Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte 31270-901, Brazil.
Department of Microbiology and Parasitology, Biosciences Center, Federal University of Rio Grande do Norte, Natal 59078-970, Brazil.
Viruses. 2024 Aug 30;16(9):1387. doi: 10.3390/v16091387.
Chikungunya virus (CHIKV) is an arbovirus causing acute febrile illness with severe joint pain, often leading to chronic arthralgia. This study investigated the adaptive immune responses during the early stages of symptomatic acute CHIKV infection, focusing on the transcription factors and cytokines linked to Th1, Th2, Th17, and Treg cells. Thirty-six individuals were enrolled: nine healthy controls and 27 CHIKV-positive patients confirmed by qRT-PCR. Blood samples were analyzed for the mRNA expression of transcription factors (Tbet, GATA3, FoxP3, STAT3, RORγt) and cytokines (IFN-γ, IL-4, IL-17, IL-22, TGF-β, IL-10). The results showed the significant upregulation of Tbet, GATA3, FoxP3, STAT3, and RORγt in CHIKV-positive patients, with RORγt displaying the highest increase. Correspondingly, cytokines IFN-γ, IL-4, IL-17, and IL-22 were upregulated, while TGF-β was downregulated. Principal component analysis (PCA) confirmed the distinct immune profiles between CHIKV-positive and healthy individuals. A correlation analysis indicated that higher Tbet expression correlated with a lower viral load, whereas FoxP3 and TGF-β were associated with higher viral loads. Our study sheds light on the intricate immune responses during acute CHIKV infection, characterized by a mixed Th1, Th2, Th17, and Treg response profile. These results emphasize the complex interplay between different adaptive immune responses and how they may contribute to the pathogenesis of Chikungunya fever.
基孔肯雅热病毒（CHIKV）是一种虫媒病毒，可引起伴有严重关节痛的急性发热性疾病，常导致慢性关节痛。本研究调查了症状性急性 CHIKV 感染早期的适应性免疫反应，重点关注与 Th1、Th2、Th17 和 Treg 细胞相关的转录因子和细胞因子。共纳入 36 名个体：9 名健康对照者和 27 名经 qRT-PCR 确诊的 CHIKV 阳性患者。分析了转录因子（Tbet、GATA3、FoxP3、STAT3、RORγt）和细胞因子（IFN-γ、IL-4、IL-17、IL-22、TGF-β、IL-10）的 mRNA 表达。结果显示，CHIKV 阳性患者中 Tbet、GATA3、FoxP3、STAT3 和 RORγt 显著上调，其中 RORγt 上调最为明显。相应地，细胞因子 IFN-γ、IL-4、IL-17 和 IL-22 上调，而 TGF-β 下调。主成分分析（PCA）证实了 CHIKV 阳性和健康个体之间明显不同的免疫特征。相关性分析表明，较高的 Tbet 表达与较低的病毒载量相关，而 FoxP3 和 TGF-β 与较高的病毒载量相关。本研究揭示了急性 CHIKV 感染期间复杂的免疫反应，表现为混合的 Th1、Th2、Th17 和 Treg 反应特征。这些结果强调了不同适应性免疫反应之间的复杂相互作用，以及它们如何可能导致基孔肯雅热的发病机制。
