Nakatsue T, Katoh I, Nakamura S, Takahashi Y, Ikawa Y, Yoshinaka Y
Department of Retroviral Regulation, Tokyo Medical and Dental University, Japan.
Biochem Biophys Res Commun. 1998 Dec 9;253(1):59-64. doi: 10.1006/bbrc.1998.9724.
In general, viral infection is supposed to induce stress responses in the host cell. However, very few detailed observations about virus-induced stress responses have been reported. Here we investigated specific stress responses in Vero cells infected with Sindbis virus (SV), a single-stranded RNA virus, acute infection with which is known to cause apoptotic cell death in the host cells. Prior to the onset of apoptosis, p38 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinases (JNKs) were activated. Subsequently, a 27-kDa heat shock protein (HSP27) became phosphorylated, and intracellular distribution of HSP27 was changed from the cytoplasm to the perinuclear region. These results indicate that the cellular signaling cascades activated by pro-inflammatory cytokines and environmental stresses are also activated as a result of lytic infection with SV. These responses may contribute to the delayed onset of apoptosis in the host cells and the facilitation of viral replication.
一般来说，病毒感染被认为会在宿主细胞中引发应激反应。然而，关于病毒诱导的应激反应的详细观察报道却非常少。在这里，我们研究了感染辛德毕斯病毒（SV）的非洲绿猴肾细胞（Vero细胞）中的特定应激反应，SV是一种单链RNA病毒，已知其急性感染会导致宿主细胞发生凋亡性细胞死亡。在凋亡开始之前，p38丝裂原活化蛋白激酶（MAPK）和c-Jun氨基末端激酶（JNKs）被激活。随后，一种27 kDa的热休克蛋白（HSP27）发生磷酸化，并且HSP27的细胞内分布从细胞质改变为核周区域。这些结果表明，由促炎细胞因子和环境应激激活的细胞信号级联反应也会因SV的裂解感染而被激活。这些反应可能有助于宿主细胞凋亡的延迟发生以及病毒复制的促进。
