Protection of Mice from Fatal Herpes Simplex Virus Type 1 Infection by Adoptive Transfer of Cloned Virus-specific and H-2-restricted Cytotoxic T Lymphocytes

Sethi, K. K.; Omata, Yoshitaka; Schneweis, K. E.

doi:10.1099/0022-1317-64-2-443

Cited by 137 publications

(62 citation statements)

References 14 publications

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“…The cellular immune response, especially virus-specific cytotoxic T lymphocytes (CTL), has been shown to represent a second important defence mechanism against certain virus infections (Ada & Jones, 1986;Byrne & Oldstone, 1984;Reddehase et al, 1988;Sethi et at., 1983;Yap et al, 1978). So far, only scarce information about cellular immunity to CSFV has been available.…”

Section: Introductionmentioning

confidence: 99%

Classical swine fever virus-specific cytotoxic T lymphocytes and identification of a T cell epitope

Pauly¹,

Elbers²,

König³

et al. 1995

Journal of General Virology

113

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Section: Introductionmentioning

confidence: 99%

Classical swine fever virus-specific cytotoxic T lymphocytes and identification of a T cell epitope

Pauly¹,

Elbers²,

König³

et al. 1995

Journal of General Virology

113

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“…Although systemic vaccination protocols lack sufficient efficacy at present for use against mucosal HSV-2 infections in humans, several in vivo and in vitro studies indicate that immunity to or recovery from primary systemic infection by HSV-2 is mediated by humoral and cellular effector mechanisms. The roles of antibodies (Balachandran et al, 1982a;Morahan et al, 1977;Simmons & Nash, 1985), complement (Shore et al, 1979), interferon (Engler et al, 1981;Fitzgerald & Lopez, 1982), macrophages (Morahan et al, 1980;Plaeger-Marshall et al, 1983), cytotoxic T cells (CTLs) (Larsen et al, 1983;Rosenthal et al, 1987;Sethi et al, 1983), natural killer cells (Engler et al, 1981;Fitzgerald & Lopez, 1982), and cells involved in delayed hypersensitivity reactions (Nash & Ashford, 1982;Nash & Gell, 1983;Nash et al, 1981) and regulatory activities (Leung et al, 1984;Nash & Ashford, 1982) have all been implicated in resistance to systemic HSV-2 infection.…”

Section: Introductionmentioning

confidence: 99%

Mucosal and systemic antiviral antibodies in mice inoculated intravaginally with herpes simplex virus type 2

McDermott

Brais

Evelegh

1990

Journal of General Virology

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Herpes simplex virus type 2 (HSV-2) causes lethal illness after intravaginal (IVAG) inoculation into BALB/cJ mice. In the present studies, we demonstrated in mice that primary IVAG vaccination with an attenuated strain of HSV-2 induced humoral immunity in sera and in vaginal secretions, Secondary genital exposure to HSV-2 enhanced this response. However, intraperitoneal exposure to attenuated HSV-2 elicited an antiviral antibody response in sera but not in vaginal secretions. In both sera and vaginal secretions, antiviral IgG antibodies were the major isotype. Systemic exposure to HSV-2 elicited antibodies only in sera that were specific for the major viral antigens whereas IVAG inoculation with HSV-2 stimulatedboth serum and vaginal antibody responses. Intravenous transfer of antiviral monoclonal antibodies protected against systemic HSV-2 infection but were ineffective against vaginal infection due to a lack of transudation into vaginal secretions. These results suggested that local humoral immunity in the genital tract is important in resistance to HSV-2.

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“…Nevertheless, herpes simplex virus triggers strong cellular and humoral immunity. In general, cell-mediated immune responses are particularly important for viral clearance, 56,59,60 as demonstrated by immunodepletion studies, 52,61 adoptive transfer experiments 53,[62][63][64] and human clinical trials. 60 It is intriguing that recurrent HSV-1 lesions can occur in the presence of both humoral and cell-mediated immunity, although duration of recurrent lesions is typically shortened compared to the original infection.…”

mentioning

confidence: 99%

Herpes simplex virus 1 (HSV-1) for cancer treatment

2006

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Cancer remains a serious threat to human health, causing over 500 000 deaths each year in US alone, exceeded only by heart diseases. Many new technologies are being developed to fight cancer, among which are gene therapies and oncolytic virotherapies. Herpes simplex virus type 1 (HSV-1) is a neurotropic DNA virus with many favorable properties both as a delivery vector for cancer therapeutic genes and as a backbone for oncolytic viruses. Herpes simplex virus type 1 is highly infectious, so HSV-1 vectors are efficient vehicles for the delivery of exogenous genetic materials to cells. The inherent cytotoxicity of this virus, if harnessed and made to be selective by genetic manipulations, makes this virus a good candidate for developing viral oncolytic approach. Furthermore, its large genome size, ability to infect cells with a high degree of efficiency, and the presence of an inherent replication controlling mechanism, the thymidine kinase gene, add to its potential capabilities. This review briefly summarizes the biology of HSV-1, examines various strategies that have been used to genetically modify the virus, and discusses preclinical as well as clinical results of the HSV-1-derived vectors in cancer treatment.

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Protection of Mice from Fatal Herpes Simplex Virus Type 1 Infection by Adoptive Transfer of Cloned Virus-specific and H-2-restricted Cytotoxic T Lymphocytes

Cited by 137 publications

References 14 publications

Classical swine fever virus-specific cytotoxic T lymphocytes and identification of a T cell epitope

Classical swine fever virus-specific cytotoxic T lymphocytes and identification of a T cell epitope

Mucosal and systemic antiviral antibodies in mice inoculated intravaginally with herpes simplex virus type 2

Herpes simplex virus 1 (HSV-1) for cancer treatment

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