Scientists link Epstein-Barr virus to multiple sclerosis mechanisms

Researchers at UC San Francisco have uncovered evidence showing how the Epstein-Barr virus may trigger immune responses in multiple sclerosis patients. The study reveals elevated levels of virus-targeting immune cells in the nervous systems of those with the disease. These findings, published in Nature Immunology, suggest potential new treatment avenues by targeting the virus.

Multiple sclerosis (MS) is a chronic autoimmune disorder affecting nearly one million people in the United States, where the immune system attacks the myelin sheath protecting nerve fibers in the brain and spinal cord, leading to progressive neurological damage.

A new study from UC San Francisco provides fresh insights into the role of the Epstein-Barr virus (EBV) in MS. EBV, which infects about 95% of adults and is present in nearly all individuals who develop MS, has long been associated with the disease. The research, published on February 5 in Nature Immunology, focused on CD8+ "killer" T cells, which are less studied than CD4+ T cells but play a direct role in destroying infected cells.

The team analyzed blood and cerebrospinal fluid (CSF) samples from 13 people with MS or early signs of the disease, compared to five without MS. In healthy individuals, CD8+ T cells that recognize specific proteins appeared in similar concentrations in blood and CSF. However, in MS patients, these EBV-responsive cells were 10 to 100 times more abundant in the CSF than in the blood, indicating heightened immune activity within the central nervous system.

EBV was detected in the CSF of most participants, with some viral genes active. Notably, one EBV gene was active only in those with MS, suggesting it may drive the aberrant immune response.

"Looking at these understudied CD8+ T cells connects a lot of different dots and gives us a new window on how EBV is likely contributing to this disease," said senior author Joe Sabatino, MD, PhD, an assistant professor of Neurology at UCSF and member of the UCSF Weill Institute for Neurosciences.

The virus has also been linked to other autoimmune conditions like lupus, rheumatoid arthritis, and long COVID. Researchers are exploring treatments that target EBV directly.

"The big hope here is that if we can interfere with EBV, we can have a big effect, not just on MS but on other disorders, and improve the quality of life for many, many people," Sabatino added.

The study was funded by the National Institutes of Health and involved numerous UCSF collaborators.

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Realistic depiction of a long COVID patient experiencing fatigue and breathing difficulties, overlaid with highlighted CD14+ monocytes (LC-Mo state) and inflammatory markers from recent immune study.
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Study links a distinct CD14+ monocyte state to fatigue and breathing symptoms in long COVID

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Researchers analyzing immune cells from people with long COVID have identified a distinct molecular state in CD14+ monocytes—labeled “LC-Mo”—that was more prevalent among patients whose initial COVID-19 illness was mild to moderate and that tracked with reported fatigue and respiratory symptoms, along with higher levels of inflammatory signaling molecules in blood plasma.

A large-scale study reveals that about one in ten people carry genetic variants making them more vulnerable to severe effects from the Epstein-Barr virus, which infects over 90 percent of the population. These variants are linked to higher viral persistence and increased risks of autoimmune diseases like multiple sclerosis and lupus. The findings, based on over 735,000 genomes, suggest pathways for targeted treatments and vaccines.

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Researchers at Fred Hutch Cancer Center have created human-like monoclonal antibodies that prevent Epstein-Barr virus (EBV) from infecting immune cells. Using mice engineered with human antibody genes, the team identified antibodies targeting viral proteins gp350 and gp42, with one fully blocking infection in lab models. The findings, published in Cell Reports Medicine, could lead to therapies for transplant patients at risk of EBV-related complications.

Researchers at Memorial Sloan Kettering Cancer Center report that colorectal tumors can contain two major subtypes of regulatory T cells with opposing effects—one associated with restraining tumor growth and another linked to suppressing anti-tumor immunity. The work, published in Immunity, helps explain why higher overall levels of these immune cells have been tied to better outcomes in colorectal cancer and suggests a potential strategy for more selective Treg-targeted therapies.

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Scientists at the University of California, Riverside have found that Toxoplasma gondii, a parasite infecting up to one-third of the world's population, is more active in the brain than previously thought. Their study shows cysts contain multiple subtypes of the parasite, some primed for reactivation and disease. This discovery could guide new treatments for a lifelong infection that resists current drugs.

Evidence indicates that reactivations of the varicella-zoster virus, which causes shingles, could speed up aging and increase the risk of dementia. Scientists are exploring whether vaccines and antiviral treatments might offer protection for the brain. The findings come amid concerns about cognitive decline linked to the virus.

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Researchers at UCLA have identified senescent immune cells, dubbed 'zombie' cells, that accumulate in aging livers and contribute to fatty liver disease. By eliminating these cells in mice, the team reversed liver damage and reduced body weight, even on an unhealthy diet. The findings, published in Nature Aging, suggest similar mechanisms may drive human liver conditions.

 

 

 

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