Heldwein Ekaterina E
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA 02111, USA.
Curr Opin Virol. 2016 Jun;18:1-8. doi: 10.1016/j.coviro.2016.01.010. Epub 2016 Feb 2.
Membrane fusion during herpesvirus entry into host cells is a complex process where multiple glycoproteins interact to relay the triggering signal from a receptor-binding protein to the conserved fusogen gB through the conserved heterodimer gH/gL. Crystal structures of individual glycoproteins are available, yet high-order 'supercomplexes' have been elusive. Recent structures of complexes between gH/gL from human cytomegalovirus or Epstein-Barr virus and the receptor-binding proteins that form at early stages of herpesviral entry highlighted mechanisms that control tropism and revealed dynamic intermediate complexes containing gH/gL that may directly participate in membrane deformation and juxtaposition. Determining how the triggering signal reaches the fusogen gB represents the next frontier in structural biology of herpesvirus entry.
疱疹病毒进入宿主细胞过程中的膜融合是一个复杂的过程,在此过程中多种糖蛋白相互作用,通过保守的异二聚体gH/gL将触发信号从受体结合蛋白传递给保守的融合蛋白gB。单个糖蛋白的晶体结构是已知的,但高阶“超复合物”却难以捉摸。人巨细胞病毒或EB病毒的gH/gL与疱疹病毒进入早期形成的受体结合蛋白之间复合物的最新结构突出了控制嗜性的机制,并揭示了含有gH/gL的动态中间复合物,这些复合物可能直接参与膜的变形和并列。确定触发信号如何到达融合蛋白gB是疱疹病毒进入结构生物学的下一个前沿领域。