Rajasekharan Sreejith, Rana Jyoti, Gulati Sahil, Sharma Sanjeev K, Gupta Vandana, Gupta Sanjay
Center for Emerging Diseases, Department of Biotechnology, Jaypee Institute of Information Technology, Noida, Uttar Pradesh, India.
Department of Microbiology, Ram Lal Anand College, University of Delhi South Campus (UDSC), Benito Juarez Marg, New Delhi, India.
Pathog Dis. 2013 Oct;69(1):29-35. doi: 10.1111/2049-632X.12064. Epub 2013 Oct 1.
Chandipura virus (CHPV), alike other pathogens, exploits the cellular infrastructure of their hosts through complex network of interactions for successful infection. CHPV being a recently emerged pediatric encephalitic virus, the mechanisms involved in the establishment of viral persistence are still ill defined. Because the protein interface between CHPV and its host provides one means by which the virus invades and seize control of their human host machinery, the authors in this study have employed computational methods to create a network of putative protein-protein interactions between CHPV and its human host to shed light on the hitherto less-known CHPV biology. On the basis of the 2105 potential interactions predicted among 1650 human proteins and the five proteins of CHPV, the authors decipher the probable mode by which the virus manipulates the biological pathways of its host toward its own end and replicates while evading the immune system. Identification of such conserved set of putative interactions that allow the virus to take control of the host has the potential to deepen our understanding of the virus-specific remodeling processes of the host cell and illuminate new arenas of disease intervention.
钱迪普拉病毒(CHPV)与其他病原体一样,通过复杂的相互作用网络利用宿主的细胞结构来成功感染。CHPV是一种最近出现的引起小儿脑炎的病毒,其建立病毒持续性的机制仍不清楚。由于CHPV与其宿主之间的蛋白质界面是病毒侵入并控制人类宿主机制的一种方式,因此本研究的作者采用计算方法创建了CHPV与其人类宿主之间假定的蛋白质-蛋白质相互作用网络,以阐明迄今鲜为人知的CHPV生物学特性。基于预测的1650种人类蛋白质与CHPV的5种蛋白质之间的2105种潜在相互作用,作者解读了病毒操纵宿主生物途径以实现自身目的并在逃避免疫系统的同时进行复制的可能模式。鉴定出这种使病毒能够控制宿主的保守的假定相互作用集,有可能加深我们对宿主细胞病毒特异性重塑过程的理解,并为疾病干预开辟新领域。