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Herpes Simplex Virus Entry by a Nonconventional Endocytic Pathway.

Giulia Tebaldi1, Suzanne M Pritchard1, Anthony V Nicola2

  • 1Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA.

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Herpes simplex virus 1 (HSV-1) uses endocytosis to enter cells but bypasses the typical endo-lysosomal pathway. This study suggests HSV-1 may utilize the trans-Golgi network (TGN) for entry, offering new intervention targets.

Keywords:
Rab GTPasesTGNendocytosisherpes simplex virus 1retrograde transportviral entry

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Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Herpes simplex virus 1 (HSV-1) is a widespread human pathogen causing significant illness.
  • HSV-1 infection often begins with entry into epithelial cells via low-pH dependent endocytosis.
  • The precise intracellular route and fusion compartment for HSV-1 entry remain unidentified.

Purpose of the Study:

  • To elucidate the intracellular pathway utilized by HSV-1 during endocytic entry.
  • To investigate the role of Rab GTPases and the endo-lysosomal network in HSV-1 cell entry.
  • To identify potential alternative pathways, such as those involving the trans-Golgi network (TGN).

Main Methods:

  • Utilized molecular and pharmacological approaches to study HSV-1 entry.
  • Employed small interfering RNA (siRNA) and dominant-negative GTPases (Rab5, Rab7, Rab9, Rab11).
  • Applied brefeldin A (BFA) and Golgicide A (GCA) to inhibit TGN-related functions.

Main Results:

  • HSV-1 entry was not affected by Rab5 or Rab7 manipulation, indicating independence from the conventional endo-lysosomal pathway.
  • BFA and GCA inhibited HSV-1 entry and viral transport, implicating TGN functions and retrograde transport.
  • Silencing Rab9 or Rab11 showed only a minor reduction in HSV infection.

Conclusions:

  • HSV-1 entry into host cells occurs via an intracellular route distinct from the canonical lysosome-terminal endocytic pathway.
  • The findings suggest a potential involvement of the trans-Golgi network (TGN) in HSV-1 endocytosis.
  • This research may pave the way for novel therapeutic strategies targeting HSV-1 entry.