Most scientific studies are false, but this one rings true to me. And it seems to have quite solid direct causal evidence.
See my previous discussion about EBV incited by COVID in Epstein-Barr Virus (EBV) mRNA Vaccine Trial Underway.
2022-01-24. Emphasis added.
A new study found that part of the Epstein-Barr virus mimics a protein made in the brain and spinal cord, leading the immune system to mistakenly attack the body’s nerve cells.
Scientists have long suspected — but failed to prove — a link between certain viral infections and the development of multiple sclerosis, a crippling autoimmune disease that affects nearly 1 million Americans. Now, a study led by Stanford Medicine researchers has proved that the Epstein-Barr virus, a common type of herpes virus, triggers multiple sclerosis by priming the immune system to attack the body’s own nervous system.
The study, published Jan. 24 in Nature, shows that approximately 20% to 25% of patients with multiple sclerosis have antibodies in their blood that bind tightly to both a protein from the Epstein-Barr virus, called EBNA1, and a protein made in the brain and spinal cord, called the glial cell adhesion molecule, or GlialCAM.
“Part of the EBV protein mimics your own host protein — in this case, GlialCAM, found in the insulating sheath on nerves,” said William Robinson, MD, PhD, professor of immunology and rheumatology at Stanford. “This means that when the immune system attacks EBV to clear the virus, it also ends up targeting GlialCAM in the myelin.”... “This is the first time anyone has shown rather definitively that a virus is the trigger for multiple sclerosis,” Steinman said. “And these exciting findings open up some new directions for clinical trials in MS treatment.”
MS and viruses: an elusive connection
Previous research has shown that multiple sclerosis patients have increased antibodies to a variety of common viruses, including measles, mumps, varicella-zoster and Epstein-Barr virus. In fact, more than 99% of MS patients have EBV antibodies in their blood, indicating a prior infection, compared with 94% of healthy individuals. But despite this epidemiologic correlation, scientists have struggled to prove a causal connection.
“Nobody really knows what causes autoimmune diseases, and for many decades, all sorts of different viruses have been hypothesized,” Robinson said. “But when people did further mechanistic digging, everything fell apart, and it turned out that getting those other viruses didn’t actually cause MS.”
Molecular mimicry provides mechanism for development of MS
Next, the researchers tested the same antibody on a microarray containing more than 16,000 human proteins. When they discovered that the antibody also bound with high affinity to GlialCAM, they knew they’d found a specific mechanism for how EBV infection could trigger multiple sclerosis.
“EBV tricks the immune system into responding not only to the virus, but also to this critical component of the cells that make up the white matter in our brains,” Steinman said... researchers looked at a broader sample of MS patients and found elevated reactivity to the EBNA1 protein and GlialCAM in 20% to 25% of blood samples in three separate MS cohorts.
“Twenty-five percent is a conservative number,” Robinson said, noting that it doesn’t include patients who may have previously reacted to GlialCAM following EBV infection but whose immune response has evolved since the initial trigger.
In fact, a study of 801 MS cases from more than 10 million active-duty military personnel over 20 years found that EBV infection was present in all but one case at the time of MS onset. A paper describing that study, published this month in Science, found that of 35 people who were initially EBV-negative, all but one became infected with EBV before the onset of MS. In addition, this separate group of researchers identified the same EBNA1 region as a major antibody target in MS patients. Together with the discovery of EBNA1/GlialCAM cross-reactivity, this data provides compelling evidence that EBV is the trigger for the vast majority of MS cases, as Robinson and Steinman point out in a Science Perspective, also published in January.
Mouse models provide further proof
...After receiving an injection of a fragment of the EBNA1 protein, the mice exhibited more severe paralysis, more immune cells invading their central nervous system, and more damage to the protective coating on their nerve cells, compared with mice injected with a control protein fragment...
Paving the way for future MS treatments
...“If a virus is the target of the immune response that’s going an unwanted way in the MS brain, why not get rid of the virus?” Steinman said, noting that a vaccine against Epstein-Barr virus could perhaps eventually eradicate MS, in the same way polio was eradicated from the United States in the 1970s.
But this research also demonstrates why manufacturers would need to be extra careful in selecting which antigens to incorporate into an EBV vaccine. “You don’t want to choose those antigens, like EBNA1, that could cause autoimmunity,” Lanz said.
[Red flag: who has proven beyond a shadow of a doubt that COVID vaccines are not inducing autoimmunity by use of a protein that might cause similar issues?!]
In addition, an EBV vaccine wouldn’t necessarily help patients who have already developed EBNA1/GlialCAM cross-reactivity. For those patients, a better option might be to “tolerize” the immune system so it no longer responds to GlialCAM, Steinman said. “There are two promising technologies here, one involving a reverse vaccine using DNA plasmids and another using RNA technology from the same company in Germany that made the Pfizer vaccine for COVID-19.”
The discovery of how EBV triggers multiple sclerosis could also have ramifications for research into other autoimmune diseases, such as lupus and rheumatoid arthritis, which, like MS, have been significantly associated with EBV infection in epidemiologic studies.
It concerns me that having had a major EBV infection in 2020 following COVID, that I am at heightened risk for MS.