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Infection and Immunity of Herpes Simplex Virusin the Culture System sof Lym phocytes and Monocyte-Macrophages

Infection and Immunity of Herpes Simplex Virus in the Culture Systems of Lymphocytes and Monocyte Macrophages
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摘要 The study was made by the method of experimental infection using cultured cells in vitro. The characteristic of HSV infection of the cells and the effects of immunity factors on the infection were analyzed by cytopathic effect, double antibodies sandwich ELISA for immunoglobulin yield, hemolytic plaque assay for specific SRBC antibody forming cells, microcytopathy assay for viral titer, IFA for viral antigen and PCR for viral DNA.The results were as follows: ①A series of models of HSV infection were established, including the model of HSV 1 persistent infection of Raji cells, the model of acute and cytocidal HSV 1 infection of HSB\-2 cells, the models of temporary persistent HSV 1 infection of LPS stimulated U\-\{937\} cells and murine peritoneal macrophages and the models of inhibitions both of IgG synthesis and specific SRBC antibody production by HSV 1 infection of human tonsillar lymphocytes activated by PWM stimulating. ②According to the characteristic of HSV infection of lymphocyte and monocyte macrophage, it was reasonable that stimulating with antigen, mitogen, LPS, or inflammatory factors might make lymphocytes and/or monocyte macrophages become permissive cells of replicative HSV infection, or might activate the latent virus, resulting in HSV dissemination by blood circulation. ③It was proved that IFN α, IFN γ, TNF, M CSF, GM CSF and IL 3 have an inhibitory effect on HSV replication in lymphocyte and monocyte macrophage, respectively and reversed the replicative enhancement activity of LPS, suggesting that applications of these immunity factors favour lymphocytes and monocyte macrophages with a resistance to HSV replicative infection and with an inhibition of latent virus reactivation in vivo, and therefore, it might be helpful for preventing the virus from dissemination by blood circulation.\; The study was made by the method of experimental infection using cultured cells in vitro. The characteristic of HSV infection of the cells and the effects of immunity factors on the infection were analyzed by cytopathic effect, double antibodies sandwich ELISA for immunoglobulin yield, hemolytic plaque assay for specific SRBC antibody forming cells, microcytopathy assay for viral titer, IFA for viral antigen and PCR for viral DNA.The results were as follows: ①A series of models of HSV infection were established, including the model of HSV 1 persistent infection of Raji cells, the model of acute and cytocidal HSV 1 infection of HSB\-2 cells, the models of temporary persistent HSV 1 infection of LPS stimulated U\-\{937\} cells and murine peritoneal macrophages and the models of inhibitions both of IgG synthesis and specific SRBC antibody production by HSV 1 infection of human tonsillar lymphocytes activated by PWM stimulating. ②According to the characteristic of HSV infection of lymphocyte and monocyte macrophage, it was reasonable that stimulating with antigen, mitogen, LPS, or inflammatory factors might make lymphocytes and/or monocyte macrophages become permissive cells of replicative HSV infection, or might activate the latent virus, resulting in HSV dissemination by blood circulation. ③It was proved that IFN α, IFN γ, TNF, M CSF, GM CSF and IL 3 have an inhibitory effect on HSV replication in lymphocyte and monocyte macrophage, respectively and reversed the replicative enhancement activity of LPS, suggesting that applications of these immunity factors favour lymphocytes and monocyte macrophages with a resistance to HSV replicative infection and with an inhibition of latent virus reactivation in vivo, and therefore, it might be helpful for preventing the virus from dissemination by blood circulation.\;
出处 《The Journal of Biomedical Research》 CAS 1999年第2期98-102,共5页 生物医学研究杂志(英文版)
关键词 herpes simplex virus LYMPHOCYTE monocyte macrophage INFECTION IMMUNITY herpes simplex virus lymphocyte monocyte macrophage infection immunity
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