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作 者:沙文琼[1] 孙晗笑[1] 张光[1] 莫雪梅[1] 郭钦丽[1]
机构地区:[1]暨南大学药学院基因组药物研究所,广州510632
出 处:《天津医药》2005年第11期713-715,T0002,共4页Tianjin Medical Journal
基 金:国家863计划资助项目(项目编号:2001AA215271)
摘 要:目的:研究重组病毒巨噬细胞炎性蛋白(rvMIP)体外的抗HIV-1SF1作用效果和机制。方法:分别在HIV-1SF1接种前后将敏感的MT-4细胞系与rvMIP作用,检测MT-4细胞系病变情况和培养上清的P24抗原水平,用有限稀释PCR法测定前病毒DNA水平。结果:预先用rvMIP处理过的细胞,病毒感染后细胞病变程度很轻,培养上清的P24抗原和前病毒水平明显低于对照组,P24抗原抑制率可达90%;先感染病毒再用rvMIP处理组病毒P24抗原水平和细胞内前病毒DNA水平也显著降低,但降低程度不如先用rvMIP预处理组。结论:rvMIP能阻止病毒进入靶细胞,同时可能也通过某种机制抑制已感染细胞HIV病毒的复制。Objective: To investigate the inhibiting effects and mechanism of recombinant viral macrophage inflammation protein rvMIP against HIV-1SF1 out of the body. Methods: The sensible MT-4 cells were cultured with the rvMIP before and after being immunized with HIV-1SF1. The pathological changes of MT-4 cells were observed after immunization and the P24 antigen in the culture supernatant was determined as well as HIV-1SF1 proviral DNA level within cells was tested by using limited diluting methods. Results: The cells pretreated with rvMIP only had little pathological changes. The P24 antigen level in supernatant and the proviral DNA level decreased markedly, with a highest P24 antigen inhibitory rate of 90%. The cells treated with rvMIP after infection also had a decrease of P24 antigen and proviral DNA level but both of all were less than pretreated cells. Conclusion: The main mechanism of rvMIP is to prevent virus'entry .Meanwhile,it may also depress the replication of infected cell HIV through a kind of mechanism.
关 键 词:巨噬细胞炎性蛋白质类 感染 病毒复制 巨噬细胞炎性蛋白 体外抑制作用 重组病毒 P24抗原 DNA水平 病毒感染后 抗原水平
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