scholarly journals HERV and Epstein-Barr Virus: Another Piece to Multiple Sclerosis Puzzle

Author(s):  
Letícia Caroline Breis ◽  
Marco Antônio Machado Schlindwein ◽  
Marcus Vinicius Magno Gonçalves

Multiple Sclerosis (MS) has a well established link with Epstein-Barr virus (EBV) and a growing association with human endogenous retroviruses (HERVs). In this review, we described how these two pieces may interact in MS pathogenesis

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e44991 ◽  
Author(s):  
Giuseppe Mameli ◽  
Luciana Poddighe ◽  
Alessandra Mei ◽  
Elena Uleri ◽  
Stefano Sotgiu ◽  
...  

2018 ◽  
Vol 24 (1) ◽  
pp. 42-47 ◽  
Author(s):  
Antonina Dolei

Two human endogenous retroviruses of the HERV-W family are proposed as multiple sclerosis (MS) co-factors: MS-associated retrovirus (MSRV) and ERVWE1, whose env proteins showed several potentially neuropathogenic features, in vitro and in animal models. Phase II clinical trials against HERV-Wenv are ongoing. HERV-W/MSRV was repeatedly found in MS patients, in striking parallel with MS stages, active/remission phases, and therapy outcome. The HERV-Wenv protein is highly expressed in active MS plaques. Early MSRV presence in spinal fluids predicted worst MS progression 10 years in advance. Effective anti-MS therapies strongly reduced MSRV/Syncytin-1/HERV-W expression. The Epstein–Barr virus (EBV) activates HERV-W/MSRV in vitro and in vivo, in patients with infectious mononucleosis and controls with high anti-EBNA1-IgG titers. Thus, the two main EBV/MS links (infectious mononucleosis and high anti-EBNA1-IgG titers) are paralleled by activation of HERV-W/MSRV. It is hypothesized that EBV may act as initial trigger of future MS, years later, by activating MSRV, which would act as direct neuropathogenic effector, before and during MS.


2021 ◽  
Vol 22 (6) ◽  
pp. 2927
Author(s):  
Ali Afrasiabi ◽  
Nicole L. Fewings ◽  
Stephen D. Schibeci ◽  
Jeremy T. Keane ◽  
David R. Booth ◽  
...  

Although the causes of Multiple Sclerosis (MS) still remain largely unknown, multiple lines of evidence suggest that Epstein–Barr virus (EBV) infection may contribute to the development of MS. Here, we aimed to identify the potential contribution of EBV-encoded and host cellular miRNAs to MS pathogenesis. We identified differentially expressed host miRNAs in EBV infected B cells (LCLs) and putative host/EBV miRNA interactions with MS risk loci. We estimated the genotype effect of MS risk loci on the identified putative miRNA:mRNA interactions in silico. We found that the protective allele of MS risk SNP rs4808760 reduces the expression of hsa-mir-3188-3p. In addition, our analysis suggests that hsa-let-7b-5p may interact with ZC3HAV1 differently in LCLs compared to B cells. In vitro assays indicated that the protective allele of MS risk SNP rs10271373 increases ZC3HAV1 expression in LCLs, but not in B cells. The higher expression for the protective allele in LCLs is consistent with increased IFN response via ZC3HAV1 and so decreased immune evasion by EBV. Taken together, this provides evidence that EBV infection dysregulates the B cell miRNA machinery, including MS risk miRNAs, which may contribute to MS pathogenesis via interaction with MS risk genes either directly or indirectly.


Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 643 ◽  
Author(s):  
Rachael E. Tarlinton ◽  
Ekaterina Martynova ◽  
Albert A. Rizvanov ◽  
Svetlana Khaiboullina ◽  
Subhash Verma

Multiple sclerosis (MS) is an immune inflammatory disease, where the underlying etiological cause remains elusive. Multiple triggering factors have been suggested, including environmental, genetic and gender components. However, underlying infectious triggers to the disease are also suspected. There is an increasing abundance of evidence supporting a viral etiology to MS, including the efficacy of interferon therapy and over-detection of viral antibodies and nucleic acids when compared with healthy patients. Several viruses have been proposed as potential triggering agents, including Epstein–Barr virus, human herpesvirus 6, varicella–zoster virus, cytomegalovirus, John Cunningham virus and human endogenous retroviruses. These viruses are all near ubiquitous and have a high prevalence in adult populations (or in the case of the retroviruses are actually part of the genome). They can establish lifelong infections with periods of reactivation, which may be linked to the relapsing nature of MS. In this review, the evidence for a role for viral infection in MS will be discussed with an emphasis on immune system activation related to MS disease pathogenesis.


2007 ◽  
Vol 14 (2) ◽  
pp. 284-287 ◽  
Author(s):  
Mario Habek ◽  
Vesna V Brinar ◽  
Sanja Hajnšek

The aetiology of multiple sclerosis (MS) is still an unresolved question. Several recently reported studies are implicating Epstein—Barr virus (EBV) as one of the key players in MS pathogenesis. We present a 21-year-old male patient with a history of EBV-related infectious mononucleosis in puberty and Hodgkin's disease two years previously treated with irradiation and chemotherapy. The patient presented with spastic paraparesis that resolved promptly on corticosteroid treatment. There were no signs of Hodgkin's disease relapse. In the next three years he had three more bouts of the disease and he was diagnosed with relapse—remitting MS. There is evidence of EBV involvement in MS pathogenesis; the association of MS with EBV-related infectious mononucleosis and Hodgkin's disease being just one of them. Although there are many unanswered questions, it is clear that without EBV seropositivity MS in adults is extremely rare. Multiple Sclerosis 2008; 14: 284—287. http://msj.sagepub.com


PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e78474 ◽  
Author(s):  
Giuseppe Mameli ◽  
Giordano Madeddu ◽  
Alessandra Mei ◽  
Elena Uleri ◽  
Luciana Poddighe ◽  
...  

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