Longitudinal analysis reveals high prevalence of Epstein-Barr virus associated with multiple sclerosis
Продольный анализ выявляет высокую распространенность вируса Эпштейна—Барр, связанного с рассеянным склерозом
2022-01-14
SCID: 54.1/f3cebeny
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Epstein-Barr virus (EBV)longitudinal cohort studymilitary cohort (US active duty)multiple sclerosis (MS)neurofilament light chain (NfL) biomarker
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Abstract (AI)
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system of unknown etiology. We tested the hypothesis that MS is caused by Epstein-Barr virus (EBV) in a cohort comprising more than 10 million young adults on active duty in the US military, 955 of whom were diagnosed with MS during their period of service. Risk of MS increased 32-fold after infection with EBV but was not increased after infection with other viruses, including the similarly transmitted cytomegalovirus. Serum levels of neurofilament light chain, a biomarker of neuroaxonal degeneration, increased only after EBV seroconversion. These findings cannot be explained by any known risk factor for MS and suggest EBV as the leading cause of MS.
Key Findings
1
In a cohort of over 10 million US military personnel with 955 MS cases, MS risk increased 32-fold after Epstein-Barr virus (EBV) infection.
2
Infection with other viruses, including cytomegalovirus, was not associated with increased MS risk.
3
Serum neurofilament light chain levels rose only after EBV seroconversion, indicating neuroaxonal degeneration follows EBV infection.
4
The observed associations are not explained by any known MS risk factor, supporting EBV as the leading cause of MS.
Research Object
Association between Epstein-Barr virus (EBV) infection and multiple sclerosis incidence in a cohort of US military personnel
Research Subject
Risk increase of multiple sclerosis following EBV infection, including a 32-fold elevated MS risk after EBV seroconversion and associated rise in serum neurofilament light chain as a marker of neuroaxonal degeneration
Publication Details
Publication Date
2022-01-14
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