Abstract
Binding of herpes simplex virus (HSV) glycoprotein D (gD) to a cell surface receptor is required to trigger membrane fusion during entry into host cells. Nectin-1 is a cell adhesion molecule and the main HSV receptor in neurons and epithelial cells. We report the structure of gD bound to nectin-1 determined by x-ray crystallography to 4.0 Å resolution. The structure reveals that the nectin-1 binding site on gD differs from the binding site of the HVEM receptor. A surface on the first Ig-domain of nectin-1, which mediates homophilic interactions of Ig-like cell adhesion molecules, buries an area composed by residues from both the gD N- and C-terminal extensions. Phenylalanine 129, at the tip of the loop connecting β-strands F and G of nectin-1, protrudes into a groove on gD, which is otherwise occupied by C-terminal residues in the unliganded gD and by N-terminal residues in the gD/HVEM complex. Notably, mutation of Phe129 to alanine prevents nectin-1 binding to gD and HSV entry. Together these data are consistent with previous studies showing that gD disrupts the normal nectin-1 homophilic interactions. Furthermore, the structure of the complex supports a model in which gD-receptor binding triggers HSV entry through receptor-mediated displacement of the gD C-terminal region.
Highlights
Herpes simplex virus (HSV) enters cells by fusing its envelope with a membrane of the host cell [1]
Four viral glycoproteins are required for HSV entry into host cells. glycoprotein D (gD) binding to a cell surface receptor triggers conformational changes in the other viral glycoproteins leading to membrane fusion and viral entry
Our data point to a conserved mechanism for receptor mediated activation of the HSV entry process
Summary
Herpes simplex virus (HSV) enters cells by fusing its envelope with a membrane of the host cell [1]. Five viral envelope glycoproteins participate in the cell entry process. Glycoprotein C (gC) and gB promote attachment by interacting with cell surface proteoglycans, gD binds to a specific receptor [2,3]. The gD-receptor interaction initiates the process that leads to gB-mediated membrane fusion [4,5]. Depending on the cell type, fusion occurs at the cell surface or, after endocytosis of virions, with an endosomal membrane in a low pH-dependent or independent manner [6,7]. Regardless of the entry pathway gD, gB, gH/gL and a cellular gD receptor are required for entry [8]
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