Pathogenesis of Mouse Hepatitis Virus Infection in Gamma Interferon-Deficient Mice Is Modulated by Co-infection with Helicobacter hepaticus

Compton; Susan R.; nbsp; Ball-Goodrich; Lisa J.; nbsp; Zeiss; Caroline J.; nbsp; Johnson; Linda K.; nbsp; Johnson; Elizabeth A.; nbsp; Macy; James D.

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Pathogenesis of Mouse Hepatitis Virus Infection in Gamma Interferon-Deficient Mice Is Modulated by Co-infection with Helicobacter hepaticus

机译：γ干扰素缺陷小鼠的小鼠肝炎病毒感染的发病机理是通过与肝杆菌共感染来调节的。

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Gammainterferon-deficient(IFN-#59138;KO)micedevelopedawastingsyndromeandwerefoundtobeco-infectedwithHelicobactersp.,andanewisolateofmousehepatitisvirus(MHV)designatedMHV-G.Thediseasewascharacterizedbypleuritis,peritonitis,hepatitis,pneumonia,andmeningitis.InitialexperimentsusedacecalhomogenateinoculumfromtheclinicalcasesthatcontainedH.hepaticusandMHV-GtoreproducethedevelopmentofperitonitisandpleuritisinIFN-#59138;KOmice.Incontrast,immunocompetentmicegiventhesameinoculumdevelopedanacute,self-limitinginfectionandremainedclinicallynormal.ThisresultconfirmedtheimportanceofIFN-#59138;inpreventingchronicinfectionandlimitingviraldissemination.Tounderstandtheroleofbothagentsinthedevelopmentofperitonitisandpleuritis,IFN-#59138;KOmicewereinfectedwitheitheragentorwereco-infectedwithH.hepaticusandMHV-G.InfectionwithMHV-Ginducedamultisystemicinfectionsimilartothatdescribedintheoriginalcases,withmultifocalhepaticnecrosis,acutenecrotizingandinflammatorylesionsofthegastrointestinaltract,andacuteperitonitisandpleuritiswithadhesionsontheserosalsurfacesoftheviscera.However,micegivenH.hepaticusalonehadminimalpathologicchangeseventhoughtheorganismwasconsistentlydetectedinthececumorfeces.Althoughco-infectionwithH.hepaticusandMHV-GinducedlesionssimilartothoseassociatedwithMHV-Galone,thepathogenesisoftheMHVinfectionwasmodified.HelicobacterhepaticusappearedtoreducetheseverityofMHV-inducedlesionsduringtheacutephaseofinfection,andexacerbatedhepatitisandmeningitisatthelatertimepoint.WeconcludethatinfectionofIFN-#59138;KOmicewithMHV-Gresultsinmultisystemicinfectionwithperitonitis,pleuritis,andadhesionsduetotheaberrantimmuneresponseinthesemice.Inaddition,co-infectionofthesemicewithH.hepaticusresultsinalterationsinthepathogenesisofMHV-Ginfection.

机译：Gammainterferon缺陷型（IFN-＃59138; KO）。micedevelopedawastingsyndromeandwerefoundtobeco-infectedwithHelicobactersp，andanewisolateofmousehepatitisvirus（MHV）designatedMHV-G.Thediseasewascharacterizedbypleuritis，腹膜炎，肝炎，肺炎，andmeningitis.InitialexperimentsusedacecalhomogenateinoculumfromtheclinicalcasesthatcontainedH.hepaticusandMHV-GtoreproducethedevelopmentofperitonitisandpleuritisinIFN-＃59138; KOmice.Incontrast，immunocompetentmicegiventhesameinoculumdevelopedanacute，自-limitinginfectionandremainedclinicallynormal.ThisresultconfirmedtheimportanceofIFN-＃59138; inpreventingchronicinfectionandlimitingviraldissemination.Tounderstandtheroleofbothagentsinthedevelopmentofperitonitisandpleuritis，IFN-＃59138; KOmicewereinfectedwitheitheragentorwereco-infectedwithH.hepaticusandMHV-G.InfectionwithMHV-Ginducedamultisystemicinfectionsimilartothatdescribedintheoriginalcases，withmultifocalhepaticnecrosis，acutenecrotizingandinflammatorylesionsofthegastrointestinaltract，andacuteperito nitisandpleuritiswithadhesionsontheserosalsurfacesoftheviscera.However，micegivenH.hepaticusalonehadminimalpathologicchangeseventhoughtheorganismwasconsistentlydetectedinthececumorfeces.Althoughco-infectionwithH.hepaticusandMHV-GinducedlesionssimilartothoseassociatedwithMHV-Galone，thepathogenesisoftheMHVinfectionwasmodified.HelicobacterhepaticusappearedtoreducetheseverityofMHV-inducedlesionsduringtheacutephaseofinfection，andexacerbatedhepatitisandmeningitisatthelatertimepoint.WeconcludethatinfectionofIFN-＃59138; KOmicewithMHV-Gresultsinmultisystemicinfectionwithperitonitis，胸膜炎，andadhesionsduetotheaberrantimmuneresponseinthesemice.Inaddition，共infectionofthesemicewithH.hepaticusresultsinalterationsinthepathogenesisofMHV-Ginfection。

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《Comparative Medicine》 |2003年第2期|共页
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Compton; Susan R.; nbsp; Ball-Goodrich; Lisa J.; nbsp; Zeiss; Caroline J.; nbsp; Johnson; Linda K.; nbsp; Johnson; Elizabeth A.; nbsp; Macy; James D.;
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中图分类畜牧、动物医学、狩猎、蚕、蜂;
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1. Pathogenesis of mouse hepatitis virus infection in gamma interferon-deficient mice is modulated by co-infection with Helicobacter hepaticus [J] . Compton SR, Ball-Goodrich LJ, Zeiss CJ, Comparative Medicine . 2003,第2期

机译：γ干扰素缺乏症小鼠中小鼠肝炎病毒感染的发病机理是通过与肝幽门螺杆菌共同感染来调节的
2. Co-infection by Semliki forest virus and malarial parasite modulates viral multiplication, pathogenesis and cytokines in mice [J] . P. Gupta, P. Seth, M.M. Husain, Parasite . 2006,第3期

机译：Semliki森林病毒和疟疾寄生虫的共感染可调节小鼠的病毒繁殖，发病机制和细胞因子
3. Helicobacter pylori infection does not promote hepatocellular cancer in a transgenic mouse model of hepatitis C virus pathogenesis [J] . Alexis Garcia, Yan Feng, Nicola MA Parry, Gut microbes. . 2013,第6期

机译：在丙型肝炎病毒发病机制的转基因小鼠模型中，幽门螺杆菌感染不会促进肝细胞癌
4. Quantification of inflammation-induced oxidized deoxyguanosine lesion in colon and liver from Helicobacter hepaticus-infected Rag2-deficient mice [C] . Wenjie Ye, Aswin Mangerich, Liang Cui, American Society for Mass Spectrometry Conference on Mass Spectrometry and Allied Topics . 2011

机译：炎症诱导的氧化脱氧胍病病变的结肠杆菌感染肝病感染的RAG2缺陷小鼠
5. The role of B cells and gammadelta T cells in the pathogenesis of mouse hepatitis virus induced demyelination. [D] . Dandekar, Ajai Arvind. 2005

机译：B细胞和γT细胞在小鼠肝炎病毒引起的脱髓鞘的发病机理中的作用。
6. Co-Infection with the Friend Retrovirus and Mouse Scrapie Does Not Alter Prion Disease Pathogenesis in Susceptible Mice [O] . Pascal Leblanc, Kim Hasenkrug, Anne Ward, 2009

机译：与朋友逆转录病毒和小鼠瘙痒病的共同感染不会改变易感小鼠的on病毒疾病发病机理。
7. Co-infection by Semliki forest virus and malarial parasite modulates viral multiplication, pathogenesis and cytokines in mice [O] . P. Gupta, P. Seth, M.M. Husain, 2006

机译：Semliki森林病毒和疟原虫的共同感染调节小鼠中的病毒倍增，发病机制和细胞因子

Pathogenesis of Mouse Hepatitis Virus Infection in Gamma Interferon-Deficient Mice Is Modulated by Co-infection with Helicobacter hepaticus

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