Bantel-Schaal U
Institut für Medizinische Mikrobiologie und Hygiene, Abt. Virologie, Universität Freiburg, Federal Republic of Germany.
Virology. 1991 May;182(1):260-8. doi: 10.1016/0042-6822(91)90669-3.
Infection of the SV40-transformed Syrian hamster cells Elona with adeno-associated parvovirus type 5 (AAV-5) affects the cellular stress response. Stress-induced growth delay becomes permanent and this promotes cell death. AAV DNA is replicated in the absence of helper virus. Induction of an incomplete stress response by cycloheximide treatment still results in replication of viral DNA but not in virus-mediated growth arrest. Thus, the reactions that induce AAV DNA replication and that direct growth delay are different and replication of AAV DNA is not sufficient to induce growth arrest and cell death. Additional steps that lead to effects resembling inhibition of protein synthesis are required. The possibility that they may have their origin in the action of AAV rep proteins is discussed.
用5型腺相关细小病毒（AAV-5）感染SV40转化的叙利亚仓鼠细胞Elona会影响细胞应激反应。应激诱导的生长延迟会变得永久性，这会促进细胞死亡。AAV DNA在没有辅助病毒的情况下进行复制。用环己酰亚胺处理诱导不完全应激反应仍会导致病毒DNA复制，但不会导致病毒介导的生长停滞。因此，诱导AAV DNA复制和导致生长延迟的反应是不同的，AAV DNA复制不足以诱导生长停滞和细胞死亡。需要额外的步骤来产生类似于蛋白质合成抑制的效应。文中讨论了这些效应可能源于AAV rep蛋白作用的可能性。
