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首页> 外文期刊>Virology >Cultures of HEp-2 cells persistently infected by human respiratory syncytial virus differ in chemokine expression and resistance to apoptosis as compared to lytic infections of the same cell type.
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Cultures of HEp-2 cells persistently infected by human respiratory syncytial virus differ in chemokine expression and resistance to apoptosis as compared to lytic infections of the same cell type.

机译：与相同细胞类型的溶解性感染相比，被人呼吸道合胞病毒持续感染的HEp-2细胞培养物的趋化因子表达和对细胞凋亡的抵抗力不同。

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摘要

HEp-2 cells that survived a lytic infection with Human Respiratory Syncytial Virus (HRSV) were grown to obtain a persistently infected culture that produced relatively high amounts of virus (10(6)-10(7) pfu/ml) for more than twenty passages. The cells in this culture were heterogeneous with regard to the expression of viral antigens, ranging from high to undetectable levels. However, all cell clones derived from the persistent culture did not produce infectious virus or viral antigens and grew more slowly than the original uninfected HEp-2 cells. When these "cured" cell clones were infected with wild-type HRSV, delayed virus production and reduction in the number and size of syncytia were observed compared to lytically infected HEp-2 cells. Most significantly, differences in gene expression between persistently and lytically infected cultures were also observed, including genes that encode for cytokines, chemokines and other gene products that either promote cell survival or inhibit apoptosis. These results highlight the significantly different responses of the same cell type to HRSV infection depending on the outcome of such infection, i.e., lytic versus persistent.
机译：使在人类呼吸道合胞病毒（HRSV）裂解性感染后存活下来的HEp-2细胞生长，以获得持续感染的培养物，该培养物产生相对大量的病毒（10（6）-10（7）pfu / ml）超过二十种段落。就病毒抗原的表达而言，这种培养物中的细胞是异质的，范围从高到不可检测。但是，所有源自持续培养的细胞克隆均不产生传染性病毒或病毒抗原，并且比原始未感染的HEp-2细胞生长更慢。当这些“治愈”的细胞克隆被野生型HRSV感染时，与裂解感染的HEp-2细胞相比，病毒的产生被延迟，合胞体的数量和大小减少。最重要的是，还观察到持续感染和溶菌感染的培养物之间基因表达的差异，包括编码细胞因子，趋化因子的基因以及其他能促进细胞存活或抑制细胞凋亡的基因产物。这些结果凸显了相同细胞类型对HRSV感染的显着不同的反应，这取决于这种感染的结果，即裂解性还是持久性。

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