Evidence that deficient IFN- γ production is a biological basis of herpes simplex virus type-2 neurovirulence

Although immune response control of herpes simplex virus (HSV) has been well demonstrated, numerous HSV-2 strains are neurovirulent in immunocompetent mice. Using an RNase protection assay and an ELISA, we found that HSV-2-infected mice exhibited a deficient IFN- γ response, an inability to clear vi...

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Bibliographic Details
Published in:Journal of neuroimmunology 1998, Vol.81 (1), p.66-75
Main Authors: Lewandowski, Gail, Hobbs, Monte, Geller, Alfred
Format: Article
Language:English
Subjects:
Animals
Brain
Brain - metabolism
Brain - virology
Cell Death
Encephalitis, Viral - physiopathology
Gene therapy
Herpes Simplex - physiopathology
Immunosuppression
Interferon-gamma - deficiency
Interferon-gamma - physiology
Lethal Dose 50
Mice
Mice, Inbred BALB C
Nerve Tissue Proteins - deficiency
Nerve Tissue Proteins - physiology
Neural-immune
Neuropathogenesis
RNA, Messenger - biosynthesis
Simplexvirus - isolation & purification
Simplexvirus - pathogenicity
Simplexvirus - physiology
Transduction, Genetic
Virulence
Virus Replication
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Summary:Although immune response control of herpes simplex virus (HSV) has been well demonstrated, numerous HSV-2 strains are neurovirulent in immunocompetent mice. Using an RNase protection assay and an ELISA, we found that HSV-2-infected mice exhibited a deficient IFN- γ response, an inability to clear virus, and eventual death. An HSV-based amplicon vector expressing mouse IFN- γ was constructed and packaged into HSV-1-helper virus (HSV(pIFN- γ)). In mice treated with HSV(pIFN- γ), (i) the LD 50 of HSV-2(G) increased 5000-fold, (ii) intracerebral IFN- γ expression increased 10-fold, and (iii) HSV titer rapidly decreased. We suggest that the deficient IFN- γ response is a basis for HSV-2 neurovirulence in mice.
ISSN:0165-5728
1872-8421
DOI:10.1016/S0165-5728(97)00160-4