Viral Antibody Titers

Shirodaria, P. V.; Haire, Margaret; Fleming, Elizabeth; Merrett, J. D.; Hawkins, Stanley; Roberts, S D

doi:10.1001/archneur.1987.00520240019006

Cited by 52 publications

(8 citation statements)

References 43 publications

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“…Removing the two studies [18], [35] which measured EBNA complex had no effect on the overall result (OR 4.56, 95% CI 3.27–6.37). Another seven studies [17], [23], [31], [32], [39], [43], [46] did not clearly state which form of EBNA was measured; if these are also removed the result is little changed (OR 4.30, 95% CI 2.90–6.39).…”

Section: Resultsmentioning

confidence: 99%

Systematic Review and Meta-Analysis of the Sero-Epidemiological Association between Epstein Barr Virus and Multiple Sclerosis

et al. 2013

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BackgroundA role for Epstein Barr virus (EBV) in multiple sclerosis (MS) has been postulated. Previous systematic reviews found higher prevalences of anti-EBV antibodies in MS patients compared to controls, but many studies have since been published, and there is a need to apply more rigorous systematic review methods.Methodology/Principal FindingsWe examined the link between EBV and MS by conducting a systematic review and meta-analysis of case-control and cohort studies that examined the prevalence of anti-EBV antibodies in the serum of cases and controls. We searched Medline and Embase databases from 1960 to 2012, with no language restriction. The Mantel-Haenszel odds ratios (OR) for anti-EBV antibodies sero-positivity were calculated, and meta-analysis conducted. Quality assessment was performed using a modified version of the Newcastle Ottawa scale. Thirty-nine studies were included. Quality assessment found most studies reported acceptable selection and comparability of cases and controls. However the majority had poor reporting of ascertainment of exposure. Most studies found a higher sero-prevalence of anti-EBNA IgG and anti-VCA IgG in cases compared to controls. The results for anti-EA IgG were mixed with only half the studies finding a higher sero-prevalence in cases. The meta-analysis showed a significant OR for sero-positivity to anti-EBNA IgG and anti-VCA IgG in MS cases (4.5 [95% confidence interval (CI) 3.3 to 6.6, p<0.00001] and 4.5 [95% CI 2.8 to 7.2, p<0.00001] respectively). However, funnel plot examination suggested publication bias for the reporting of the anti-EBNA IgG. No significant difference in the OR for sero-positivity to anti-EA IgG was found (1.4 [95% CI 0.9 to 2.1, p = 0.09]).Conclusion/SignificanceThese findings support previous systematic reviews, however publication bias cannot be excluded. The methodological conduct of studies could be improved, particularly with regard to reporting and conduct of laboratory analyses.

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Section: Resultsmentioning

confidence: 99%

Systematic Review and Meta-Analysis of the Sero-Epidemiological Association between Epstein Barr Virus and Multiple Sclerosis

et al. 2013

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“…In SLE and MS, titers of antibodies against EBV antigens are elevated compared to healthy controls [13,21,22,23], and for both diseases, this elevation seems to predate the first symptoms [24,25,26,27]. Anti-EBV nuclear antigen (EBNA)-1 IgG titers may also predict conversion from clinically isolated syndrome (CIS) to MS [28] and be a marker of MS disease activity [29], although the latter has been questioned by a recent study [30].…”

Section: Evidence Of Associationmentioning

confidence: 99%

“…For SLE, there is some evidence that titers of IgA antibodies against viral capsid antigen (VCA) may be associated with disease flares [34]. There is also some evidence that patients with RA have elevated serum titers of antibodies against EBV antigens [15,23,35,36,37]. However, in contrast to SLE and MS, it does not seem to be any association between the titers of antibodies and risk of subsequent RA [38].…”

Section: Evidence Of Associationmentioning

confidence: 99%

Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation

Lossius

Johansen

Torkildsen

et al. 2012

Viruses

113

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Epidemiological data suggest that the Epstein-Barr virus (EBV) is associated with several autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. However, it is not clear whether EBV plays a role in the pathogenesis of these diseases, and if so, by which mechanisms the virus may contribute. In this review, we discuss possible viral and immunological mechanisms that might explain associations between EBV and autoimmune diseases and whether these associations represent causes or effects of inflammation and autoimmunity.

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“…Moreover, RA patients have high numbers of circulating EBV-infected B cells (7) and EBV DNA loads in saliva (8). Antibody titers against EBV antigens are also elevated in SLE and MS patients compared to those in healthy controls (9,10).…”

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confidence: 99%

Endosomal Toll-Like Receptors Mediate Enhancement of Interleukin-17A Production Triggered by Epstein-Barr Virus DNA in Mice

Shehab

Sherri

Hussein

et al. 2019

J Virol

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We previously demonstrated that Epstein-Barr virus (EBV) DNA increases the production of the proinflammatory cytokine interleukin-17A (IL-17A) in mice. This property may contribute to the established association between EBV and autoimmune diseases. The objective of the present study was to elucidate mechanisms through which EBV DNA modulates IL-17A levels in mice. To determine whether endosomal Toll-like receptors (TLRs) played a role in this pathway, the expression of TLR3, -7, or -9 was assessed by real-time reverse transcription-PCR in mouse spleens after injection of EBV DNA. Moreover, specific inhibitors were used for these TLRs in mouse peripheral blood mononuclear cells (PBMCs) cultured with EBV DNA and in mice injected with this viral DNA; IL-17A levels were then assessed using an enzyme-linked immunosorbent assay. The expression of the endosomal receptors TLR3, -7, and -9 was increased in mice injected with EBV DNA. When mouse immune cells were cultured with EBV DNA and a TLR3, -7, or -9 inhibitor or when mice were injected with the viral DNA along with either of these inhibitors, a significant decrease in IL-17A levels was detected. Therefore, endosomal TLRs are involved in the EBV DNA-mediated triggering of IL-17A production in mice. Targeting these receptors in EBV-positive subjects with autoimmunity may be useful pending investigations assessing whether they play a similar role in humans. IMPORTANCE Epstein-Barr virus is a pathogen that causes persistent infection with potential consistent viral DNA shedding. The enhancement of production of proinflammatory cytokines by viral DNA itself may contribute to autoimmune disease development or exacerbation. In this project, we identified that endosomal Toll-like receptors are involved in triggering proinflammatory mediators in response to viral DNA. Pathways and receptors involved may serve as future therapeutic targets for autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus.

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Viral Antibody Titers

Cited by 52 publications

References 43 publications

Systematic Review and Meta-Analysis of the Sero-Epidemiological Association between Epstein Barr Virus and Multiple Sclerosis

Systematic Review and Meta-Analysis of the Sero-Epidemiological Association between Epstein Barr Virus and Multiple Sclerosis

Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation

Endosomal Toll-Like Receptors Mediate Enhancement of Interleukin-17A Production Triggered by Epstein-Barr Virus DNA in Mice

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