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中国仓鼠卵巢细胞的蓖麻毒素抗性突变体对新城疫病毒诱导的融合不敏感。

Insensitivity of a ricin-resistant mutant of Chinese hamster ovary cells to fusion induced by Newcastle disease virus.

作者信息

Polos P G, Gallaher W R

出版信息

J Virol. 1979 Apr;30(1):69-75. doi: 10.1128/JVI.30.1.69-75.1979.

Abstract

The role of membrane components in the interaction of cells with Newcastle disease virus (NDV) was studied using a ricin-resistant mutant of Chinese hamster ovary cells (CHO-15B), in which there is a deficiency in distal saccharides at the plasma membrane. Compared to the parental wild type, the mutant was shown to be 4- to 10-fold less sensitive to either fusion from without or fusion from within induced by NDV. The mutant and wild type were nearly indistinguishable with respect to other interactions with NDV. Viral attachment was investigated with 125I-labeled NDV and found to be comparable in both lines. Functionally equivalent amounts of hemagglutinin were produced, as measured by the fraction of cells positive for hemadsorption, or by the number of erythrocytes adsorbed per cell. No significant differences in the morphogenesis or yield of progeny virus were seen. The ability of the mutant to produce a fusion factor was measured by transfer of infected cells to uninfected monolayers. Infected CHO-15B cells were capable of inducing fusion normally in the indicator wild-type monolayers, but were incapable of inducing fusion in mutant monolayers. These results suggest that the insensitivity of the CHO-15B mutants to fusion may be due to inhibition of an early virus-cell interaction subsequent to viral attachment, whereas other events in infection appear to be unaffected by the cell surface mutation.

摘要

利用对蓖麻毒素具有抗性的中国仓鼠卵巢细胞(CHO-15B)突变体研究了膜成分在细胞与新城疫病毒(NDV)相互作用中的作用,该突变体的质膜远端糖类存在缺陷。与亲代野生型相比,该突变体对NDV诱导的细胞外融合或细胞内融合的敏感性降低了4至10倍。就与NDV的其他相互作用而言,突变体和野生型几乎没有区别。用125I标记的NDV研究病毒附着,发现两条细胞系中的情况相当。通过血细胞吸附阳性细胞的比例或每个细胞吸附的红细胞数量来衡量,产生的血凝素功能等效量相同。子代病毒的形态发生或产量没有显著差异。通过将感染细胞转移到未感染的单层细胞中来测量突变体产生融合因子的能力。感染的CHO-15B细胞能够在指示野生型单层细胞中正常诱导融合,但在突变体单层细胞中不能诱导融合。这些结果表明,CHO-15B突变体对融合不敏感可能是由于病毒附着后早期病毒-细胞相互作用受到抑制,而感染中的其他事件似乎不受细胞表面突变的影响。

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