CD11b maintains West Nile virus replication through modulation of immune response in human neuroblastoma cells.

IF 4 3区医学 Q2 VIROLOGY

Virology Journal Pub Date : 2024-07-14 DOI:10.1186/s12985-024-02427-6

Yan-Gang Liu, Hao-Ran Peng, Rui-Wen Ren, Ping Zhao, Lan-Juan Zhao

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引用次数: 0

Abstract

Background: West Nile virus (WNV) is a rapidly spreading mosquito-borne virus accounted for neuroinvasive diseases. An insight into WNV-host factors interaction is necessary for development of therapeutic approaches against WNV infection. CD11b has key biological functions and been identified as a therapeutic target for several human diseases. The purpose of this study was to determine whether CD11b was implicated in WNV infection.

Methods: SH-SY5Y cells with and without MEK1/2 inhibitor U0126 or AKT inhibitor MK-2206 treatment were infected with WNV. CD11b mRNA levels were assessed by real-time PCR. WNV replication and expression of stress (ATF6 and CHOP), pro-inflammatory (TNF-α), and antiviral (IFN-α, IFN-β, and IFN-γ) factors were evaluated in WNV-infected SH-SY5Y cells with CD11b siRNA transfection. Cell viability was determined by MTS assay.

Results: CD11b mRNA expression was remarkably up-regulated by WNV in a time-dependent manner. U0126 but not MK-2206 treatment reduced the CD11b induction by WNV. CD11b knockdown significantly decreased WNV replication and protected the infected cells. CD11b knockdown markedly increased TNF-α, IFN-α, IFN-β, and IFN-γ mRNA expression induced by WNV. ATF6 mRNA expression was reduced upon CD11b knockdown following WNV infection.

Conclusion: These results demonstrate that CD11b is involved in maintaining WNV replication and modulating inflammatory as well as antiviral immune response, highlighting the potential of CD11b as a target for therapeutics for WNV infection.

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CD11b 通过调节人神经母细胞瘤细胞的免疫反应来维持西尼罗河病毒的复制。

背景：西尼罗河病毒（WNV）是一种迅速传播的蚊媒病毒，可导致神经侵入性疾病。要开发针对 WNV 感染的治疗方法，就必须深入了解 WNV 与宿主因子的相互作用。CD11b 具有关键的生物学功能，已被确定为多种人类疾病的治疗靶点。本研究的目的是确定 CD11b 是否与 WNV 感染有关：方法：用 WNV 感染 SH-SY5Y 细胞，无论是否使用 MEK1/2 抑制剂 U0126 或 AKT 抑制剂 MK-2206。通过实时 PCR 评估 CD11b mRNA 水平。用 CD11b siRNA 转染 WNV 感染的 SH-SY5Y 细胞，评估 WNV 复制和应激因子（ATF6 和 CHOP）、促炎因子（TNF-α）和抗病毒因子（IFN-α、IFN-β 和 IFN-γ）的表达。细胞存活率由 MTS 法测定：结果：CD11b mRNA的表达在WNV作用下呈显著的时间依赖性上调。U0126 而非 MK-2206 可减少 CD11b 在 WNV 诱导下的表达。敲除 CD11b 能明显减少 WNV 复制并保护受感染细胞。CD11b 敲除可明显增加 WNV 诱导的 TNF-α、IFN-α、IFN-β 和 IFN-γ mRNA 的表达。WNV感染后，CD11b敲除后ATF6 mRNA表达减少：这些结果表明，CD11b 参与了维持 WNV 复制、调节炎症和抗病毒免疫反应的过程，突出了 CD11b 作为 WNV 感染治疗靶点的潜力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Virology Journal 医学-病毒学

CiteScore

7.40

自引率

2.10%

发文量

186

审稿时长

1 months

期刊介绍： Virology Journal is an open access, peer reviewed journal that considers articles on all aspects of virology, including research on the viruses of animals, plants and microbes. The journal welcomes basic research as well as pre-clinical and clinical studies of novel diagnostic tools, vaccines and anti-viral therapies. The Editorial policy of Virology Journal is to publish all research which is assessed by peer reviewers to be a coherent and sound addition to the scientific literature, and puts less emphasis on interest levels or perceived impact.