
Exploring the Link between EBV and MS: Micah Luftig, PhD
The Allen Geller distinguished professor of immunology at Duke University School of Medicine discusses the connection between Epstein Barr Virus and Multiple Sclerosis, citing decades of research that position EBV as a leading environmental risk factor and a potential therapeutic target in MS. [WATCH TIME: 4 minutes]
WATCH TIME: 4 minutes
“The epidemiological relationship had an odds ratio of 32, which is as high as the odds ratio for smoking and lung cancer.”
Epstein-Barr virus (EBV), or human herpesvirus 4, is a double-stranded DNA virus and one of the most common human pathogens worldwide. A member of the gammaherpesvirus subfamily family, EBV infects over 95% of the global population and is transmitted primarily through saliva and other bodily fluids. Primary infection is often asymptomatic, and by early adulthood, nearly 90% of adolescents in the United States have been affected.1
Over the past two decades, Epstein–Barr virus (EBV) has been increasingly implicated in the development of autoimmune diseases, including multiple sclerosis (MS). EBV establishes lifelong latency in B lymphocytes and expresses viral proteins and non-coding RNAs that alter immune signaling, promote chronic immune activation, and enable evasion of host immune surveillance. Dysregulation of EBV-infected B cells has been proposed as a key mechanism linking EBV to autoimmune pathology, including MS, as highlighted in comprehensive reviews of EBV biology and disease. ¹ Research surrounding EBV has increasingly shifted to include the virus as a biomarker of adults developing MS.
One of the researchers at the forefront of the investigation is Micah Luftig, PhD, a professor in immunology at Duke University School of Medicine, in Durham, North Carolina. Luftig leads the Luftig Lab, a research program that focuses on uncovering the molecular mechanisms that enable EBV to establish latency, switch to the lytic cycle, and promote disease. At the
In the interview, Luftig outlined the growing body of evidence linking EBV to MS, beginning with more than a century of research suggesting that infection may play a role in disease development. He explained that over the past 30 years, and more recently in the last decade, studies have increasingly shown that immune responses to EBV are strongly associated with MS, including abnormal antibody and T-cell responses to specific EBV proteins. He noted that these immune reactions may cross-react with myelin autoantigens through a process known as molecular mimicry, potentially driving autoimmune activity. He also highlighted that the clinical success of B-cell–depleting therapies, which target the cellular reservoir where EBV persists, further supports a biological connection, although the precise mechanism remains unclear.
REFERENCES
1. Damania B, Kenney S, Raab-Traub N. Epstein-Barr virus: Biology and clinical disease. Cell. 2022;185(20):3652-3670. doi:10.1016/j.cell.2022.08.026
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