Epstein-Barr virus glycoproteins H, L, and 42 complex (gH/gL/gp42)

The Epstein–Barr virus (EBV) glycoprotein complex **gH/gL/gp42** is an essential multi-protein complex on the surface of the virus that mediates fusion of the viral envelope with B cell membranes, thereby enabling viral entry. The complex consists of: - **gH (glycoprotein H)** and **gL (glycoprotein L)**, which form a heterodimeric structure that works as a core fusogen, - **gp42 (glycoprotein 42)**, a type II membrane protein with a flexible N-terminal region that binds the gH/gL heterodimer and a C-terminal lectin-like domain that binds to the B cell receptor, human leukocyte antigen (HLA) class II[1][2][4]. Upon binding to HLA class II molecules on B cells, gp42 triggers conformational changes that promote membrane fusion. Importantly, gp42 controls EBV cell tropism: it is required for B cell entry but its presence inhibits fusion with epithelial cells[4]. gH/gL and gp42 interact through specific N-terminal domains, and perturbing this interaction (e.g., via peptides or mutations) can inhibit EBV entry into B cells[3][5][6]. The complex does not have a direct homolog in human proteins, making it an attractive potential target for therapeutic intervention in EBV infection. There are currently no approved drugs directly targeting this complex, though various experimental peptides and antibodies that block its function have been described in the literature[3][5][6]. No established biomarkers or safety concerns have been described in the clinical context due to the experimental status of interventions. The canonical role of this complex is **viral entry and membrane fusion**, which underlies EBV's infection of B cells and its disease associations, including infectious mononucleosis and EBV-driven malignancies[1][2][4].

Other names

EBV gH/gL/gp42 complexgHgL/gp42Epstein-Barr virus entry/fusion complex

Inhibition of viral membrane fusion with B cell membrane via blocking subunit interactions[3][5]. Inhibition of receptor binding to HLA class II, preventing B cell entry[1][2][4].