Multiple sclerosis (MS), a life-shortening, debilitating neurological condition that affects over 9,000 people in Ireland, could be slowed or stopped by blocking the brain inflammation triggered by infection with Epstein-Barr virus (EBV).
That’s according to research published yesterday in the Nature journal, which involved Dr Éanna Fennell, an Irish researcher based at the lab of Professor Christian Munz at Institute for Experimental Immunology, University of Zurich.
“MS is a terrible disease that affects millions of people worldwide, so being able to contribute to research that sheds new light on the disease and can open up new ways to treat or prevent it is hugely satisfying,” Dr Fennell said.
MS is the most common, disabling neurological disease affecting young adults in Ireland and is often diagnosed between the ages of 20 and 40.
EBV is a common virus infecting 95pc of the population. It spreads through saliva and body fluids and has been linked to mononucleosis, or glandular fever, sometimes called the “kissing disease”, and rare cases of cancer.
In MS research, scientists previously found a strong link between EBV infection and the onset of MS, but how it happened was unknown.
In this new research carried out in mice – which have a human-like immune system – Dr Fennell and his colleagues found that, after infection with EBV, a group of immune cells called B cells became active and travel to the brain.
Once inside the brain, these B cells release signals that attract another group of immune cells, called the T cells.
The B and T cells then work together to cause inflammation and damage to the mouse brain in a way similar to what is found in early stages of MS in humans.
The T cells mistake proteins found in the brain for EBV proteins
“The T cells, which are trying to kill and remove EBV-infected cells, mistake proteins found in the brain for EBV proteins,” Dr Fennell said.
“This causes the T cells to create a very inflammatory environment and subsequently try to attack these CNS [central nervous system] proteins, causing damage.”
Dr Fennell and colleagues then gave the mice Rituximab, a drug prescribed for late-stage, advanced MS, which works by removing all B cells.
“As B cells are responsible for creating antibodies against diseases, removing all B cells is not something clinicians want to do – it is usually a last-ditch attempt in late-stage MS to manage systems,” Dr Fennell said.
The drug was duly found to have removed the B cells, and, after that, there were far less actively inflamed T cells present in the brain.
“This suggests that EBV may kick-start MS by reprogramming B cells to invade the brain and spark inflammation by attracting inflammatory T cells,” Dr Fennell said.
“And that targeting these B cells early could help prevent or slow the development of MS.”
This research can lead to better treatments for MS, Dr Fennell said, that target the cause of the disease rather than using drugs to suppress the immune system, and encourage scientists to develop an EBV vaccine.
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