Chattopadhyay Shiladitya, Bagchi Parikshit, Dutta Dipanjan, Mukherjee Anupam, Kobayashi Nobumichi, Chawlasarkar Mamta
Division of Virology, National Institute of Cholera and Enteric Diseases, P-33, C.I.T. Road Scheme- XM, Beliaghata, Kolkata-700010, India.
Bioinformation. 2010 Apr 30;4(10):448-51. doi: 10.6026/97320630004448.
Rotavirus (RV) diarrhoea causes huge number deaths in children less than 5 years of age. In spite of available vaccines, it has been difficult to combat RV due to large number of antigenically distinct genotypes, high mutation rates, generation of reassortant viruses due to segmented genome. RV is an eukaryotic virus which utilizes host cell machinery for its propagation. Since RV only encodes 12 proteins, post-translational modification (PTM) is important mechanism for modification, which consequently alters their function. A single protein exhibiting different functions in different locations or in different subcellular sites, are known to be 'moonlighting'. So there is a possibility that viral proteins moonlight in separate location and in different time to exhibit diverse cellular effects. Based on the primary sequence, the putative behaviour of proteins in cellular environment can be predicted, which helps to classify them into different functional families with high reliability score. In this study, sites for phosphorylation, glycosylation and SUMOylation of the six RV structural proteins (VP1, VP2, VP3, VP4, VP6 & VP7) & five non-structural proteins (NSP1, NSP2,NSP3,NSP4 & NSP5) and the functional families were predicted. As NSP6 is a very small protein and not required for virus growth & replication, it was not included in the study. Classification of RV proteins revealed multiple putative functions of each structural protein and varied number of PTM sites, indicating that RV proteins may also moonlight depending on requirements during viral life cycle. Targeting the crucial PTM sites on RV structural proteins may have implications in developing future anti-rotaviral strategies.
轮状病毒(RV)腹泻导致大量5岁以下儿童死亡。尽管有可用的疫苗,但由于存在大量抗原性不同的基因型、高突变率以及因基因组分段而产生重配病毒,抗击RV一直很困难。RV是一种真核病毒,它利用宿主细胞机制进行繁殖。由于RV仅编码12种蛋白质,翻译后修饰(PTM)是其修饰的重要机制,进而改变它们的功能。已知单个蛋白质在不同位置或不同亚细胞位点发挥不同功能,即所谓的“兼职”。因此,病毒蛋白有可能在不同位置和不同时间进行“兼职”以表现出不同的细胞效应。基于一级序列,可以预测蛋白质在细胞环境中的推定行为,这有助于将它们可靠地分类到不同的功能家族中。在本研究中,预测了六种RV结构蛋白(VP1、VP2、VP3、VP4、VP6和VP7)和五种非结构蛋白(NSP1、NSP2、NSP3、NSP4和NSP5)的磷酸化、糖基化和SUMO化位点以及功能家族。由于NSP6是一种非常小的蛋白质,且病毒生长和复制不需要它,因此未纳入本研究。RV蛋白的分类揭示了每种结构蛋白的多种推定功能和不同数量的PTM位点,表明RV蛋白也可能在病毒生命周期中根据需要进行“兼职”。靶向RV结构蛋白上的关键PTM位点可能对未来抗轮状病毒策略的开发具有重要意义。