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Herpes simplex virus-induced cell surface protrusions.

U Krempien, B M Jockusch, C Jungwirth

    Intervirology
    |January 1, 1984
    PubMed
    Summary
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    Herpes simplex virus infection induces microvillus protrusions on cell surfaces, dependent on late viral functions. These structures, containing actin, do not appear to aid in virus release.

    Area of Science:

    • Virology
    • Cell Biology
    • Microscopy

    Background:

    • Herpes simplex virus (HSV) infection causes significant changes to host cell surfaces.
    • Understanding these alterations is crucial for comprehending viral pathogenesis and host-cell interactions.

    Purpose of the Study:

    • To investigate cell surface alterations induced by herpes simplex virus infection using scanning electron microscopy.
    • To characterize the morphology and timing of virus-induced microvillus formation.
    • To explore the molecular mechanisms and potential functions of these structures.

    Main Methods:

    • Scanning electron microscopy (SEM) was employed to examine infected chick embryo fibroblasts and Vero cells at various time points post-infection.
    • Fluorescent phalloidin staining was used to detect filamentous actin within the induced microvilli.

    Related Experiment Videos

  • Inhibitors of DNA and protein synthesis were utilized to assess the involvement of viral functions.
  • A specific drug, N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine, was tested for its effect on microvillus formation and virus replication.

    • Main Results:

    • Microvillus protrusions (0.12-0.18 micron diameter, 0.3 micron length) appeared on infected cells starting at 4 hours post-infection.
    • These structures contained filamentous actin, confirmed by fluorescent phalloidin staining.
    • Microvillus formation decreased in chick embryo fibroblasts by 12 hours post-infection.
    • Virus titer increased significantly at 24 hours, suggesting microvilli were not involved in virus release.
    • Inhibitors of DNA and protein synthesis blocked microvilli induction, indicating a late viral function.
    • N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine inhibited microvillus formation in chick embryo fibroblasts but not Vero cells, without affecting virus replication.

    Conclusions:

    • Herpes simplex virus infection induces actin-containing microvillus structures on host cells via a late viral function.
    • These virus-induced microvilli are unlikely to play a role in the release of infectious virions.
    • The differential effect of N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine suggests cell-type specific mechanisms in microvillus formation and potential anticellular drug activity.