Transcriptomic insights into early mechanisms underlying post-chikungunya chronic inflammatory joint disease

Transcriptomic insights into early mechanisms underlying post-chikungunya chronic inflammatory joint disease

Abstract Chikungunya virus (CHIKV) infection often results in a chronic joint condition known as Post-Chikungunya Chronic Inflammatory Joint Disease (pCHIKV-CIJD). This condition disrupts individuals’ daily lives and contributes to increased healthcare expenditure. This study investigated the molecu...

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Main Authors: Mariana Severo Ramundo, Guilherme Cordenonsi da Fonseca, Felipe Ten-Caten, Alexandra L. Gerber, Ana Paula Guimarães, Erika Regina Manuli, Marina Farrel Côrtes, Geovana Maria Pereira, Otavio Brustolini, Milena Gomes Cabral, Carolina Dos Santos Lázari, Patrícia Brasil, Clarisse da Silveira Bressan, Helder I. Nakaya, Gláucia Paranhos-Baccalà, Ana Tereza R. Vasconcelos, Ester Cerdeira Sabino
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Scientific Reports
Subjects:
CHIKV
Chikungunya
Post-Chikungunya Chronic Inflammatory Joint Disease
Total RNA sequencing
Small RNA sequencing
Chikungunya prognosis
Online Access:https://doi.org/10.1038/s41598-025-86761-x
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Summary:Abstract Chikungunya virus (CHIKV) infection often results in a chronic joint condition known as Post-Chikungunya Chronic Inflammatory Joint Disease (pCHIKV-CIJD). This condition disrupts individuals’ daily lives and contributes to increased healthcare expenditure. This study investigated the molecular mechanisms underlying pCHIKV-CIJD development by analyzing RNA transcripts, including small RNAs, of whole blood from CHIKV-infected patients. By comparing patients who evolved to pCHIKV-CIJD with those who did not, we identified molecular signatures associated with chronification in acute and post-acute disease phases. These molecules were primarily associated with an altered immune response regulation. Notably, LIFR, an immune receptor that enhanced IL-6 transcription, was down-regulated in the acute phase of pCHIKV-CIJD patients, while its inhibitor, hsa-miR-98-5p, was up-regulated in these individuals. Other downregulated genes include members of immune mechanisms whose impairment can lead to a reduction in the first line of antiviral response, thereby promoting virus persistence for a longer period in these patients. Additionally, pCHIKV-CIJD patients exhibited reduced transcript levels of MMP8, LFT, and DDIT4, genes already implicated in the pathological process of other types of inflammatory arthritis and seemingly relevant for pCHIKV-CIJD development. Overall, our findings provide insights into the early molecular mechanisms involved in the chronification and highlight potential targets for further investigation.
ISSN:2045-2322

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