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Giant cell-forming variants of the Miyama strain of type 1 herpes simplex virus which differ in fusion activity
Abstract:
During serial passages of a non-giant cell-forming variant (-GCr) of the Miyama strain of type 1 herpes simplex virus, a new giant cell-forming variant named +GC(81) was isolated. CPE induced by this isolate was compared with that by -GCr and also by +GC(LPV), a derivative strain of the +GC variant of the Miyama strain. Rounding of single cells was observed after infection with -GCr. Remarkable syncytial formation was induced by +GC(LPV), the syncytia containing hundreds of nuclei, while small giant cells were formed by +GC(81). The reason for the appearance of +GC variants that differ in fusion capacity is discussed.
Insights
A new variant of herpes simplex virus type 1, +GC(81), was isolated. This variant forms small giant cells, unlike other strains that cause cell rounding or large syncytia.
Area of Science:
- Virology
- Cell Biology
Background:
- Herpes simplex virus (HSV) exhibits strain-dependent variations in cytopathic effects (CPE).
- Previous studies identified giant cell-forming variants of HSV, but their fusion capacities differ.
Purpose of the Study:
- To isolate and characterize a novel giant cell-forming variant of HSV type 1.
- To compare the CPE induced by the new variant with existing strains, focusing on cell fusion.
Main Methods:
- Serial passages of a non-giant cell-forming HSV-1 variant (-GCr).
- Isolation and characterization of a new giant cell-forming variant (+GC(81)).
- Comparative analysis of CPE induced by -GCr, +GC(81), and a known giant cell-forming strain (+GC(LPV)).
Main Results:
- Infection with -GCr resulted in single-cell rounding.
- +GC(LPV) induced remarkable syncytial formation with hundreds of nuclei.
- +GC(81) specifically formed small giant cells.
Conclusions:
- A novel HSV-1 variant, +GC(81), was successfully isolated, exhibiting distinct giant cell formation.
- The study highlights variations in fusion capacity among HSV-1 giant cell variants.
- Further investigation is warranted to understand the genetic and molecular basis for these differences in viral fusion.