Protection from lethal herpes simplex virus type 1 infection by vaccination with a UL41-deficient recombinant strain.
Fukushima J Med Sci
; 62(1): 36-42, 2016 Jun 08.
Article
em En
| MEDLINE
| ID: mdl-26983589
UNLABELLED: The UL41 gene of herpes simplex virus type 1 (HSV-1) encodes a virion host shut off protein which is involved in immune evasion.ãThe growth and virulence of HSV-1 is markedly reduced by the deletion of UL41.ãIn this report, the UL41-deleted recombinant HSV-1 strain VR∆41 was evaluated as a prophylactic live attenuated vaccine against lethal HSV-1 infection in a mouse model.ãIntraperitoneal (i.p.) inoculation with the VR∆41 strain clearly inhibited lethal wild-type HSV-1 (VR-3 strain) infection after both i.p. and intracerebral (i.c.) inoculations.ãVaccination with the VR∆41 strain was safer than VR-3 vaccination and was able to protect against a wild-type challenge to the same degree as VR-3 vaccination.ãIn contrast, i.p. inoculation with ultraviolet-irradiated VR-3 induced resistance against i.p. infection, but not against i.c. INFECTION: Although replication of the VR∆41 strain in mice was greatly reduced compared to that of the VR-3 strain, VR∆41 strain maintained the ability to spread to the central nervous system (CNS) from a peripheral inoculation site. These results indicated that the VR∆41 strain evoked a potent immune reaction through viral protein expression within CNS without the induction of lethal encephalitis.ãThe entry of antigens into the CNS was essential for the establishment of protective immunity against the lethal HSV encephalitis.ãWe concluded that only a live attenuated vaccine is able to afford a prophylactic effect against CNS infection with HSV.ãIn order to fulfill this requirement, UL41-deleted viruses provide a strong candidate for use as a recombinant live vaccine.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Virais
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Vacinas Virais
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Vacinação
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Herpesvirus Humano 1
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Herpes Simples
Limite:
Animals
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Female
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Humans
Idioma:
En
Ano de publicação:
2016
Tipo de documento:
Article