ISSN:
1432-0428
Keywords:
Type 1 (insulin-dependent) diabetes mellitus
;
molecular mimicry
;
Epstein-Barr virus
;
class II MHC molecules
;
EBV BOLF1
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary A role for the Epstein-Barr virus in initiating Type 1 (insulin-dependent) diabetes mellitus has been proposed since Epstein-Barr virus BOLF1(497–513) AVTPL RIFIVPPAAEY has an 11 amino acid identity with HLA-DQw8β (49–60) AVTPL GPPAAEY. Rabbit antisera to the BOLF1 (496–515) peptide crossreacted with the homologous DQw8β (44–63) peptide but not with the related DQw7β(44–63) peptide, which differed from the DQw8 peptide only in an ALA to ASP substitution in position 57. Antisera to DQw8β(49–60) reacted with the DQw8β(44–63) peptide and BOLF1 (496–515), but not with DQw7β (44–63). The antiserum to the BOLF1 peptide bound to denatured class II major histocompatibility complex β chains from Epstein-Barr virus-transformed DQw8-positive lymphocytes in an immunoblotting analysis. Epstein-Barr virus antibodies were detected at equal frequencies and similar titres in sera of 30 patients with Type 1 diabetes (16 of 30;63%) and in sera of 20 non-diabetic control subjects (13 of 20;65%). Sera from diabetic patients did not bind to DQw8β (44–63) or BOLF1(496–515) peptides. From these data we conclude that there is no simple relationship between serological evidence of Epstein-Barr virus infection and crossreactions between homologous Epstein-Barr virus and class II major histocompatibility complex peptides.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00404022
Permalink
