Brown M, Wilson-Friesen H L, Doane F
Department of Microbiology, University of Toronto, Ontario, Canada.
J Virol. 1992 May;66(5):3198-205. doi: 10.1128/JVI.66.5.3198-3205.1992.
The fastidious enteric adenovirus (FEAd) types 40 (Ad40) and 41 (Ad41) are found in stool specimens of infants and young children in association with gastroenteritis. Although they can be isolated routinely from clinical specimens by using 293 cells, they are propagated with variable success in cell lines which support the replication of other adenovirus serotypes. HeLa cells are generally considered to be nonpermissive for the replication of FEAds, but in this study, Ad40 and Ad41 grew to comparable titers in individual 293 and HeLa cells. However, virus was not efficiently released from infected HeLa cells and thus did not undergo multiple cycles of infection in HeLa cell cultures. The block in virus release was not overcome in KB18 cells which, like 293 cells, constitutively express proteins encoded by the E1B region of a subgroup C adenovirus (in this case Ad2). Moreover, it was apparent from these studies that Ad40 and Ad41 have particle-to-infectious unit ratios several orders of magnitude greater than that for Ad5, even in 293 cells which express the E1A and E1B proteins of Ad5 and are considered to be permissive for replication of the FEAds. Neither the block in release of progeny virus nor the high particle-to-infectious unit ratio is explained solely by the defect in expression of the E1B 55K protein identified by Mautner et al. (V. Mautner, N. MacKay, and V. Steinthorsdottir, Virology 171:619-622, 1989; V. Mautner, N. MacKay, and K. Morris, Virology 179:129-138, 1990).
苛养肠道腺病毒40型(Ad40)和41型(Ad41)可在婴幼儿粪便标本中检出,与肠胃炎相关。尽管通过使用293细胞可从临床标本中常规分离出它们,但它们在支持其他腺病毒血清型复制的细胞系中增殖时成功率不一。一般认为HeLa细胞不支持苛养肠道腺病毒的复制,但在本研究中,Ad40和Ad41在单个293细胞和HeLa细胞中生长至相当的滴度。然而,病毒未能从感染的HeLa细胞中有效释放,因此在HeLa细胞培养物中未经历多轮感染。在KB18细胞中未克服病毒释放障碍,KB18细胞与293细胞一样,组成性表达C亚群腺病毒(在本案例中为Ad2)E1B区域编码的蛋白质。此外,从这些研究中可以明显看出,即使在表达Ad5的E1A和E1B蛋白且被认为支持苛养肠道腺病毒复制的293细胞中,Ad40和Ad41的颗粒与感染单位比率也比Ad5大几个数量级。子代病毒释放的障碍以及高颗粒与感染单位比率都不能仅由Mautner等人鉴定的E1B 55K蛋白表达缺陷来解释(V. Mautner、N. MacKay和V. Steinthorsdottir,《病毒学》171:619 - 622,1989;V. Mautner、N. MacKay和K. Morris,《病毒学》179:129 - 138,1990)。