Reactivation of ancient viruses incorporated into the human genome in the course of evolution may be involved in the acute inflammatory response that is characteristic of multiple sclerosis (MS), a study says.
The findings of the study, “Expression of endogenous retroviruses reflects increased usage of atypical enhancers in T cells,” were published in The EMBO Journal.
Human endogenous retroviruses, or HERVs, are a type of virus derived from ancient viruses that had been incorporated into the human genome during the process of evolution.
HERVs normally are silenced by heterochromatin, a tightly packed region of the DNA sequence in which genes are less accessible. However, in certain autoimmune diseases, including MS, these inhibitory mechanisms fail, and HERVs — termed fossil viruses — are abnormally active.
Although these viruses do not trigger an infection by themselves, they may change the way cells in the body respond to infection and inflammation once they are active.
A team of researchers from the Institut Pasteur in France found that these viral DNA sequences contain specific instructions that, once active, can control the activity of nearby genes involved in the body’s defense.
They found that HERV sequences were abnormally active in stem cells — undifferentiated cells that are able to give rise to all cell types in the body — but not in differentiated brain cells.
Researchers also found that these viral sequences were abnormally active, although to a lesser extent, in immune T-cells — the killers of the immune system — that had been driven to overactivation after being exposed to a pesticide called dieldrin. This means that stress may lead to the reactivation of HERV sequences in cells that normally would not express them.
Finally, after examining T-cells isolated from MS patients, the team discovered these ancient viral sequences were abnormally active in the vicinity of genes involved in the body’s immune response. This supports the hypothesis that HERVs reactivation may play a role in inflammation associated with MS by triggering the activity of several pro-inflammatory genes.
“Our study shows that reactivation of ancient viruses does not correspond to an infectious phenomenon, but to a defense response of the body when faced with an acute inflammatory phenomenon,” leading to chronic excessive inflammation, Christian Muchardt, PhD, head of the epigenetic regulation unit at the Institut Pasteur, said in a press release.
“The discovery of this mechanism … may one day pave the way for management of MS using small molecules that inhibit chromatin modification enzymes,” Muchardt said.
However interesting this article may be we are still at, “someday and may”. When is this madness going to end? So many are wrecked by MS and all we can do is shoot them full of meds and drain their bank accounts and watch the suffering.
I agree instead of test like these lets find a cure. The modern meds have such absurd side effects. They still have no idea what causes it, so close to a cure right yeah right.
I can’t stand to watch my wife on her bad days. She’s so beautiful and has been through so much. She doesn’t deserve this stupid disease.
I really think more research should be carried out on MS patients birth dates? With only one exception, everyone I know with MS myself included was born between March and May.
I was born in August have had ms now for 7 years been stuck in the very first attack…
Born in January and have had MS fot 8 years.
see http://www.geneuro.com and https://multiplesclerosisnewstoday.com/2019/03/18/rrms-see-benefits-temelimab-phase-2-extension-study/
Geneuro is precisely developing Temelimab, based on this hypothesis of retrovirus HErv
To Christian Muchardt et al:
I began my review of literature after diagnosis in 1967; I am now 74, symptom free and fully mobile.
Allow me to share with you some of the numerous references to MS as long term virus mutation of red measles virus
from my books, Black Patent Shoes Dancing With MS © 1989 and Eva Marsh is STILL Dancing© 2017
p246
After reading the literature for half a century, I am satisfied with evidence that multiple sclerosis is the long term genetic mutation of the red measles virus. We often hear that MS is a disease acquired in childhood and research in childhood diseases compares measles and MS to chicken pox and shingles. If you have shingles, you definitely had chicken pox; if you have chicken pox, under stress, you might develop shingles. So too, if you are diagnosed with MS, there is a significant chance you have had red measles. Studies6 7 8 have documented the high measles titre in the blood of MS patients. I have vivid memories of having measles just before my 8th birthday; the light was so painful that my mother climbed on up on the window sill to nail a blanket over the window. After the spots were gone, I asked Mom when she was going to bake my cake. She said my birthday was over and I could have a cake next year. I never forgot.
p290
4. Alvord Ellsworth C Jr (1989) EDITORIAL Two hopeful aspects of multiple sclerosis: resolution of lesions and prevention of disease. Lab Invest 61(5):477-479. … measles immunization should reduce incidence of MS in persons born since 1970 – later the infection, the greater the susceptibility to MS evoked by other infections decades later – remain susceptible to MS no matter where they move.
5. Millar JHD(1971) Multiple Sclerosis: A Disease Acquired in Childhood.Charles C Thomas. Springfield, Illinois, USA. p45 – measles.
6. Atkins GJ, Mooney DA, Fahy DA, Ng SH,&Sheahan BJ (1991) Multiplication of rubella and measles viruses in primary rat neural cell cultures: relevance to a postulated triggering mechanism for multiuple sclerosis. Neuropath & Appl Neurobiol 17:299-308. From epidemiological studies the event which triggers MS occurs many years before symptoms become manifest – virus may only trigger the disease, and disappear before biopsy and autopsy specimens are available – autoimmune demyelination may be induced by presentation of myelin antigens to T-helper lymphocytes through the generation of myelin debris…sensitization to myelin antigens may occur by molecular mimicry, or by releasing antigens following damage to oligodendrocytes.
7. Jersild Casper, Ammitzboll T, Clausen J, Fog T (1973) Assn HL-AAntigens & measles antibody in MS Lancet Jan 20, 1973.
8. Offner H, T Ammizboll, J Clausen, T Fog, K Hyllested (1974) Immune response of lymphocytes from patients with ms and phytohemagglutinin, basic protein of myelin and measles antigens. Acta neurol Scand 50:373-381. … measles … high antibody titres were observed.
p 101 RE: INFLAMMATION –
… investigations suggest that the inflammatory response is the start of clinical improvement. Inflammation allows the migration of cells which promote remyelination, and removal of fragments of damaged myelin (Hafler and Weiner, 1987, Hammann et al, 1985). ALSO **Bunge et al 1961 has electron microscope slides that prove this as well as Feigin & Popoff 1967.
Merci
Yours very truly
Eva Marsh BSc MEng
Hamilton Ontario CANADA
https://evamarsh.net