| Autor: |
Ovejero T; School of Medicine, Universidad Católica de Valencia San Vicente Mártir, 46001 Valencia, Spain., Sadones O; Université de Poitiers, CEDEX, 86073 Poitiers, France., Sánchez-Fito T; Escuela de Doctorado, Universidad Católica de Valencia San Vicente Mártir, 46008 Valencia, Spain., Almenar-Pérez E; Escuela de Doctorado, Universidad Católica de Valencia San Vicente Mártir, 46008 Valencia, Spain., Espejo JA; School of Biotechnology, Universidad Católica de Valencia San Vicente Mártir, 46001 Valencia, Spain., Martín-Martínez E; National Health Service, Manises Hospital, 46940 Valencia, Spain., Nathanson L; Institute for Neuro Immune Medicine, Nova Southeastern University, Ft Lauderdale, FL 33314, USA., Oltra E; School of Medicine, Universidad Católica de Valencia San Vicente Mártir, 46001 Valencia, Spain.; Centro de Investigación Traslacional San Alberto Magno, Universidad Católica de Valencia San Vicente Mártir, 46001 Valencia, Spain. |
| Abstrakt: |
Advancements in nucleic acid sequencing technology combined with an unprecedented availability of metadata have revealed that 45% of the human genome constituted by transposable elements (TEs) is not only transcriptionally active but also physiologically necessary. Dysregulation of TEs, including human retroviral endogenous sequences (HERVs) has been shown to associate with several neurologic and autoimmune diseases, including Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). However, no study has yet addressed whether abnormal expression of these sequences correlates with fibromyalgia (FM), a disease frequently comorbid with ME/CFS. The work presented here shows, for the first time, that, in fact, HERVs of the H, K and W types are overexpressed in immune cells of FM patients with or without comorbid ME/CFS. Patients with increased HERV expression (N = 14) presented increased levels of interferon (INF-β and INF-γ) but unchanged levels of TNF-α. The findings reported in this study could explain the flu-like symptoms FM patients present with in clinical practice, in the absence of concomitant infections. Future work aimed at identifying specific genomic loci differentially affected in FM and/or ME/CFS is warranted. |
