Characterization of the infection of Aedes albopictus cell clones by Sindbis virus
Characterization of the infection of Aedes albopictus cell clones by Sindbis virus
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DOI：
10.1016/s0168-1702(97)01461-5
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发表时间：
1997-07-01
期刊：
影响因子：
5
通讯作者：
Brown, DT
中科院分区：
文献类型：
--
作者：
Karpf, AR;Blake, JM;Brown, DT
我们调查了白纹伊蚊(蚊子)细胞克隆感染辛德比斯病毒的情况。感染的多重性(MOI)在50-0.00005 pfu/cell的范围内的变化被确定对感染进展到高急性期滴度没有影响，这表明当感染进入持续阶段时，细胞内因素单独负责限制病毒的产生。虽然持续感染(感染后1年以上)的细胞克隆在形态上与未感染的细胞不同，但与同一克隆的未感染的细胞相比，它们的生长速度一致地降低了30%。利用基于流式细胞仪的DNA含量分析，我们发现Sindbis病毒的持续感染会对这些细胞产生明显的细胞学影响，包括一个克隆的细胞凋亡率和多倍体增加，另一个克隆的细胞周期时相影响。最后，观察到持续感染的细胞培养物中被生产性感染的细胞数量接近于因凋亡而死亡的细胞数量，这促使我们研究细胞死亡在维持持续感染中可能发挥的作用。持续感染的细胞培养物通过45摄氏度的短热处理人工诱导细胞凋亡，但没有表现出辛德比斯病毒产量的增加。这一结果不支持持续感染细胞培养物中随机凋亡诱导的感染敏感性是持续感染的长期维持的假说。(C)1997年爱思唯尔科学公司。
We have investigated the infection of Aedes albopictus (mosquito) cell clones by Sindbis virus. Variation in the multiplicity of infection (MOI) from ranges of 50-0.00005 pfu/cell was determined to have no effect on the progression of the infection to high acute phase titer, suggesting that intracellular factors alone are responsible for the restriction of virus production seen as the infection enters the persistent phase. While persistently infected (over 1 year post infection) cell clones are morphologically indistinct from uninfected cells, they do display a uniform 30% reduction in growth rate compared with uninfected cells of the same clone. Using flow cytometry-based DNA content analysis, we found that persistent Sindbis virus infection induces distinct cytological effects on these cells, including an increase in apoptosis and polyploidy in one clone and cell cycle phase effects in another. Finally, the observation that the number of cells in persistently infected cell cultures which are productively infected closely approximates the number of cells dying by apoptosis prompted us to investigate the role that cell death may play in the maintenance of the persistent infection. Persistently infected cell cultures which were artificially induced into apoptosis by short 45 degrees C heat treatments do not display increased Sindbis virus production. This result does not support the hypothesis that infection sensitivity induced by random apoptosis in persistently infected cell cultures is responsible for the long-term maintenance of the persistent infection. (C) 1997 Elsevier Science B.V.