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, 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.
Muggeridge
Martin I
MI
Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA. mmugge@lsuhsc.edu
Grantham
Michael L
ML
Johnson
F Brent
FB
D000595:Amino Acid Sequence; D000818:Animals; D019556:COS Cells; D002522:Chlorocebus aethiops; D016572:Cyclosporine / Q000494:pharmacology; D015726:Giant Cells / Q000821:virology; D006558:Herpes Genitalis / Q000821:virology; D018258:Herpesvirus 2, Human / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification; D006801:Humans; D008969:Molecular Sequence Data; D009154:Mutation; D016415:Sequence Alignment; D014760:Viral Fusion Proteins / Q000235:genetics*; D010948:Viral Plaque Assay
D014760:Viral Fusion Proteins; D016572:Cyclosporine