Gupta Megha, Mallick Disharee, Kumar Dilip, Kumar Rajesh
Department of Biosciences and Bioengineering, Indian Institute of Technology, Roorkee, Uttarakhand, India.
Trivedi School of Biosciences, Ashoka University, Sonipat, Haryana, India.
Curr Microbiol. 2025 May 9;82(6):286. doi: 10.1007/s00284-025-04258-2.
Chandipura virus (CHPV), a member of the Rhabdoviridae family, is an emerging pathogen responsible for encephalitis outbreaks, particularly among children under 15 years of age. Predominantly transmitted by sandflies, CHPV has caused multiple outbreaks in India, whereas strains from West African countries, including Kenya, Senegal, and Nigeria, have not been linked to human infections. The CHPV glycoprotein (G protein), a crucial spike protein, plays a key role in viral entry into host cells. In this study, we performed an in silico analysis to identify the potential mechanism of viral entry into host cells through interactions with the G protein. We also conducted bioinformatics analyses to examine the global distribution of CHPV strains and performed comparative structural and sequence-level analyses of the CHPV G protein. The phylogenetic analysis revealed a clear division of the CHPV G protein into two distinct clades. Despite this divergence, genome-wide analysis revealed high sequence conservation across the CHPV strains. Additionally, we identified potential interactions between the CHPV G protein and human receptors such as Lipoprotein Receptor-related Protein 1 (LRP1), facilitated by conserved lysine residues in the CHPV G protein in a calcium-dependent manner. The conservation of interacting residues across all strains raises concerns about the zoonotic potential of CHPV, particularly in regions where the virus is circulating in sandfly populations but has not yet caused any reported human infection. Our findings offer valuable insights into the genetic and structural similarities of CHPV strains, emphasizing the CHPV potential to spread beyond its current geographic boundaries and possibly cause human infections.
钱迪普拉病毒(CHPV)是弹状病毒科的成员,是一种新兴病原体,可引发脑炎疫情,尤其是在15岁以下儿童中。CHPV主要通过白蛉传播,在印度已引发多次疫情,而来自包括肯尼亚、塞内加尔和尼日利亚在内的西非国家的毒株尚未与人类感染相关联。CHPV糖蛋白(G蛋白)是一种关键的刺突蛋白,在病毒进入宿主细胞过程中起关键作用。在本研究中,我们进行了计算机模拟分析,以确定病毒通过与G蛋白相互作用进入宿主细胞的潜在机制。我们还进行了生物信息学分析,以研究CHPV毒株的全球分布,并对CHPV G蛋白进行了比较结构和序列水平分析。系统发育分析显示CHPV G蛋白明显分为两个不同的进化枝。尽管存在这种差异,但全基因组分析显示CHPV毒株之间具有高度的序列保守性。此外,我们确定了CHPV G蛋白与人类受体如脂蛋白受体相关蛋白1(LRP1)之间的潜在相互作用,这是由CHPV G蛋白中保守的赖氨酸残基以钙依赖方式促进的。所有毒株中相互作用残基的保守性引发了对CHPV人畜共患病潜力的担忧,特别是在病毒在白蛉种群中传播但尚未导致任何报告的人类感染的地区。我们的研究结果为CHPV毒株的遗传和结构相似性提供了有价值的见解,强调了CHPV有可能传播到其当前地理边界之外并可能导致人类感染。