Abstract
Historically, the indications that herpes simplex virus (HSV) strains may vary considerably emerged many years ago (Ashe and Scherp 1965; Hampar and Burroughs 1969). For one of us (BR), the studies on the variability of HSV began with a chance isolation of a mutant [HSV-1 (MP)] that fused cells into polykaryocytes from a wild type virus [HSV-l (mP)] which caused cells to round and clump (Hoggan and Roizman 1959). Subsequent studies showed that the parent and mutant differed with respect to buoyant density in CsCl gradients (Roizman and Roane 1961), affinity chromatography (Roizman and Roane 1963), neutralization with specific antisera (Roizman and Roane 1963), the ability to accumulate glycoprotein VP8(gC) (Heine et al. 1974) and, ultimately, with respect to several genetic loci concerned with cell fusion in addition to accumulation of glycoprotein VP8(gC) (Ruyechan et al. 1979). The discovery that HSV represents two viruses, HSV-1 and HSV-2 (Schneweiss 1962; Dowdle et al. 1967), and studies on isolates and mutants of each (Ejercito et al. 1968; Heine et al. 1974; Seth etal. 1974; Terni and Roizman 1970), reinforced the hypothesis that HSV strains vary in a number of characteristics.
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Roizman, B., Tognon, M. (1983). Restriction Endonuclease Patterns of Herpes Simplex Virus DNA: Application to Diagnosis and Molecular Epidemiology. In: Bachmann, P.A. (eds) New Developments in Diagnostic Virology. Current Topics in Microbiology and Immunology, vol 104. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-68949-9_17
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DOI: https://doi.org/10.1007/978-3-642-68949-9_17
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