登革热感染改变了人血小板中CD154和CD148的表达。

IF 2.5 4区医学 Q3 VIROLOGY

Virus research Pub Date : 2025-01-01 DOI:10.1016/j.virusres.2024.199519

Sayali Vedpathak , Sonali Palkar , AkhileshChandra Mishra , Vidya A Arankalle , Shubham Shrivastava

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引用次数: 0

摘要

血小板对止血和血管完整性至关重要。血小板通过DC-SIGN受体识别登革热病毒。在病原体识别后，血小板迅速调节粘附分子的表达，触发免疫细胞相互作用，调节免疫反应。在这项研究中，我们旨在检测三种分子CD151、CD154和CD148在登革热患者血小板上的表达水平。与健康受试者相比，在登革热患者中CD154的表达显著增加，CD148的表达显著减少(p

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Dengue infection changes the expressions of CD154 and CD148 in human platelets

Platelets are essential for hemostasis and vascular integrity. Platelets recognize dengue virus through the DC-SIGN receptor. Upon pathogen recognition, platelets rapidly modulate the expression of adhesion molecules to trigger immune cell interactions and regulate the immune response. In this study, we aimed to examine the expression levels of three molecules, CD151, CD154, and CD148 on platelets in dengue patients. A significantly increased expression of CD154 and reduced expression of CD148 was observed in dengue patients compared to healthy subjects (p < 0.0001). Moreover, a strong positive correlation between CD148 and CD41/CD61 (p < 0.0001) was noted in dengue patients. In summary, we demonstrated the altered expressions of CD154 and CD148 on platelets in dengue patients that may play a crucial role in dengue pathogenesis.

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来源期刊

Virus research 医学-病毒学

CiteScore

9.50

自引率

2.00%

发文量

239

审稿时长

43 days

期刊介绍： Virus Research provides a means of fast publication for original papers on fundamental research in virology. Contributions on new developments concerning virus structure, replication, pathogenesis and evolution are encouraged. These include reports describing virus morphology, the function and antigenic analysis of virus structural components, virus genome structure and expression, analysis on virus replication processes, virus evolution in connection with antiviral interventions, effects of viruses on their host cells, particularly on the immune system, and the pathogenesis of virus infections, including oncogene activation and transduction.