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Evidence is mounting that a garden-variety virus that sometimes causes mono in teens is the underlying cause of multiple sclerosis, a rare neurological disease in which the immune system attacks the brain and spinal cord, destroying nerve cells. The surrounding strips away the protective insulation, called myelin.

It is still unclear exactly how the virus—Epstein-Barr virus (EBV)—triggers MS and why MS develops in a small proportion of people. About 95 percent of adults have been infected with EBV, which most often occurs in childhood. Meanwhile, MS often develops between the ages of 20 and 40 and is estimated to affect about a million people in America. Nevertheless, years of evidence have consistently pointed to links between childhood viruses and chronic demyelinating disease occurring later in life.


With A study published today in Science, the link is stronger than ever, and outside experts say the new findings offer further “compelling” evidence that EBV isn’t just linked to MS; It is a necessary trigger for the disease. Among other things, the study found that people after EBV infection in early adulthood had a 32-fold increased risk of developing MS.

“It’s a good paper,” said Dr., a preventive neurology professor and MS specialist at Queen Mary University of London. Ruth Dobson told Ars in an interview. “The evidence just adds and adds and adds… While we don’t understand biologically how EBV drives MS and we tend to think of causality theories, we actually have the rest of the building blocks. ,” said Dobson, who was not involved in the new Science study. “This is another piece of evidence that really strengthens the theory” that EBV triggers MS.

new findings

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For the study, researchers led by Harvard neuroepidemiologist Dr. Kjetil Bjrnvik mined an extraordinarily rich repository of blood serum samples taken from a group of more than 10 million active-duty military personnel between 1993 and 2013. Samples were taken from relatively healthy, fit. , and infection, especially young military personnel during standard screening for HIV.

In the cohort, there were 801 members who developed MS and had banked up to three serum samples before their diagnosis. This gave researchers the unique opportunity to go back in time and examine serum samples from MS patients before they developed the disease. Researchers could also compare samples from 801 MS patients with samples from 1,566 cohort members who did not develop MS and could serve as controls.

Of the 801 people who developed MS, all except one had antibodies indicating an EBV infection by the time of their MS diagnosis. And most of those EBV infections happened earlier in their lives. At the beginning of the 20-year period, only 35 of 801 MS patients started out as negative for EBV. By the end of the period, 34 of those 35 developed anti-EBV antibodies—aka seroconverted—before their diagnosis.

Bjrnvik and colleagues compared 35 initial EBV-negative personnel with 107 control-group members who initially tested negative. They found that the rate of seroconversion in 35 who would go on to develop MS was significantly higher than the rate in the control group—97 percent of 35 seroconverted before diagnosis while only 57 percent of the control group seroconverted during the 20-year period. . From that data, the researchers calculated that people who were seroconverted had a 32-fold increased risk of developing MS.

It is not clear why one MS patient did not appear to seroconvert during the study. The authors speculate that, given the lag in sampling, it is possible that the individual may have seroconverted between the last sample and diagnosis. It is also possible that the person was misdiagnosed with MS or was infected with EBV but did not seroconvert for some reason. It’s also possible that the person had a rare type of MS that was triggered by something other than EBV. Regardless, the authors argued that an outlier did not undermine the strong association between MS and EBV.

But EBV was not the only virus the researchers investigated. In fact, they examined serum samples for antibodies targeting more than 200 viruses. Screening indicated that the risk of MS did not increase after infection with a virus other than EBV. Furthermore, when the researchers compared the overall antiviral antibody responses in MS patients to those in controls, they found that the overall antibody responses were similar. This suggests that there was no underlying immune dysregulation that drives the development of MS following EBV infection.

previous connections

Overall, the study adds to the plethora of other data linking EBV to MS. Similar to the new study, other research has found a two to threefold increase in the risk of developing MS after a bout of infectious mononucleosis (“mono”) caused by EBV. The virus specifically attacks a type of immune cell called B cells, and after the initial infection the virus remains dormant in those cells for the rest of a person’s life. Several studies have found demyelinated lesions of EBV-infected B cells in the brain and of MS patients. MS patients sometimes have elevated levels of specific anti-EBV antibodies that target proteins called EBV nuclear antigens. And, currently, one of the most effective treatments for MS is antibody therapy that targets circulating memory B cells to ward off dormant EBV.

“There’s a lot of pieces out there that suggest EBV plays a role in MS,” Bjrnvik told Ars. “We think that with this study, we provide compelling evidence that there is indeed a causal relationship between EBV and MS … we think this is a definite big step forward and the most compelling evidence to date.” “

Dobson and other experts agreed. In an email to Ars, Dr. Helen Tremlett, a neuroepidemiologist and MS specialist at the University of British Columbia, called it “an important study” that “provides reliable evidence of a relationship between EBV risk and MS risk.” Tremlett was not involved in the new study, but said he had collaborated with some co-authors in the past.

In Simultaneous Perspective Articles In Science, Stanford MS specialist William Robinson and neurologist Lawrence Steinman wrote that the findings “provide compelling data that implicate EBV as a trigger for the development of MS.”

essential piece of jigsaw

Robinson and Steinman discuss some of the hypotheses about how EBV might trigger MS. One hypothesis is that components of EBV—particularly EBV nuclear antigen protein—may mimic parts of the myelin protein and other proteins in the central nervous system. This can prompt the immune system to make cross-reactive antibodies that attack the virus and the body, causing damage over time. Other hypotheses include EBV-infected B cells that induce the formation of pathogenic immune cells or activate other immune cells that eventually cause damage.

While new data suggests that EBV may be necessary for MS to develop—that is, you cannot develop MS without having previously been infected with EBV—it is clearly not the only factor. This Sufficient, as scientists like to say. Over the years researchers have identified other factors that are associated with and may contribute to MS development, such as vitamin D deficiency, smoking, obesity and UVB exposure. How any of these factors can lead to MS with EBV infection is still under active investigation.

But, as Dobson told Ars, finding an early trigger opens up new possibilities for treatments, such as future EBV vaccines and EBV antivirals. “It’s a disease we can’t treat and even with our best treatments, people in the progressive stage still get worse,” Dobson said. “So, to be able to prevent or have a window into how we might be able to get people to prevent or prevent this disease in the first place, it would be amazing.”

If you talk to MS patients, Dobson says, all they want to do is stop the disease from affecting their children. If we can target “an essential piece of that jigsaw that everyone develops MS” and therefore prevent an irreversible neurological disability… “That’s really exciting,” she said.

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