Multiple sclerosis risk was found to increase 32-fold after Epstein-Barr virus infection.
The longitudinal analysis of data from over 10 million young adults, by Alberto Ascherio and Harvard T.H. Chan School of Public Health (MA, USA) researchers, has uncovered evidence that supports the long-held hypothesis that Epstein-Barr virus (EBV) infection causes multiple sclerosis (MS). The results identify a new avenue of potential treatment for the currently incurable MS.
“The hypothesis that EBV causes MS has been investigated by our group and others for several years, but this is the first study providing compelling evidence of causality,” commented senior author Ascherio. “This is a big step because it suggests that most MS cases could be prevented by stopping EBV infection, and that targeting EBV could lead to the discovery of a cure for MS.”
In MS, the neurodegenerative demyelination of the central nervous system is caused by immune-mediated chronic inflammation. It is thought that persistent viral infection may be a key contributor to initiating and sustaining long-term chronic inflammation. The herpesvirus EBV is a common viral infection that can form a lifelong dormant infection, which can become reactivated over the life of the host, making EBV a suspect of MS causality.
To investigate this, Ascherio’s team analyzed blood sample data collected between 1993 and 2013 from over 10 million people actively serving in the US military, of which 955 people were diagnosed with MS.
Several research papers have recently been published all providing valuable new insight into the roles and functions of key proteins and pathways involved in amyotrophic lateral sclerosis (ALS).
The team focused on the blood levels of neurofilament light chain, a neuroaxonal degeneration biomarker, in people who did not have EBV infection at the beginning of their service. From this, they observed that neurofilament light chain levels increased only after EBV seroconversion, suggesting that EBV infection occurs before both the onset of MS symptoms and the neurodegeneration inherent in MS.
To confirm that solely EBV was behind the exhibited causal relationship, antibodies for the herpesvirus cytomegalovirus were examined in a subset of individuals finding no such relationship. In addition, an antivirome search ruled out that any interaction from another viral infection also contributed to MS.
“Currently there is no way to effectively prevent or treat EBV infection, but an EBV [mRNA] vaccine or targeting the virus with EBV-specific antiviral drugs could ultimately prevent or cure MS,” explained Ascherio.
However, even with this clear indication that EBV is key in the development of MS, infection alone is insufficient to diagnose MS. Other factors that may play a role in MS development include genetic predisposition and environmental factors, such as smoking and vitamin D deficiency.
Commenting on Ascherio’s study, Daniel Davis (University of Manchester, UK) added: “Crucially, we do not know why only a small fraction of people infected with this virus develop a problem. There must be other factors involved, including the inheritance of certain genes.”
“It is now clear that there is variation in EBV in different geographic and ethnic groups, particularly in some of the proteins which are prime candidates for the cross-reacting epitopes,” commented expert Paul Farrell (Imperial College London, UK). “Future work should therefore include sequencing the EBV in MS cases compared to controls to determine whether this might allow explanation of more of the individual cases.”
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