May 2008
Volume 49, Issue 13
ARVO Annual Meeting Abstract  |   May 2008
Herpesvirus Surfing: A Mechanism for Finding the Host Cell
Author Affiliations & Notes
  • D. Shukla
    Ophthalmology/Visual Sciences, Univ of Illinois at Chicago, Chicago, Illinois
  • M.-J. Oh
    Ophthalmology/Visual Sciences, Univ of Illinois at Chicago, Chicago, Illinois
  • V. Tiwari
    Ophthalmology/Visual Sciences, Univ of Illinois at Chicago, Chicago, Illinois
  • Footnotes
    Commercial Relationships  D. Shukla, None; M. Oh, None; V. Tiwari, None.
  • Footnotes
    Support  NIH grant AI053836 and a career award from RPB
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 1117. doi:
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      D. Shukla, M.-J. Oh, V. Tiwari; Herpesvirus Surfing: A Mechanism for Finding the Host Cell. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1117. doi:

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Herpesviruses cause myriads of eye problems. The goal of the present study was to perform ultrastructural and real time analysis of Herpes Simplex Virus type 1 (HSV-1), cytomegalovirus (CMV) and human herpesvirus-8 (HHV-8) attachment to cells and to determine the cellular signaling events that facilitate virus attachment.

Methods: : High resolution laser confocal microscopy and fluorescent microscopy were used to monitor viral attachment to live cells. Green fluorescent viruses and/or fluorescent antibodies for HSV-1 (K26-GFP), CMV (MCMV-GFP) and HHV-8(GFP) were used. Immunoprecipitation and Western blot analysis were performed for the determination of signaling events. Inhibitors of actin polymerization were used to probe the significance of filopodia.

Results: : All three herpesviruses attach to filopodia-like structures before reaching the cell body. A lateral movement on filopodia toward the cell body ensues soon after the attachment. The viruses do not enter into filopodia but use them for moving exogenously until the cell body is reached and that is where they enter into cells. This unilateral movement on filopodia is termed "surfing" and is mediated by interaction between heparan sulfate and viral glycoprotein, gB. An increase in Rho GTPase, cdc42 as well as an induction of filopodia was observed after the addition of viruses. The filopodia generated in response to the viruses contain f-actin and inhibitors of actin polymerization such as cytochalasin-D inhibited both filopodia formation and viral entry. The viral gB retains the ability to move on the filopodia.

Conclusions: : "surfing" appears to be a conserved mechanism commonly used by divergent members of herpesvirus family. It might represent a mechanism by which viruses efficently find susceptible cells in a host and establsih how viruses can use abrasions in skin to their advantage.

Keywords: herpes simplex virus • microscopy: confocal/tunneling • microbial pathogenesis: experimental studies 

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