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Investigation of humoral immune response towards persisting Epstein-Barr virus infections in multiple sclerosis and chronic fatigue syndrome using peptide microarrays

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By Aaron Castro et al. • www.ProHealth.com • June 12, 2014


By Aaron Castro et al.

Abstract

Most humans carry a considerable number of persisting viral infections, frequently in a latent state. Chronic infections may intermittently reactivate especially under immune suppression and play an important role as trigger or cofactor for autoimmune diseases and cancer.

Correlation of such infections with diseases is difficult. An analysis of antibody repertoire in chronic infection may provide information about patterns of virus reactivation. Following primary infection the herpes virus 4 (EBV) results in persistent mostly asymptomatic latent infection.

About 95% of the adult population are EBV seropositive. EBV infections are known as cofactors for various diseases such as lymphomas, multiple sclerosis and chronic fatigue syndrome. The detailed mapping of humoral immune response in human serum samples allows a high resolution analysis of the antibody repertoire against EBV antigens.

We developed a peptide microarray platform with peptide libraries of up to 6900 members. Here we present data using a library of peptide scans through major EBV antigens from incubations with serum samples of healthy human donors, patients diagnosed with chronic fatigue syndrome or multiple sclerosis.

Even though there are shared epitopes between the specimens and cohorts, different epitope patterns are observed for a number of antigens and antigen areas. The patterns of antibody responses could be of diagnostic value for multiple sclerosis and chronic fatigue syndrome.

Source: Aaron Castro, Nikolaus Pawlowski, Ulf Reimer, Janina Jansong, Madlen Löbel, Klemens Ruprecht, and Carmen Scheibenbogen. Investigation of humoral immune response towards persisting Epstein-Barr virus infections in multiple sclerosis and chronic fatigue syndrome using peptide microarrays. The Journal of Immunology, May 1, 2014, vol. 192 no. 1 Supplement 69.36.




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