Detection of H1N1 Influenza Virus in the Bile of a Severe Influenza Mouse Model

IF 4.3 4区医学 Q1 INFECTIOUS DISEASES

Influenza and Other Respiratory Viruses Pub Date : 2024-10-25 DOI:10.1111/irv.70012

Yan Liu, Jiuyang Xu, Cheng Wei, Yitian Xu, Chen Lyu, Mingzhi Sun, Ying Zheng, Bin Cao

{"title":"Detection of H1N1 Influenza Virus in the Bile of a Severe Influenza Mouse Model","authors":"Yan Liu, Jiuyang Xu, Cheng Wei, Yitian Xu, Chen Lyu, Mingzhi Sun, Ying Zheng, Bin Cao","doi":"10.1111/irv.70012","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Aims</h3>\n \n <p>Influenza virus infection may lead to fatal complications including multi-organ failure and sepsis. The influenza virus was detected in various extra-pulmonary organs in autopsy studies during the 2009 pandemic. However, limited research has been conducted on the presence of viral particle or viral components in the peripheral blood.</p>\n </section>\n \n <section>\n \n <h3> Methods and Results</h3>\n \n <p>We established a mouse model for severe H1N1 influenza. The bile and blood samples were collected over time and inoculated into embryonated chicken eggs. We detected live influenza virus in bile and blood samples in early infection. Immunofluorescence showed influenza viral components in the liver tissue. No live virus was isolated in the bile in mice intragastrically administered with influenza virus, indicating that the virus was spread from the blood stream. Targeted metabolomics analysis of bile acid and liver tissues showed that a secondary bile acid (3-dehydrocholic acid) was decreased after influenza H1N1 infection. Genes related with fatty acid metabolism and bile secretion pathways were down-regulated in liver after influenza virus infection.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Our study indicated that influenza virus viremia is present in severe influenza, and that the liver is a target organ for influenza viral sepsis.</p>\n </section>\n </div>","PeriodicalId":13544,"journal":{"name":"Influenza and Other Respiratory Viruses","volume":"18 10","pages":""},"PeriodicalIF":4.3000,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502934/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Influenza and Other Respiratory Viruses","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/irv.70012","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}

引用次数: 0

Abstract

Aims

Influenza virus infection may lead to fatal complications including multi-organ failure and sepsis. The influenza virus was detected in various extra-pulmonary organs in autopsy studies during the 2009 pandemic. However, limited research has been conducted on the presence of viral particle or viral components in the peripheral blood.

Methods and Results

We established a mouse model for severe H1N1 influenza. The bile and blood samples were collected over time and inoculated into embryonated chicken eggs. We detected live influenza virus in bile and blood samples in early infection. Immunofluorescence showed influenza viral components in the liver tissue. No live virus was isolated in the bile in mice intragastrically administered with influenza virus, indicating that the virus was spread from the blood stream. Targeted metabolomics analysis of bile acid and liver tissues showed that a secondary bile acid (3-dehydrocholic acid) was decreased after influenza H1N1 infection. Genes related with fatty acid metabolism and bile secretion pathways were down-regulated in liver after influenza virus infection.

Conclusion

Our study indicated that influenza virus viremia is present in severe influenza, and that the liver is a target organ for influenza viral sepsis.

Abstract Image

查看原文本刊更多论文

在严重流感小鼠模型胆汁中检测甲型 H1N1 流感病毒

目的：流感病毒感染可能导致致命的并发症，包括多器官衰竭和败血症。在 2009 年流感大流行期间进行的尸检研究中，在多个肺外器官中检测到了流感病毒。然而，关于外周血中是否存在病毒颗粒或病毒成分的研究却十分有限：我们建立了一个重症甲型 H1N1 流感小鼠模型。方法：我们建立了一个重症甲型 H1N1 流感小鼠模型，在一段时间内收集胆汁和血液样本，并将其接种到鸡胚蛋中。我们在感染早期的胆汁和血液样本中检测到了活流感病毒。免疫荧光显示肝组织中有流感病毒成分。胃内注射流感病毒的小鼠胆汁中没有分离到活病毒，这表明病毒是从血液中传播的。胆汁酸和肝组织的靶向代谢组学分析表明，感染甲型 H1N1 流感后，一种次级胆汁酸（3-脱氢胆酸）减少。与脂肪酸代谢和胆汁分泌途径相关的基因在感染流感病毒后在肝脏中下调：我们的研究表明，重症流感患者体内存在流感病毒病毒血症，肝脏是流感病毒败血症的靶器官。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Influenza and Other Respiratory Viruses 医学-病毒学

CiteScore

7.20

自引率

4.50%

发文量

120

审稿时长

6-12 weeks

期刊介绍： Influenza and Other Respiratory Viruses is the official journal of the International Society of Influenza and Other Respiratory Virus Diseases - an independent scientific professional society - dedicated to promoting the prevention, detection, treatment, and control of influenza and other respiratory virus diseases. Influenza and Other Respiratory Viruses is an Open Access journal. Copyright on any research article published by Influenza and Other Respiratory Viruses is retained by the author(s). Authors grant Wiley a license to publish the article and identify itself as the original publisher. Authors also grant any third party the right to use the article freely as long as its integrity is maintained and its original authors, citation details and publisher are identified.