Protective Vaccination Against Primary And Recurrent Disease Caused By Herpes Simplex Virus (HSV) Type 2 Using A Genetically Disabled HSV-1

The vaccine potential of a mutant herpes simplex virus (HSV) type 1, with a deletion in the glycoprotein H (gH) gene, was evaluated. The virus requires a gH-expressing cell line for multi-cycle growth but can complete a single cycle of infection in noncomplementing cells. Such viruses, termed DISC (...

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Published inThe Journal of infectious diseases Vol. 170; no. 5; pp. 1100 - 1109
Main Authors Mclean, C. S., Erturk, M., Jennings, R., Ni Challanain, D., Minson, A. C., Duncan, I., Boursnell, M. E. G., Inglis, S. C.
Format Journal Article
LanguageEnglish
Published United States The University of Chicago Press 01.11.1994
University of Chicago Press
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Summary:The vaccine potential of a mutant herpes simplex virus (HSV) type 1, with a deletion in the glycoprotein H (gH) gene, was evaluated. The virus requires a gH-expressing cell line for multi-cycle growth but can complete a single cycle of infection in noncomplementing cells. Such viruses, termed DISC (disabled infectious single cycle) viruses, should be safe, yet still able to stimulate humoral and cell-mediated responses against a broad range of virus antigens in vaccinated hosts. Prophylactic vaccination of guinea pigs with DISC HSV-1, by ear scarification or direct infection of the vaginal mucosa, afforded a high degree of protection against HSV-2-induced primary genital disease and reduced significantly the frequency of subsequent disease recurrence. There was also a trend toward reduced recurrence following therapeutic vaccination of animals already infected with HSV-2. DISC HSV vaccination, therefore, offers an effective route for control of HSV disease.
Bibliography:ark:/67375/HXZ-LCHJB4MC-J
istex:AEBBE9EEC3A24AFD4DCE01A6B22E2143E80DD34F
Reprints or correspondence: Dr. S. C. Inglis, Cantab Pharmaceuticals Research Ltd., Cambridge Science Park, Cambridge, UK CB4 4GN.
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/170.5.1100