The complement system is a critical component of both innate and adaptive immune responses. It has both protective and pathogenic roles in viral infections. There are no studies regarding the role of complement system in Chandipura virus (CHPV) infection. The current study has investigated the role of complement pathways in the in vitro neutralization of CHPV in Vero E6 cells. Using normal human serum (NHS), heat-inactivated serum (HIS), human serum deficient of complement factor, respective reconstituted serum, assays like in vitro neutralization, real-time PCR, and flow cytometry-based tissue culture-based limited dose assay (TC-LDA) were carried out for assessing the activation of different complement pathways. NHS from 9/10 donors showed complement dependent neutralization, reduction in viral load and decrease in percentage of CHPV-positive cells compared to their HIS counterparts. EGTA or EDTA pretreatment experiments indicated that CHPV neutralization proceeds through the alternative pathway of the complement activation. Our data showed a strong dependence on C3 for the in vitro neutralization of CHPV. Disparity in CHPV neutralization levels between factor B-deficient and reconstituted sera could be attributed to amplification loop/“tick-over” mechanism. Assays using C3, C5, and C8 deficient sera indicated that complement-mediated CHPV neutralization and suppression of CHPV infectivity are primarily through C3 and C5, and not dependent on downstream complement factor C8. With no specific anti-viral treatment/vaccine against Chandipura, the current data, elucidating role of human complement system in the neutralization of CHPV, may help in designing effective therapeutics.

中文翻译：

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补体激活的替代途径具有对抗钱迪普拉病毒感染的有益作用。

补体系统是先天和适应性免疫应答的关键组成部分。它在病毒感染中具有保护作用和致病作用。尚无关于补体系统在昌迪普拉病毒（CHPV）感染中的作用的研究。当前的研究已经研究了补体途径在Vero E6细胞中CHPV的体外中和中的作用。使用正常人血清（NHS），热灭活血清（HIS），缺乏补体因子的人血清，相应的重组血清，体外中和，实时PCR和基于流式细胞术的基于组织培养的有限剂量测定等测定（TC-LDA）用于评估不同补体途径的激活。来自9/10个捐助者的NHS显示补体依赖性中和，与HIS对应物相比，病毒载量减少，CHPV阳性细胞百分比降低。EGTA或EDTA预处理实验表明，CHPV中和通过补体激活的替代途径进行。我们的数据显示CHPV的体外中和作用强烈依赖于C3。缺乏因子B的血清和重组血清之间CHPV中和水平的差异可能归因于扩增环/“滴答”机制。使用C3，C5和C8缺陷血清的分析表明，补体介导的CHPV中和和CHPV感染性抑制主要是通过C3和C5，而不依赖于下游补体因子C8。由于没有针对Chandipura的特异性抗病毒治疗/疫苗，目前的数据是，