We examined several aspects of African hedgehog adenovirus (AhAdv-1) that was isolated from an African pygmy hedgehog, including: replication kinetics of, virus-induced cytopathic effect (CPE), activation status of mitogen-activated protein kinase (MAPK) signaling pathways, and possible roles of these signaling pathways in virus replication and virus-induced CPE in MDCK cells. AhAdv-1 efficiently replicated and induced CPE in infected cells and caused accumulation of cleaved caspase-3 at 24 h post-infection (p.i.), suggesting apoptosis induction. Analysis of several intracellular signal transduction pathways, which are involved in apoptosis, showed activation of p38 MAPK, Akt and ERK1/2 pathways at 3 h p.i., and upregulation of phosphorylated SAPK/JNK at 24 h p.i. Although p38 MAPK inhibitor and SAPK/JNK inhibitor suppressed activation of the respective pathways in infected cells, they did not inhibit virus-induced CPE. Treatment of infected cells with inhibitor of the Akt pathway, the p38 pathway, the SAPK/JNK pathway or the ERK pathway revealed that inhibitors of p38 pathway inhibited viral replication by real-time PCR and TCID₅₀ assay in infected MDCK cells, suggesting that AhAdv-1 uses p38 pathway for multiplication in infected cells.

我们检查了从非洲侏儒刺猬中分离的非洲刺猬腺病毒 (AhAdv-1) 的几个方面，包括：病毒诱导的细胞病变效应 (CPE) 的复制动力学、丝裂原活化蛋白激酶 (MAPK) 信号通路的激活状态以及这些信号通路在 MDCK 细胞中病毒复制和病毒诱导的 CPE 中的可能作用。AhAdv-1 在感染细胞中有效复制和诱导 CPE，并在感染后 24 小时 (pi) 引起裂解的 caspase-3 积累，表明细胞凋亡诱导。对参与细胞凋亡的几种细胞内信号转导通路的分析表明，p38 MAPK、Akt 和 ERK1/2 通路在感染后 3 小时激活，磷酸化 SAPK/JNK 在感染后 24 小时上调 尽管 p38 MAPK 抑制剂和 SAPK/JNK 抑制剂抑制了感染细胞中各自通路的激活，但它们并没有抑制病毒诱导的 CPE。用 Akt 通路、p38 通路、SAPK/JNK 通路或 ERK 通路的抑制剂处理感染细胞表明 p38 通路抑制剂通过实时 PCR 和 TCID 抑制病毒复制₅₀检测感染的 MDCK 细胞，表明 AhAdv-1 使用 p38 途径在感染细胞中增殖。