VBCN - May 2015 Volume 2, No 1 - In the Literature

A new study unveils a strong association between Epstein-Barr virus (EBV) genomic variants and multiple sclerosis, reinforcing the idea that EBV contributes to the development of multiple sclerosis (Mechelli R, et al. Neurology. 2015;84:1362-1368).

“Despite converging evidence supporting an etiologic role for EBV in MS [multiple sclerosis], we still do not know through which mechanisms the virus may contribute to disease development,” said Rosella Mechelli, PhD, Centre for Experimental Neurological Therapies, Sapienza University, Rome, Italy.

The researchers analyzed the Epstein-Barr nuclear antigen (EBNA) 2 gene, which contains the most variable region of the viral genome, in patients with multiple sclerosis. EBNA2 is considered the best candidate for this kind of study, because it is the most polymorphic among all EBV genes, interacts with host proteins, and may have functional consequences.

The frequency of the EBNA2 gene in 53 patients with multiple sclerosis was compared with that of 38 matched healthy individuals to verify whether virus genetic variants are involved in the disease. The researchers used a seminested polymerase chain reaction approach, Sanger sequencing, and, in a subgroup of controls, high-throughput sequencing by Illumina MiSeq. Patients underwent gadolinium-enhanced magnetic resonance imaging (MRI) and human leukocyte antigen (HLA) typing. The study controlled for HLA haplotype and clinical and MRI features.

The number of new variants was higher than expected. Multiple sclerosis status correlated with an excess of the EBNA2 1.2 allele (odds ratio [OR], 5.13; P = .016) and an underrepresentation of the 1.3B allele (OR, 0.23; P = .0006). Furthermore, patients with multiple sclerosis were also more likely than healthy individuals to harbor newly identified 1.2 allele-related variants, particularly at amino acid position 245.

“By investigating a region of ENBA2 that previous studies in MS cohorts did not investigate, we have detected MS-associated EBV genetic variations that are stronger than those previously reported and seem to be independent of the donors’ HLA haplotype,” the researchers wrote, concluding that a “complex interplay between both host and viral genetic variants may contribute to disease development.”

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