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Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
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The COMPLEXity in herpesvirus entry.

Karthik Sathiyamoorthy1, Jia Chen2, Richard Longnecker2

  • 1Department of Structural Biology, Stanford University School of Medicine, 1201 Welch Road, Stanford, CA 94305, United States.

Current Opinion in Virology
|May 25, 2017
PubMed
Summary
This summary is machine-generated.

Herpesviruses use multiple envelope glycoproteins, including the gHgL complex and gB protein, to enter host cells. Recent studies on Epstein-Barr virus and Cytomegalovirus reveal gHgL

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Area of Science:

  • Virology
  • Molecular Biology
  • Structural Biology

Background:

  • Enveloped viruses utilize diverse transmembrane proteins for host cell entry, involving receptor binding, activation, and membrane fusion.
  • Unlike single-protein systems (e.g., HIV env, influenza HA), herpesviruses employ multiple envelope glycoproteins for entry.
  • Herpesvirus entry relies on two core glycoproteins: the gHgL complex (activator) and gB protein (fusogen).

Purpose of the Study:

  • To review recent structural and functional studies of Epstein-Barr virus (EBV) and Cytomegalovirus (CMV) gHgL complexes.
  • To elucidate the role of the gHgL complex in coordinating herpesvirus entry.
  • To understand how gB conformational changes contribute to viral and cellular membrane fusion.

Main Methods:

  • Review of recent structural and functional studies.
  • Analysis of electron microscopy (EM) models.
  • Examination of glycoprotein complex assembly and function.

Main Results:

  • The gHgL complex acts as an entry activator, binding receptors or assembling with other proteins to confer target cell specificity.
  • gHgL complexes form membrane bridging intermediates, crucial for triggering gB-mediated fusion.
  • EM model of Herpes Simplex virus (HSV) gB highlights conformational changes promoting membrane fusion.

Conclusions:

  • The gHgL complex is central to herpesvirus entry, mediating receptor interactions and activating the fusogenic gB protein.
  • Understanding gHgL and gB functions provides a framework for herpesvirus entry mechanisms.
  • Structural insights into gB are key to deciphering viral and cellular membrane fusion processes.