scholarly journals Anti-Human Herpesvirus 6 A/B Antibodies Titers Correlate With Multiple Sclerosis-Associated Retrovirus Envelope Expression

2021 ◽  
Vol 12 ◽  
Author(s):  
Silvia Pérez-Pérez ◽  
María I. Domínguez-Mozo ◽  
M. Ángel García-Martínez ◽  
M. Celeste García-Frontini ◽  
Noelia Villarrubia ◽  
...  

Human endogenous retrovirus W family envelope proteins (pHERV-W ENV/syncytin-1) have been repeatedly associated with multiple sclerosis (MS). Here, we have focused on the study of pHERV-W ENV/syncytin-1 expression levels in MS patients (relapsing and progressive forms) and in healthy donors (HD) and on exploring their possible relationship with Epstein-Barr virus (EBV) and human herpesvirus-6A/B (HHV-6A/B). We included blood samples from 101 MS patients and 37 HD to analyze antiviral antibody titers by ELISA and pHERV-W ENV/syncytin-1 expression levels by flow cytometry as well as by qPCR. Patients with relapsing MS forms showed significantly higher pHERV-W ENV/syncytin-1 protein and gene expression levels than HD. Progressive MS patients also showed significantly higher protein and gene expression levels than both HD and relapsing MS patients. Regarding antiviral antibodies titers, anti-HHV-6A/B IgM levels were positively correlated with pHERV-W ENV/syncytin-1 protein expression levels in patients with relapsing MS, while in the progressive forms patients this correlation was found with anti-HHVA/B IgG levels. Therefore, pHERV-W ENV could be involved in MS pathogenesis, playing a role in relapsing and progressive forms. Besides, anti-HHV-6A/B antibodies positively correlated with pHERV-W ENV expression. Further studies are needed to better understand this possible relationship.

2008 ◽  
Vol 14 (9) ◽  
pp. 1175-1180 ◽  
Author(s):  
AK Tai ◽  
EJ O’Reilly ◽  
KA Alroy ◽  
KC Simon ◽  
KL Munger ◽  
...  

Background The human endogenous retrovirus (HERV)-K18 Env is an Epstein-Barr virus (EBV)-associated superantigen. Given the evidence for a role of EBV in the etiology of multiple sclerosis (MS), HERV-K18 Env is a plausible candidate for association with MS. Objective To assess whether variation in HERV-K18 Env is a risk factor for MS. Methods We developed a single nucleotide polymorphism-based genotyping method to determine the distribution of the three alleles of HERV-K18 env. We then conducted a nested case-control study including 207 MS cases and 403 matched controls. Analyses were replicated in an independent series of 909 MS cases and 339 controls. Results Overall, there was a significant association between HERV-K18 env genotype and MS risk (χ2 P = 0.03). As compared with K18.2/K18.2 individuals, risk of MS was three fold higher among K18.3/K18.3 individuals ( P = 0.03). An increase in MS risk among carriers of the K18.3 allele was also observed in the replication study, but did not reach statistical significance. In pooled analyses, K18.3/K18.3 individuals had a significantly increased risk of MS (relative risks [RR] comparing K18.3/K18.3 vs K18.2/K18.2 = 2.7; 95% confidence interval: 1.1–6.4). Conclusion Variation in EBV-associated superantigen HERV-K18 Env could influence the genetic susceptibility to MS.


2019 ◽  
Vol 25 (7) ◽  
pp. 891-901 ◽  
Author(s):  
Mariano Marrodan ◽  
Lucas Alessandro ◽  
Mauricio F Farez ◽  
Jorge Correale

Several lines of evidence suggest that multiple sclerosis (MS), like other autoimmune diseases, may be triggered by microbial infections. Pathogens associated with development or exacerbation of MS include bacteria, such as Chlamydia pneumoniae, Staphylococcus aureus-produced enterotoxins that function as superantigens, and viruses of the Herpesviridae (Epstein–Barr virus and human herpes virus 6) and human endogenous retrovirus families. However, to date, no single pathogen has been accepted as causal agent. In addition, common upper respiratory, gastrointestinal, and urogenital tract infections have also been associated with MS exacerbations. Although evidence of an infectious etiology as cause of MS in humans remains inconclusive, microbial agents may modulate the neuroimmunological system of genetically susceptible individuals. Decoding the epidemiological contribution of different microorganisms to MS, along with their pathogenic mechanisms, may help develop new treatment strategies and prevent relapses.


2020 ◽  
pp. 754-763
Author(s):  
Alan B. Rickinson ◽  
M.A. Epstein

Epstein–Barr virus is a human herpesvirus with a linear double-stranded DNA genome that is carried asymptomatically by most people. Symptomless primary infection is usual in childhood, establishing a lifelong carrier state where the virus persists as a latent infection of circulating B cells. The virus replicates recurrently in oropharyngeal epithelial cells, with consequent shedding of virus in saliva transmitting infection. Controversially, Epstein–Barr virus has been linked with certain autoimmune diseases. In particular, there is strong serologic and epidemiologic evidence to suggest that previous exposure to Epstein–Barr virus markedly increases the risk of developing multiple sclerosis. Although the Epstein–Barr virus/multiple sclerosis connection is receiving much attention, the mechanism that might underpin such an association remains uncertain.


2018 ◽  
Vol 25 (12) ◽  
pp. 1446-1453 ◽  
Author(s):  
S. Pérez-Pérez ◽  
M. I. Domínguez-Mozo ◽  
M. Á. García-Martínez ◽  
Y. Aladro ◽  
M. Martínez-Ginés ◽  
...  

2019 ◽  
Vol 20 (2) ◽  
pp. 303 ◽  
Author(s):  
Rachael Tarlinton ◽  
Timur Khaibullin ◽  
Evgenii Granatov ◽  
Ekaterina Martynova ◽  
Albert Rizvanov ◽  
...  

Multiple sclerosis (MS) is a chronic debilitating inflammatory disease of unknown ethology targeting the central nervous system (CNS). MS has a polysymptomatic onset and is usually first diagnosed between the ages of 20–40 years. The pathology of the disease is characterized by immune mediated demyelination in the CNS. Although there is no clinical finding unique to MS, characteristic symptoms include sensory symptoms visual and motor impairment. No definitive trigger for the development of MS has been identified but large-scale population studies have described several epidemiological risk factors for the disease. This list is a confusing one including latitude, vitamin D (vitD) levels, genetics, infection with Epstein Barr Virus (EBV) and endogenous retrovirus (ERV) reactivation. This review will look at the evidence for each of these and the potential links between these disparate risk factors and the known molecular disease pathogenesis to describe potential hypotheses for the triggering of MS pathology.


2019 ◽  
Vol 48 (4) ◽  
pp. 030006051988415
Author(s):  
O Al Wutayd

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system, causing inflammation, demyelination, and neurodegeneration. Infection can play a role in its etiology. Herein, a review is presented of studies that have reported an association between infection and MS risk in countries of the Arabian Gulf region. Searches of the PubMed, Google Scholar, and Science Direct databases were carried out using various search terms, and relevant studies published through January 2019 on the epidemiology of MS in Gulf Cooperation Council countries identified. MS has been found to be associated with measles in Saudi Arabia and Epstein–Barr virus in Kuwait whereas no association has been identified between risk of MS and varicella-zoster virus, mumps, or human herpesvirus-6. However, few epidemiological studies on this topic have been conducted in countries of the Gulf region. Longitudinal and serological studies to establish robust evidence between infection and risk of MS are highly recommended, and a regional MS registry is needed.


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