强力霉素可抑制体外神经性肠病毒的增殖。

IF 2.5 4区医学 Q3 VIROLOGY Virus research Pub Date : 2024-05-16 DOI:10.1016/j.virusres.2024.199388

Fengyu Chi , Xinzhuo Liu , Juan Li , Moujian Guo , Zhenjie Zhang , Hong Zhou , Michael J. Carr , Yuming Li , Weifeng Shi

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引用次数: 0

摘要

人类肠道病毒（EV）与一系列严重的儿科疾病有关，是全球公共卫生关注的焦点。尽管肠道病毒的发病率和死亡率很高，但目前还没有广谱抗病毒药物。在本文中，我们提出的证据表明，强力霉素能以剂量依赖的方式抑制各种神经性EV的体外复制，包括肠道病毒A71（EV-A71）、肠道病毒D68（EV-D68）和柯萨奇病毒（CV）-A6。进一步的研究表明，该药物主要作用于体外病毒感染的后进入阶段，在病毒感染后两小时给药时，对EV-A71的抑制率高达89%。这些发现为开发针对 EV 感染的抗病毒药物提供了宝贵的启示。

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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Doxycycline inhibits neurotropic enterovirus proliferation in vitro

Human enteroviruses (EVs) represent a global public health concern due to their association with a range of serious pediatric illnesses. Despite the high morbidity and mortality exerted by EVs, no broad-spectrum antivirals are currently available. Herein, we presented evidence that doxycycline can inhibit in vitro replication of various neurotropic EVs, including enterovirus A71 (EV-A71), enterovirus D68 (EV-D68), and coxsackievirus (CV)-A6, in a dose-dependent manner. Further investigations indicated that the drug primarily acted at the post-entry stage of virus infection in vitro, with inhibitory effects reaching up to 89 % for EV-A71 when administered two hours post-infection. These findings provide valuable insights for the development of antiviral drugs against EV infections.

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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.