Injection of Anti-thy-1.2 Serum Breaks Genetic Resistance of Mice against Herpes Simplex Virus

Chmielarczyk, W.; Engler, Helmut; Ernst, R.; Opitz, Uta; Kirchner, Holger

doi:10.1099/0022-1317-66-5-1087

Cited by 15 publications

(6 citation statements)

References 19 publications

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“…The former observation suggests that NK cells are not required for the development of ocular inflammation. The latter results agree with the view that asialo GM1+ cells contribute to host resistance to HSV-1 infection, a concept for which there has been both support (7,18,27) and disagreement (1,3,33). Administration of anti-gD MAb to asialo GM1+ cell-depleted hosts proved to be strikingly effective in that both stromal and CNS disease were prevented.…”

Section: Discussionsupporting

confidence: 88%

Anti-glycoprotein D monoclonal antibody protects against herpes simplex virus type 1-induced diseases in mice functionally depleted of selected T-cell subsets or asialo GM1+ cells

Staats

Oakes

Lausch

1991

J Virol

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Passive transfer of a monoclonal antibody (MAb) specific for glycoprotein D (gD) is highly effective in preventing the development of herpes simplex virus type 1-induced stromal keratitis. In the present study, we investigated whether animals which had been functionally depleted of T-cell subsets or asialo GM1+ cells would continue to be responsive to MAb therapy. BALB/c mice were depleted of CD4+, CD8+, or asialo GM1+ cells by treatment with anti-L3T4, anti-Lyt 2.2, or anti-asialo GM1 antibodies, respectively. Functional depletion of CD4+ cells was documented by the loss of delayed-type hypersensitivity responsiveness, while CD8+ cell depletion was accompanied by abrogation of cytotoxic lymphocyte activity. Anti-asialo GM1 treatment led to the loss of natural killer cell lytic activity. Mice depleted of the desired cell population and infected on the scarified cornea with herpes simplex virus type 1 uniformly developed necrotizing stromal keratitis by 3 weeks postinfection. A single inoculation of anti-gD MAb (55 ,ug) given intraperitoneally 24 h postinfection strongly protected hosts depleted of CD4+ cells against stromal keratitis. Likewise, antibody treatment in CD8+ or asialo GM1+ cell-depleted hosts was as therapeutically effective as that seen in non-cell-depleted mice. We also observed that in cell-depleted mice, the virus spread into the central nervous system and caused encephalitis. The CD4+ cell-depleted mice were the most severely affected, as 100% developed fatal disease. Anti-gD MAb treatment successfully protected all (32 of 32) CD4+-, CD8+-, or asialo GM1-depleted hosts against encephalitis. We therefore conclude that antibody-mediated prevention of stromal keratitis and encephalitis does not require the obligatory participation of CD4+, CD8+, or asialo GM1+ cells. However, when mice were * Corresponding author.

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Section: Discussionsupporting

confidence: 88%

Anti-glycoprotein D monoclonal antibody protects against herpes simplex virus type 1-induced diseases in mice functionally depleted of selected T-cell subsets or asialo GM1+ cells

Staats

Oakes

Lausch

1991

J Virol

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“…Based on these observations, it is not evident that the allelic differences between the C57BL/6 and BALB/c genetic backgrounds have an appreciable effect on the innate resistance of scid mice to HSV-1 infection, replication, spread, or pathogenesis. This corroborates earlier findings that the resistance of C57BL/6 mice to HSV-1 pathogenesis is absolutely dependent on both (i) the development of a rapid IFN-␣/␤ response (64,65) and (ii) T-lymphocyte-mediated suppression of HSV-1 replication in infected tissues between days 5 and 7 after inoculation (11,54).…”

Section: Discussionsupporting

confidence: 79%

Re-Evaluating Natural Resistance to Herpes Simplex Virus Type 1

Halford

Balliet

Gebhardt

2004

J Virol

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It is often stated that individuals of a species can differ significantly in their innate resistance to infection with herpes simplex virus type 1 (HSV-1). Three decades ago Lopez reported that C57BL/6 mice could survive a 5,000-fold-higher inoculum of HSV-1 given intraperitoneally than mice of the A or BALB/c strain (Nature 258:152-153, 1975). Susceptible strains of mice died of encephalitis-like symptoms, suggesting that viral spread to the central nervous system was the cause of death. Although Lopez's study documented that C57BL/6 mice were resistant to the development of HSV-1 encephalitis and mortality, the resistance of C57BL/6 mice to other steps of the HSV-1 infection process was not assessed. The results of the present study extend these observations to clarify the difference between resistance to (i) HSV-1 pathogenesis, (ii) HSV-1 replication, (iii) HSV-1 spread, and (iv) the establishment of latent HSV-1 infection. Although C57BL/6 mice are more resistant to HSV-1 pathogenesis than BALB/c mice, the results of the present study establish that HSV-1 enters, replicates, spreads, and establishes latent infections with virtually identical efficiencies in C57BL/6 and BALB/c mice. These observations raise questions about the validity of the inference that differences in natural resistance are relevant in explaining what differentiates humans with recurrent herpetic disease from the vast majority of asymptomatic carriers of HSV-1 and HSV-2.

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“…For these purposes, we chose nude mice for this experiment as they lack T immunity but are present with NK cell and B cell immunity (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

AAV2-mediated interleukin-12 in the treatment of malignant brain tumors through activation of NK cells

et al. 2009

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Abstract. Interleukin-12 has been elucidated as a powerful anti-cancer factor in pre-clinical research. However, the obstacles of this modality that emerged from human clinical trails included the toxicity of repeated large dose administration and short effective duration. Therefore, a prolonged, constant therapeutic level of interleukin-12 is required to reduce the adverse effects and enhance the therapeutic efficacy. In this study, 54 nude mice were divided into three groups treated with rAAV2 encoding interleukin-12, rAAV2 vector, and PBS, respectively. All nude mice received human glioblastoma multiforme cell line DBTRG implantation. The biochemistry studies included serum levels of interleukin-12, isotypes of immunoglobulin, interferon-Á, and TNF-·. The activated NK cells were sorted from the spleen by flow cytometry and the cytotoxicity of NK cells were evaluated by LDH assay. In the rAAV2 encoding interleukin-12 group, substantial expression of interleukin-12 was obtained with a serum level of 120-150 pg/ml through the experimental course and a significant increase of activated NK cells was achieved. The splenocytes extracted from the spleen in rAAV2 encoding IL-12 mice strongly exhibited cytotoxic activity compared to the control groups (p<0.001). The IgG1, IgG2a, and IgM also showed a significant increase in the rAAV2 encoding IL-12 group compared to the control groups (p<0.05). The tumor growth rate decreased obviously in the rAAV2 encoding IL-12 group with a significant difference from the control groups (p<0.001). This study demonstrated an encouraging result of immunomodulative therapy in malignant brain tumors by rAAV2 carrying IL-12 through activating NK cells.

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Injection of Anti-thy-1.2 Serum Breaks Genetic Resistance of Mice against Herpes Simplex Virus

Cited by 15 publications

References 19 publications

Anti-glycoprotein D monoclonal antibody protects against herpes simplex virus type 1-induced diseases in mice functionally depleted of selected T-cell subsets or asialo GM1+ cells

Anti-glycoprotein D monoclonal antibody protects against herpes simplex virus type 1-induced diseases in mice functionally depleted of selected T-cell subsets or asialo GM1+ cells

Re-Evaluating Natural Resistance to Herpes Simplex Virus Type 1

AAV2-mediated interleukin-12 in the treatment of malignant brain tumors through activation of NK cells

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