Rassmann Alexander, Henke Andreas, Jarasch Nadine, Lottspeich Friedrich, Saluz Hans-Peter, Munder Thomas
Leibniz Institute for Natural Product Research and Infection Biology, Hans-Knoell-Institute, Department of Cell and Molecular Biology, Beutenbergstrasse 11a, D-07745 Jena, Germany.
Antiviral Res. 2007 Nov;76(2):150-8. doi: 10.1016/j.antiviral.2007.06.011. Epub 2007 Jul 16.
Coxsackievirus is linked to a large variety of severe human and animal diseases such as myocarditis. The interplay between host factors and virus components is crucial for the fate of the infected cells. However, host proteins which may play a role in coxsackievirus-induced diseases are ill-defined. Two-dimensional gel electrophoresis of protein extracts obtained from coxsackievirus B3 (CVB3)-infected and uninfected HeLa or HepG2 cells combined with spot analysis revealed several proteins which are exclusively up-regulated in infected cells. One of these proteins was identified as the fatty acid synthase (FAS). By using cerulenin and C75, two known inhibitors of FAS we were able to significantly block CVB3 replication. FAS appears to be directly involved in CVB3-caused pathology and is therefore suitable as a therapeutic target in CVB3-induced diseases.
柯萨奇病毒与多种严重的人类和动物疾病有关,如心肌炎。宿主因子与病毒成分之间的相互作用对于受感染细胞的命运至关重要。然而,在柯萨奇病毒引起的疾病中可能起作用的宿主蛋白尚不明确。从感染和未感染柯萨奇病毒B3(CVB3)的HeLa或HepG2细胞中提取蛋白质进行二维凝胶电泳,并结合斑点分析,发现了几种仅在感染细胞中上调的蛋白质。其中一种蛋白质被鉴定为脂肪酸合酶(FAS)。通过使用两种已知的FAS抑制剂——浅蓝菌素和C75,我们能够显著阻断CVB3的复制。FAS似乎直接参与了CVB3引起的病理过程,因此适合作为CVB3诱导疾病的治疗靶点。