Acute Chikungunya Virus Infection Triggers a Diverse Range of T Helper Lymphocyte Profiles

Viruses Pub Date : 2024-08-30 DOI:10.3390/v16091387
Ramayana Morais de Medeiros Brito, Marília Farias de Melo, José Veríssimo Fernandes, Joanna Gardel Valverde, Paulo Marcos Matta Guedes, Josélio Maria Galvão de Araújo, Manuela Sales Lima Nascimento
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Abstract

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.
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急性基孔肯雅病毒感染可诱发多种 T 辅助淋巴细胞特征
基孔肯雅病毒(CHIKV)是一种虫媒病毒,可引起急性发热性疾病,并伴有严重的关节疼痛,通常会导致慢性关节痛。本研究调查了无症状急性基孔肯雅病毒感染早期的适应性免疫反应,重点是与 Th1、Th2、Th17 和 Treg 细胞相关的转录因子和细胞因子。研究人员共招募了 36 人:9 名健康对照组和 27 名经 qRT-PCR 确认为 CHIKV 阳性的患者。血液样本分析了转录因子(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,在 CHIKV 阳性患者中,Tbet、GATA3、FoxP3、STAT3 和 RORγt 均明显上调,其中 RORγt 的上调幅度最大。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,CHIKV 阳性者和健康人的免疫特征截然不同。相关分析表明,Tbet表达较高与病毒载量较低相关,而FoxP3和TGF-β则与病毒载量较高相关。我们的研究揭示了急性 CHIKV 感染期间错综复杂的免疫反应,其特点是 Th1、Th2、Th17 和 Treg 混合反应。这些结果强调了不同适应性免疫反应之间复杂的相互作用,以及它们可能如何促进基孔肯雅热的发病机制。
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