Coreceptor restriction within the HLA-DQ locus for Epstein-Barr virus infection.
نویسندگان
چکیده
Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus that causes infectious mononucleosis and is etiologically associated with malignancies of multiple origins. EBV enters cells through a cascade of interactions between its envelope glycoprotein gp350 and the gp42-gH-gL complex with cellular receptors. Membrane fusion is catalyzed by the binding of gp42, a member of the C type lectin family, to HLA class II molecule HLA-DR, -DP, or -DQ. Here we demonstrate that only a subset of HLA-DQ alleles mediates EBV entry, indicating that individuals expressing these alleles may offer unique sites for EBV infection and subsequent sequelae. Additionally, the specific site within HLA-DQ determined to be essential for EBV entry is homologous to a site within MHC class I shown by structural studies to bind to the C type-lectin-like natural killer receptor, providing insight into the biochemical nature of the gp42-HLA class II interaction.
منابع مشابه
Epstein-Barr virus entry utilizing HLA-DP or HLA-DQ as a coreceptor.
Epstein-Barr virus (EBV) glycoprotein gp350/gp220 association with cellular CD21 facilitates virion attachment to B lymphocytes. Membrane fusion requires the additional interaction between virion gp42 and cellular HLA-DR. This binding is thought to catalyze membrane fusion through a further association with the gp85-gp25 (gH-gL) complex. Cell lines expressing CD21 but lacking expression of HLA ...
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عنوان ژورنال:
- Proceedings of the National Academy of Sciences of the United States of America
دوره 97 16 شماره
صفحات -
تاریخ انتشار 2000