Harvala Heli, Kalimo Hannu, Stanway Glyn, Hyypiä Timo
Department of Virology and MediCity Research Laboratory, University of Turku, Kiinamyllynkatu 13, FIN-20520 Turku, Finland.
Department of Pathology, University of Turku and Turku University Hospital, FIN-20520 Turku, Finland.
J Gen Virol. 2003 Sep;84(Pt 9):2375-2379. doi: 10.1099/vir.0.19246-0.
Coxsackievirus A9 (CAV9) contains an arginine-glycine-aspartic acid (RGD) motif which participates in cell entry. Mutants with alterations in the RGD-containing region were utilized to explore the importance of the tripeptide in the pathogenesis of CAV9 in mice. Using in situ hybridization, the parental CAV9 strain was observed to infect skeletal muscle (intercostal, platysma, lingual and thigh muscles) of newborn mice, whereas the RGD-less mutants were detectable only in platysma and lingual muscles. In addition, newborn mice infected with the mutants survived longer than CAV9-infected mice. In adult mice, the parental strain of CAV9, but not the mutants, achieved moderately high titres in the pancreas. These results suggest that the RGD motif has a significant role in the pathogenesis of CAV9 in mice but also that RGD-independent entry routes can be utilized in the infection of murine tissue.
柯萨奇病毒A9（CAV9）含有一个参与细胞进入的精氨酸-甘氨酸-天冬氨酸（RGD）基序。利用含RGD区域发生改变的突变体来探究该三肽在CAV9小鼠发病机制中的重要性。通过原位杂交观察到，亲代CAV9毒株可感染新生小鼠的骨骼肌（肋间肌、颈阔肌、舌肌和大腿肌肉），而无RGD的突变体仅在颈阔肌和舌肌中可检测到。此外，感染突变体的新生小鼠比感染CAV9的小鼠存活时间更长。在成年小鼠中，CAV9亲代毒株而非突变体在胰腺中达到中等高滴度。这些结果表明，RGD基序在CAV9小鼠发病机制中具有重要作用，但同时也表明在小鼠组织感染中可利用不依赖RGD的进入途径。
