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Herpes simplex virus-induced cell surface protrusions
Abstract:
Cell surface alterations following herpes simplex virus infection were studied by scanning electron microscopy at different times after infection of chick embryo fibroblasts and Vero cells. Beginning at 4 h, an increasing number of cells showed numerous microvillus protrusions 0.12-0.18 micron in diameter and 0.3 micron in length. These structures could also be stained on Vero cells with fluorescent phalloidin, indicating the presence of filamentous actin within them. At 12 h, the number of chick embryo fibroblasts with virus-induced microvillus-like structures began to decrease. There was an increase in virus titer in the medium beginning at 24 h, and it was therefore considered unlikely that the microvilli induced earlier had any function in virus release. Similar to poxvirus-induced microvilli formation, DNA and protein synthesis inhibitors prevented the induction of microvilli, indicating the involvement of a late viral function. N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine inhibited the formation of herpesvirus-induced microvilli in chick embryo fibroblasts but not in Vero cells. As this inhibitor had no effect on virus replication in either cell type, it is likely that the inhibition of microvillus formation was due to an anticellular activity of the drug.
Insights
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.
- 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.