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An Epstein Barr virus infection is so common that about 95% of us have had it at some point in life, usually childhood. Sometimes it leads to mononucleosis. New research strengthens the case that the Epstein Barr virus (EBV) also plays a part in the development of multiple sclerosis (MS).

The study found that getting an EBV infection (mononucleosis) in early adulthood acts as a trigger for later development of multiple sclerosis - about 10 years later. MS usually develops between the ages of 20 to 40 in adulthood. The results are so compelling because the Harvard Univ. researchers looked at data from 10 million young adults on active duty in the US military. They found that risk of MS increased 32-fold after infection with EBV, but not other viruses.

Multiple sclerosis is a neurological disease in which the immune system attacks the brain and spinal cord, stripping away protective insulation (myelin) around the nerve cells. The Epstein Barr virus is a herpes virus that attacks a type of immune cell called B cells. After the initial EBV infection the virus remains dormant in a person's cells for the rest of the person's life. A number of studies have found EBV-infected B cells in the brains and demyelinated lesions of MS patients.

The hope now is to develop an EBV vaccine or stop the virus with antiviral drugs targeting EBV, and that this could ultimately prevent or cure MS. Keep in mind that EBV is considered a multifactorial disease by many, with several factors increasing the risk - such as having certain genes, not getting enough vitamin D, and also an Epstein Barr virus infection

From Science Daily: Epstein-Barr virus may be leading cause of multiple sclerosis

Multiple sclerosis (MS), a progressive disease that affects 2.8 million people worldwide and for which there is no definitive cure, is likely caused by infection with the Epstein-Barr virus (EBV), according to a study led by Harvard T.H. Chan School of Public Health researchers.  ...continue reading "Epstein Barr Virus May Be A Trigger For Developing Multiple Sclerosis"

Maybe bacteria are involved in Multiple sclerosis (MS). From Scientific American:

Could Multiple Sclerosis Begin in the Gut?

MS researchers are focusing on the content of the gut’s microbiome as a possible contributor to the body’s autoimmune attack on its nervous system.

Multiple sclerosis (MS) is an electrical disorder, or rather one of impaired myelin, a fatty, insulating substance that better allows electric current to bolt down our neurons and release the neurotransmitters that help run our bodies and brains. Researchers have speculated for some time that the myelin degradation seen in MS is due, at least in part, to autoimmune activity against the nervous system. Recent work presented at the MS Boston 2014 Meeting suggests that this aberrant immune response begins in the gut.

Eighty percent of the human immune system resides in the gastrointestinal tract. Alongside it are the trillions of symbiotic bacteria, fungi and other single-celled organisms that make up our guts’ microbiomes. Normally everyone wins: The microorganisms benefit from a home and a steady food supply; we enjoy the essential assistance they provide in various metabolic and digestive functions. Our microbiomes also help calibrate our immune systems, so our bodies recognize which co-inhabitants should be there and which should not. Yet mounting evidence suggests that when our resident biota are out of balance, they contribute to numerous diseases, including diabetes, rheumatoid arthritis, autism and, it appears, MS by inciting rogue immune activity that can spread throughout the body and brain.

One study presented at the conference, out of Brigham and Women’s Hospital (BWH), reported a single-celled organism called methanobrevibacteriaceae that activates the immune system is enriched in the gastrointestinal tracts of MS patients whereas bacteria that suppress immune activity are depleted. Other work, which resulted from a collaboration among 10 academic researcher centers across the U.S. and Canada, reported significantly altered gut flora in pediatric MS patients while a group of Japanese researchers found that yeast consumption reduced the chances of mice developing an MS-like disease by altering gut flora.

Sushrut Jangi, a staff physician at Beth Israel Deaconess Medical Center in Boston who co-authored the BWH study, thinks that regional dietary influences might even be at play. “The biomes of people living in different areas and who consume Western versus non-Western diets are demonstratively different,” he says. “People who emigrate from non-Western countries, including India, where MS rates are low, consequently develop a high risk of disease in the U.S. One idea to explain this is that the biome may shift from an Indian biome to an American biome,” although there is not yet data to support this theory.

The microbiome theory is gaining so much steam in academia that a coalition of four U.S. research centers called the MS Microbiome Consortium recently formed to investigate the role of gut microorganisms in the disease. The group presented data in Boston showing significantly different gastrointestinal bacterial populations in patients treated with the MS drug glatiramer acetate compared with untreated subjects. How exactly the drug suppresses MS activity is unknown but the findings suggest that perhaps it works in part by altering gut flora and, as a result, suppressing abnormal immune activity. “But important questions remain, such as how MS medications affect the microbiome, how an individual’s microbiome may affect treatment responses, whether particular bacterial species are associated with more severe disease and ultimately whether we can manipulate the microbiome to benefit our patients.”

Katz Sand says that dietary and probiotic approaches to treating MS are worth pursuing, as is a less palatable approach: fecal transplantation.Yet answers in science and medicine are rarely simple, she added, pointing out that in all likelihood MS arises from a complicated confluence of genetic and environmental influences that might ultimately trigger autoimmune activity. Beyond just our gut flora well over 100 genetic variants —many related to immune function—are now known to contribute to the disease as are external factors including vitamin D deficiency  (MS is more common at higher latitudes), smoking and increased salt intake.