Herpes simplex virus type 1 penetration initiates mobilizaton of cell surface proteins

Ken S. Rosenthal, Deborah Roess, B. George Barisas

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Changes in membrane structure resulting from herpes simplex virus 1 (HSV-1) penetration were detected using fluorescence photobleaching recovery methods. The effect could be blocked by inhibitors of viral and cellular processes involved in virus penetration. A rapid mode of HSV-1 strain KOS penetration into VERO cells at 37°C normally occurs after a 5 min lag period and is 90-95% complete within 20-30 min. Rates of cell surface protein diffusion increase 2-3-fold after 5 min and return to normal after 25-30 min, this return correlating temporally with the penetration of the virus. At pH 6.3 the lag period preceeding penetration of HSV is increased to 20 min and penetration proceeds much more slowly than at pH 7.4. Inhibition of virus penetration with cytochalasin B or with the antiherpes drug tromantadine also prevents the HSV-1-induced increase in cell surface protein mobility. Colchicine, which does not block HSV-1 penetration, prevents the recovery of the membrane following virus penetration. Therefore, the changes in membrane structure characterized by increased cell surface protein mobility seem to be caused by virus penetration. Cytoskeletal function and integrity are required for the initiation of, and cell recovery from, virus penetration. A pH-sensitive activity, likely to be a virion fusion glycoprotein, is also required.

Original languageEnglish (US)
Pages (from-to)38-44
Number of pages7
JournalBBA - Biomembranes
Issue number1
StatePublished - Jul 7 1988
Externally publishedYes


  • Fluorescence photobleaching recovery
  • Herpes simplex virus
  • Membrane protein
  • Protein mobility
  • Viral penetration

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Cell Biology


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