Borzakian S, Couderc T, Barbier Y, Attal G, Pelletier I, Colbère-Garapin F
Unité de Virologie Médicale, Institut Pasteur, Paris, France.
Virology. 1992 Feb;186(2):398-408. doi: 10.1016/0042-6822(92)90005-a.
Mutants of poliovirus (PV) with highly modified biological properties can be selected in vitro in cells of neural origin. Mutations accumulate in the genome of type 1 PV strains selected in human neuroblastoma cells, modifying cell specificity and conferring to the virus the ability to persist in such nonneural cells as HEp-2c (Pelletier et al., Virology 180, 729 1991). With this cell system, we have both parent lytic strains and persistent PV mutants; these were used to study the mechanisms of the establishment and maintenance of the persistent infection. We found that a persistent infection was established when the lytic potential of the virus was reduced; this involved both an early and a late event of the virus cycle for the type 1 mutants. In contrast, maintenance of the infection did not correlate with the reduced lytic potential of the viruses, but rather with the selection of mutant cell populations of various phenotypes. Two cell lines, representative of two phenotypes, were studied in greater detail. In the first one, HEp-S32 (cl7), the PV receptor was not detected by cytofluorometry and viral genomes were detected by in situ hybridization in 2% of the cells. In the second cell line, HEp-S31 (cl18), 97% of the cells expressed the PV receptor, viral genomes were detected in 9-10% of the cells, and viral antigens in 5-10% of the cells. With this cell line, the cure of the culture or, alternatively, the lysis of the majority of cells, could be induced under specific culture conditions. We propose a model involving an equilibrium between an abortive and a lytic infection to explain the properties of cells persistently infected with PV.
具有高度改变生物学特性的脊髓灰质炎病毒（PV）突变体可在源自神经的细胞中进行体外筛选。在人神经母细胞瘤细胞中筛选出的1型PV毒株基因组中会积累突变，从而改变细胞特异性，并赋予病毒在诸如HEp-2c等非神经细胞中持续存在的能力（佩尔蒂埃等人，《病毒学》180, 729, 1991）。利用这个细胞系统，我们既有亲本裂解毒株，也有持续性PV突变体；这些被用于研究持续性感染的建立和维持机制。我们发现，当病毒的裂解潜力降低时，就会建立持续性感染；这涉及1型突变体病毒周期的早期和晚期事件。相比之下，感染的维持与病毒降低的裂解潜力无关，而是与各种表型的突变细胞群体的选择有关。对代表两种表型的两个细胞系进行了更详细的研究。在第一个细胞系HEp-S32（cl7）中，通过细胞荧光测定法未检测到PV受体，通过原位杂交在2%的细胞中检测到病毒基因组。在第二个细胞系HEp-S31（cl18）中，97%的细胞表达PV受体，在9 - 10%的细胞中检测到病毒基因组，在5 - 10%的细胞中检测到病毒抗原。利用这个细胞系，在特定培养条件下可诱导培养物的治愈或大多数细胞的裂解。我们提出一个涉及流产感染和裂解感染之间平衡的模型来解释持续感染PV的细胞的特性。
