Entry of herpesviruses into mammalian cells.
The mechanism that herpesviruses use to enter cells is one of the most complex viral entry mechanisms studied so far. This complexity seems to mount as new participants, both cellular receptors and viral glycoproteins, are identified. Recent structural work on entry glycoproteins gD and gB from herpes simplex virus (HSV) 1 has illuminated the functional roles of these glycoproteins in the process of entry. In doing so, it provided information on the mechanism of two critical steps of HSV entry: receptor-mediated activation and membrane fusion. Remarkably, it is becoming clear that herpesviruses have a lot in common with other, simpler viruses.
Heldwein
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Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, USA. katya.heldwein@tufts.edu
Krummenacher
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D000818:Animals; D006564:Herpesviridae / Q000145:classification / Q000502:physiology*; D006801:Humans; D008561:Membrane Fusion / Q000502:physiology; D008958:Models, Molecular; D017434:Protein Structure, Tertiary; D053240:Receptors, Tumor Necrosis Factor, Member 14 / Q000378:metabolism; D014759:Viral Envelope Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D053586:Virus Internalization
D053240:Receptors, Tumor Necrosis Factor, Member 14; C506028:TNFRSF14 protein, human; D014759:Viral Envelope Proteins; C515577:glycoprotein gD, herpes simplex virus type 1