Sathiyamoorthy K, et al., 10(8):e1004309, PLoS Pathog, 2014
The entry of Epstein-Barr Virus (EBV) into B cells of the immune system was investigated using several biochemical, structural, and functional experiments. These lipid-enveloped viruses in general require coordination of the receptor recognition, viral protein activation, and significant protein-conformational changes that can drive fusion of the membrane bilayer. Three viral glycoproteins (gH, gL, and gp42) contribute to the complex formation with the host receptor know as the human leukocyte antigen (HLA). The biolayer interferometry (along with electron microscopy analyses) was used to dissect the assembly mechanism. An Octet RED96 system equipped with SA biosensors was used to capture biotinylated HLA-DQ2 or EBV gHgL depending on the interaction under consideration. The binding interaction analyses involved gp42 or its mutants (C114S or I159C) and HLA-DQ2 in the presence or absence of gHgL. Based on the current data, the authors proposed a model for EBV entry into B cells.