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HIV-1 induced decrease of nitric oxide production and inducible nitric oxide synthase expression during in vivo and in vitro infection.

机译:在体内和体外感染期间,HIV-1导致一氧化氮生成量减少和诱导型一氧化氮合酶表达降低。

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摘要

Nitric oxide (*NO) has been implicated in immunopathogenesis of HIV-1 infection. Initial reports using low sensitive techniques showed elevated levels of *NO in sera and tissues from seropositive patients. These results were not further supported using similar experimental approaches. To gain insight on *NO deregulation during HIV-1 infection, we used recently described fluorescent probes with enhanced sensitivity to assess *NO levels combined with iNOS mRNA expression in peripheral blood mononuclear cells (PBMC) from HIV-infected patients or after in vitro HIV-1 infection of normal cells. We demonstrate that PBMC from HIV-infected patients display a significant decrease of *NO production and iNOS mRNA expression. Results from in vitro infection showed that HIV-1 induces a significant decrease in *NO production and iNOS mRNA expression. Since *NO could play a role in some key processes like apoptosis, regulation of immune responses and viral replication, these results could help in elucidating HIV-1 immunopathogenesis.
机译:一氧化氮(* NO)与HIV-1感染的免疫发病机制有关。使用低敏感性技术的初步报告显示,血清阳性患者血清和组织中* NO含量升高。使用类似的实验方法无法进一步支持这些结果。为了深入了解HIV-1感染期间的* NO失控,我们使用了最近描述的荧光探针,具有更高的灵敏度来评估HIV感染患者或体外HIV后外周血单个核细胞(PBMC)中的* NO水平与iNOS mRNA表达的组合-1感染正常细胞。我们证明,来自HIV感染患者的PBMC显示* NO产生和iNOS mRNA表达显着降低。体外感染的结果表明,HIV-1导致* NO生成和iNOS mRNA表达显着降低。由于* NO可能在某些关键过程中发挥作用,例如凋亡,免疫应答调节和病毒复制,因此这些结果可能有助于阐明HIV-1免疫发病机制。

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