Epstein Barr viral infection and onset of central nervous system demyelination

Lucas, Robyn M., Ponsonby, Ane-Louise, Burrows, J., Chapman, Caron, Coulthard, Alan, Dear, Keith, Dwyer, Terence, Kilpatrick, Trevor J., McMichael, Anthony J., Taylor, Bruce V., Valery, Patricia, van der Mei, Ingrid, Williams, D and Pender, Michael P. (2010). Epstein Barr viral infection and onset of central nervous system demyelination. In: 15th Annual ACTRIMS Meeting Americas Committee for Treatment and Research in Multiple Sclerosis, San Antonio, TX, United States, (1007-1007). 5 June 2010. doi:10.1177/13524585100160081301


Author Lucas, Robyn M.
Ponsonby, Ane-Louise
Burrows, J.
Chapman, Caron
Coulthard, Alan
Dear, Keith
Dwyer, Terence
Kilpatrick, Trevor J.
McMichael, Anthony J.
Taylor, Bruce V.
Valery, Patricia
van der Mei, Ingrid
Williams, D
Pender, Michael P.
Title of paper Epstein Barr viral infection and onset of central nervous system demyelination
Conference name 15th Annual ACTRIMS Meeting Americas Committee for Treatment and Research in Multiple Sclerosis
Conference location San Antonio, TX, United States
Conference dates 5 June 2010
Journal name Multiple Sclerosis   Check publisher's open access policy
Place of Publication London, United Kingdom
Publisher Sage Publications
Publication Year 2010
Sub-type Poster
DOI 10.1177/13524585100160081301
ISSN 1352-4585
1477-0970
Volume 16
Issue 8
Start page 1007
End page 1007
Total pages 1
Language eng
Formatted Abstract/Summary
Background: Previous work has shown high levels of anti-Epstein Barr Virus (EBV) antibodies in individuals with multiple sclerosis (MS).

Objectives: To examine history of glandular fever, anti-EBV antibody profile and whole blood viral load at first clinical diagnosis of central nervous system demyelination (FCD), compared to community controls. 

Methods: The Australian Multicentre Study of Environment and Immune Function (Ausimmune Study) recruited FCD cases and unaffected controls matched on age (18–59 years), sex and study region, between 1 November 2003 and 31 December 2006. Data included history of glandular fever (yes/no), serum IgG antibody titres for EBNA complex, viral capsid antigen (VCA) and early antigen (EA), and whole blood quantitative EBV DNA viral load (measured using real-time polymerase chain reaction [PCR], primers and probe derived from BamH1 of the EBV genome and Namalwa cell line with 2 EBV copies per cell for the standard curve) expressed as EBV copies per ug of DNA. Conditional logistic regression was used to analyse case-control differences.

Results: Past history of glandular fever (n=277 cases, n=538 controls) was associated with increased odds of being a FCD case (OR=1.87, 95% confidence interval [CI] 1.30–2.67). In a subsample (n=204 cases, n=210 controls), higher titres (log2) of anti-EBNA (OR=1.26, 95% CI 1.13–1.40), anti-VCA (OR=1.16, 95% CI 1.03– .32) and anti-EA-restricted (OR=1.16, 95% CI 1.04–1.29) but not anti-EAdiffuse (OR=1.06, 95% CI 0.93–1.21) antibodies, were associated with increased risk of being a FCD case. EBV load (n=215 cases, n=216 controls) was more likely to be positive in FCD cases than controls (56.3% vs. 49.5%), and was significantly correlated with anti-EBNA (p=0.02), anti-VCA (p<0.001) and anti-EA-restricted (p=0.001), but not anti-EAdiffuse (p=0.16) antibodies. Multivariate analyses are underway.

Conclusions: History of glandular fever, or evidence of prior infection with EBV is associated with increased odds of being a FCD case, strengthening evidence that EBV infection is a risk factor for MS onset.
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status UQ

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Created: Sun, 22 Aug 2010, 10:05:44 EST