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 in | The Journal of infectious diseases Vol. 170; no. 5; pp. 1100 - 1109 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
The University of Chicago Press
01.11.1994
University of Chicago Press |
Subjects | |
Online Access | Get full text |
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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. |
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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 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-1899 1537-6613 |
DOI: | 10.1093/infdis/170.5.1100 |