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淋巴细胞性脉络丛脑膜炎病毒感染中宿主细胞依赖性同源干扰

Host cell-dependent homologous interference in lymphocytic choriomeningitis virus infection.

作者信息

Bruns M, Gessner A, Lother H, Lehmann-Grube F

机构信息

Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Universität Hamburg, Federal Republic of Germany.

出版信息

Virology. 1988 Sep;166(1):133-9. doi: 10.1016/0042-6822(88)90154-7.

DOI:10.1016/0042-6822(88)90154-7
PMID:3413982
Abstract

The generation of virus progeny as well as transcription, translation, and replication of the viral small RNA (S-RNA), which codes for the nucleoprotein (NP) and the glycoprotein precursor (GPC), was followed in L and MDCK cells after infection with multiplicities (m.o.i.) ranging from 0.01 to 100. In L cells, the yields of both plaque-forming units and interfering particles varied inversely with the m.o.i. Northern blot analysis revealed that early after infection with high multiplicity NP-mRNA was present, but later few or no signals of any specificity were registered. After low m.o.i. the results were negative at 8 hr, but large quantities of mRNAs for NP and GPC as well as viral genomic S-RNA and genomic-sized complementary S-RNA had been synthesized at 48 hr. In MDCK cells, throughout the range of m.o.i. both entities attained lower levels and most were generated at m.o.i. one. The degree of hybridization correlated roughly with the quantity of infectious virus to which the cells had been exposed. In the cells of both lines the NP-mRNA corresponded to the synthesis of its translation product, but once produced, most of it appeared to be retained in the phosphorylated form. We assume that the homologous interference seen in L cells after infection with high m.o.i. results from a host-dependent inhibition of viral transcription and replication mediated by NP.

摘要

在以0.01至100的感染复数(m.o.i.)感染L细胞和MDCK细胞后,追踪了病毒子代的产生以及病毒小RNA(S-RNA)的转录、翻译和复制情况,该病毒小RNA编码核蛋白(NP)和糖蛋白前体(GPC)。在L细胞中,噬斑形成单位和干扰颗粒的产量均与感染复数呈反比。Northern印迹分析显示,高感染复数感染后早期存在NP-mRNA,但后期几乎没有或没有任何特异性信号。低感染复数时,8小时结果为阴性,但在48小时时已合成了大量的NP和GPC的mRNA以及病毒基因组S-RNA和基因组大小的互补S-RNA。在MDCK细胞中,在整个感染复数范围内,这两种物质的水平都较低,且大多数在感染复数为1时产生。杂交程度大致与细胞所接触的感染性病毒量相关。在这两种细胞系的细胞中,NP-mRNA与其翻译产物的合成相对应,但一旦产生,其大部分似乎以磷酸化形式保留。我们推测,高感染复数感染L细胞后出现的同源干扰是由NP介导的宿主依赖性病毒转录和复制抑制所致。

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Host cell-dependent homologous interference in lymphocytic choriomeningitis virus infection.淋巴细胞性脉络丛脑膜炎病毒感染中宿主细胞依赖性同源干扰
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Residues K465 and G467 within the Cytoplasmic Domain of GP2 Play a Critical Role in the Persistence of Lymphocytic Choriomeningitis Virus in Mice.GP2胞质结构域内的K465和G467残基在淋巴细胞性脉络丛脑膜炎病毒在小鼠体内的持续存在中起关键作用。
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