Mesh : Humans Complement C1q / metabolism immunology Chikungunya Fever / immunology virology blood Complement Activation Antigen-Antibody Complex / blood immunology Chikungunya virus / immunology Male Cytokines / blood metabolism Middle Aged Adult Female Antibodies, Viral / blood immunology Aged Young Adult

来  源:   DOI:10.1007/s00284-024-03732-7

Abstract:
Chikungunya virus (CHIKV) is a causative agent of a disease continuum, ranging from an acute transient chikungunya fever to chronic incapacitating viral arthralgia. The interaction between anti-CHIKV antibodies and the complement system has recently received attention. However, the contribution of complement activation in CHIKV-induced pathologies has not been fully elucidated. The present study was undertaken to delineate the possible contribution of complement activation in CHIKV-induced disease progression. In this study, using plasma specimens of chikungunya patients in the acute, chronic, and recovered phases of infection, we explicated the involvement of complement activation in CHIKV disease progression by ELISAs and Bio-Plex assays. Correlation analysis was carried out to demonstrate interrelation among C1q-binding IgG-containing circulating immune complexes (CIC-C1q), complement activation fragments (C3a, C5a, sC5b-9), and complement-modulated pro-inflammatory cytokines (IL-1β, IL-18, IL-6, and TNF-α). We detected elevated complement activation fragments, CIC-C1q, and complement-modulated cytokines in the varied patient groups compared with the healthy controls, indicating persistent activation of the complement system. Furthermore, we observed statistically significant correlations among CIC-C1q with complement activation fragments and C3a with complement modulatory cytokines IL-1β, IL-6, and IL-18 during the CHIKV disease progression. Taken together, the current data provide insight into the plausible association between CICs, complement activation, subsequent complement modulatory cytokine expression, and CHIKV etiopathology.
摘要:
基孔肯雅病毒(CHIKV)是疾病连续体的病原体,从急性短暂性基孔肯雅热到慢性失能病毒性关节痛。抗CHIKV抗体与补体系统之间的相互作用最近受到关注。然而,补体激活在CHIKV诱导的病理中的作用尚未完全阐明.本研究旨在描述补体激活在CHIKV诱导的疾病进展中的可能贡献。在这项研究中,使用基孔肯雅患者的血浆标本,慢性,和感染的恢复阶段,我们通过ELISA和Bio-Plex分析阐明了补体激活参与CHIKV疾病进展。进行了相关分析,以证明C1q结合的含IgG的循环免疫复合物(CIC-C1q)之间的相互关系,补体激活片段(C3a,C5a,sC5b-9),和补体调节的促炎细胞因子(IL-1β,IL-18、IL-6和TNF-α)。我们检测到补体激活片段升高,CIC-C1q,与健康对照组相比,不同患者组的补体调节细胞因子,表明补体系统的持续激活。此外,我们观察到CIC-C1q与补体激活片段和C3a与补体调节细胞因子IL-1β之间的统计学显着相关性,CHIKV疾病进展期间的IL-6和IL-18。一起来看,当前的数据提供了对CICS之间合理关联的洞察,补体激活,随后的补体调节细胞因子表达,和CHIKV病因病理学。
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