B-Cells Infected by Epstein-Barr Virus Linked to MS Relapse Risk in Study

B-Cells Infected by Epstein-Barr Virus Linked to MS Relapse Risk in Study
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Immune B-cells that proliferate unchecked when infected by the Epstein-Barr virus (EBV) appear to increase the risk of relapses in patients with multiple sclerosis (MS), a mouse study suggests.

The study, “Epstein Barr virus‐immortalized B lymphocytes exacerbate experimental autoimmune encephalomyelitis in xenograft mice,” was published in the Journal of Medical Virology.

EBV, also known as human herpesvirus 4, is one of the most common of human viruses. It can cause infectious mononucleosis, also called mono, and is a known risk factor for MS.

“However, the exact mechanism by which EBV, specifically in infectious mononucleosis, increases the risk for MS remains unknown,” the researchers wrote.

Previous studies have shown that EBV, upon infecting antibody-producing immune B-cells, can “immortalize” these cells. That is, EBV allows them to grow continuously — proliferate indefinitely — in a lab dish. The virus has also been found to promote the expansion of these cells in people with mono, a phenomenon that is known to occur in MS patients.

To explore the link between MS and mono in more detail, researchers at the University of Nebraska used mice with experimental autoimmune encephalomyelitis (EAE) — an established model of MS — and injected them with immortalized EBV-infected B-cells obtained from a patient with secondary progressive MS.

Animals were then monitored for signs of EAE, such as partial or complete limb paralysis. The mice never showed any signs of the disease after being injected with these cells, indicating that EBV-infected immune cells by themselves do not trigger EAE.

Switching gears, the researchers decided to test if the presence of EBV-infected B-cells could lead to a relapse in animals with evident symptoms of EAE.

Investigators injected mice with the MOG peptide — a portion of a protein normally found on the surface of the myelin sheath (the fatty layer that protects nerve fibers). This peptide triggers the production of autoantibodies against myelin, and the onset of EAE.

Once the animals had entered in a period of remission and no longer showed signs of EAE, they were then injected with EBV-infected immune cells. This time around, patient cells containing the virus re-triggered EAE symptoms, leading to a relapse. Once all EBV-infected B-cells disappeared from circulation, so did the animals’ symptoms.

The cycle of symptom remission followed by relapse that was seen in the animals resembled that of patients with relapsing remitting MS. According to the research team, these findings suggest the excessive number of immune B-cells circulating in the blood of MS patients may be at least partly responsible for relapses.

“Nobody knows the exact mechanisms behind these relapses,” Luwen Zhang, a professor of biological sciences, member of the Nebraska Center for Virology, and senior author of the study, said in a news story.

“This over-proliferation of the B-cells seems to be a factor. It’s not a causative factor, but it promotes multiple sclerosis formation in our mouse model,” Zhang said.

Based on the timing at which EBV-infected cells were injected into the animals, the researchers also found they could estimate both when mice would start showing signs of EAE, as well as symptom severity.

This highly predictable model system, they suggested, could be valuable for testing drug candidates targeting the frequency of MS relapses.

“That’s what I’m thinking is the true importance of this work — that it gives us a way to test different drugs … [and] creates more potential for treatment,” Zhang said.

Joana holds a BSc in Biology, a MSc in Evolutionary and Developmental Biology and a PhD in Biomedical Sciences from Universidade de Lisboa, Portugal. Her work has been focused on the impact of non-canonical Wnt signaling in the collective behavior of endothelial cells — cells that made up the lining of blood vessels — found in the umbilical cord of newborns.
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Inês holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she specialized in blood vessel biology, blood stem cells, and cancer. Before that, she studied Cell and Molecular Biology at Universidade Nova de Lisboa and worked as a research fellow at Faculdade de Ciências e Tecnologias and Instituto Gulbenkian de Ciência. Inês currently works as a Managing Science Editor, striving to deliver the latest scientific advances to patient communities in a clear and accurate manner.
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Joana holds a BSc in Biology, a MSc in Evolutionary and Developmental Biology and a PhD in Biomedical Sciences from Universidade de Lisboa, Portugal. Her work has been focused on the impact of non-canonical Wnt signaling in the collective behavior of endothelial cells — cells that made up the lining of blood vessels — found in the umbilical cord of newborns.
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