Identification of syncytial mutations in a clinical isolate of herpes simplex virus 2

Small polykaryocytes resulting from cell fusion are found in herpes simplex virus (HSV) lesions in patients, but their significance for viral spread and pathogenesis is unclear. Although syncytial variants causing extensive fusion in tissue culture can be readily isolated from laboratory strains, th...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2004-10, Vol.328 (2), p.244-253
Main Authors: Muggeridge, Martin I., Grantham, Michael L., Johnson, F. Brent
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Amino Acid Sequence
Animals
Cercopithecus aethiops
COS Cells
Cyclosporin A
Cyclosporine - pharmacology
Giant Cells - virology
GLYCOPROTEINS
Herpes Genitalis - virology
HERPES SIMPLEX
Herpes simplex virus 2
Herpesvirus 2, Human - drug effects
Herpesvirus 2, Human - genetics
Herpesvirus 2, Human - isolation & purification
Humans
IN VITRO
IN VIVO
Molecular Sequence Data
Mutation
MUTATIONS
PATHOGENESIS
PATIENTS
Sequence Alignment
Syncytial mutations
TISSUE CULTURES
Viral Fusion Proteins - genetics
Viral Plaque Assay
VIRUSES
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Summary:Small polykaryocytes resulting from cell fusion are found in herpes simplex virus (HSV) lesions in patients, but their significance for viral spread and pathogenesis is unclear. Although syncytial variants causing extensive fusion in tissue culture can be readily isolated from laboratory strains, they are rarely found in clinical isolates, suggesting that extensive cell fusion may be deleterious in vivo. Syncytial mutations have previously been identified for several laboratory strains, but not for clinical isolates of HSV type 2. To address this deficiency, we studied a recent syncytial clinical isolate, finding it to be a mixture of two syncytial and one nonsyncytial strain. The two syncytial strains have novel mutations in glycoprotein B, and in vitro cell fusion assays confirmed that they are responsible for syncytium formation. This panel of clinical strains may be ideal for examining the effect of increased cell fusion on pathogenesis.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2004.07.027