence in humans
Similar experiments have linked HERVs to the CIDP, a peripheral demyelinating disease, as well as to more distinct processes, such as the progressive loss of motor neurons in ALS (Lou Gehrig's disease).
In schizophrenia, a complex neurodevelopmental disorder, the link with HERV is more circumstantial.
"HERV proteins have been reported to increase the expression of schizophrenia-related genes in cultured human brain cells," Kuery reports. "However, studies on people with schizophrenia show inconsistent changes in the expression of HERV in blood, CSF, and post-mortem brain tissue compared to healthy controls."
The question of whether HERVs contribute to these unexplained neurological conditions and others needs to be examined further. An important step will be to test the effects of HERV neutralizing antibodies in humans.
"It should be noted that a Phase 2b clinical trial using the HERV protein-neutralizing antibody, Temelimab, was conducted and we are waiting to see whether the treatment has shown beneficial effects on remyelination or a attenuated neurodegeneration, "Kuery concludes.
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