Neurology · 5 h ago
EBV-associated B cell changes precede multiple sclerosis relapse
Longitudinal blood multi-omics profiling in people with multiple sclerosis identified EBV-associated immune changes before relapse, according to a Nature Reviews Neurology report on research in Nature Medicine. The available preview does not report sample size or effect estimates, and the findings do not establish causality.
- EBV-responsive host genes were enriched in the pre-relapse immune signature.
- Pre-relapse B cells showed elevated EBV LMP1 transcripts.
- B cell transcriptional modules overlapped with MS genetic risk loci.
- Clinical predictive value and causality remain unestablished.
Longitudinal multi-omics profiling of blood collected from people with multiple sclerosis during remission, before relapse and during acute relapse identified a pre-relapse immune signature enriched for Epstein–Barr virus (EBV)-responsive host genes. According to a Nature Reviews Neurology preview summarizing research by King and colleagues in Nature Medicine, pre-relapse B cells showed elevated EBV LMP1 transcripts, alongside expansion of CD11c+ atypical B cell populations displaying the EBV surface protein gp350. Pre-relapse B cell transcriptional modules also overlapped with MS genetic risk loci, suggesting a connection between inherited susceptibility and EBV-responsive regulatory programmes. These observations support a proposed model in which episodic EBV reactivation in primed B cells could trigger relapse, but do not establish a causal role. The preview provides no sample size, effect estimates or predictive performance data, limiting assessment of clinical relevance.
Is this summary clinically accurate?
Help fellow clinicians: your rating sends inaccurate summaries straight to our editors.
Sign in to rate this summary →Source
Nature Reviews Neurology: EBV reactivation precedes multiple sclerosis relapse ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.
