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Study of the possible link of 25‐hydroxyvitamin D with Epstein–Barr virus and human herpesvirus 6 in patients with multiple sclerosis

2018; Wiley; Volume: 25; Issue: 12 Linguagem: Inglês

10.1111/ene.13749

1468-1331

Silvia Pérez‐Pérez, María Inmaculada Domínguez‐Mozo, Maria Ángel García‐Martínez, Yolanda Aladro, María Luisa Martínez‐Ginés, José Manuel García‐Domínguez, Carlos López de Silanes, Ignacio Casanova, Isabel Ortega‐Madueño, Lorena López-Lozano, María José Torrejón, Rosa Arroyo-García, Roberto Álvarez‐Lafuente,

Autoimmune and Inflammatory Disorders Research

Background and purpose Although the causes of multiple sclerosis ( MS ) remain partially unknown, environmental and genetic factors are thought to play a role in its aetiopathogenesis. Hypovitaminosis D, Epstein–Barr virus ( EBV ) and human herpesvirus 6 ( HHV ‐6) infections have been described as possible MS triggers. Our aim was to analyse the possible link between 25‐hydroxyvitamin D [25( OH )D] and viruses in patients with MS . Methods We included 482 patients with MS in a 2‐year study. Serum samples were collected to analyse 25( OH )D levels and, according to sample availability, antibody titres against EBV and HHV ‐6 by enzyme‐linked immunosorbent assay. DNA was extracted from blood in order to analyse EBV and HHV ‐6 viral load by quantitative real‐time polymerase chain reaction and to genotype MS ‐related single nucleotide polymorphisms (rs3135388, rs2248359 and rs12368653) when possible. Results The 25( OH )D levels were significantly higher in the first semester of the year than in the second. Carriers of the risk allele rs2248359‐C showed lower 25( OH )D levels than non‐carriers. For EBV , viral load was significantly higher when 25( OH )D levels were low, demonstrating an inverse correlation between 25( OH )D levels and EBV load. Conclusions The 25( OH )D levels could be involved in the regulation of EBV replication/reactivation in patients with MS .