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Kinetic Profile of Influenza Virus Infection in Three Rat Strains

机译:三种大鼠品系中流感病毒感染的动力学特征

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Influenzaisarespiratorytractdiseaseofviraloriginthatcancausemajorepidemicsinhumans.Theinfluenzavirusinfectsanddamagesepithelialcellsoftherespiratorytractandcausespneumonia.Lunglesionsofmiceinfectedwithinfluenzavirusresemblesthoseseeninhumanswithinfluenza,andcanresultinsevereandevenfatalpneumonia.Incontrast,experimentalinfectionofratswiththevirusinducesamilderformofthedisease,withnomortality.ThepurposeofthestudyreportedherewastodeterminethetimecourseofinfluenzainfectionandlunginjuryinBrownNorway(BN),Fischer-344(F344),andSprague-Dawley(SD)ratstoascertainwhethergeneticbackgroundimpactssusceptibilitytoinfectionandhostresponses.Ratsofeachstrainwereinoculatedintranasallywith10,000plaque-formingunitsofrat-adaptedinfluenzavirus(RAIV),andlungswereassessedatpostinoculationhour(PIH)2,24,48,72,and144forviraltiter,inflammatorycells,pro-inflammatorycytokines,andbiochemicalindicatorsoflungedema(protein)andinjury(lactatedehydrogenase[LD]activity).VirustiterpeakedatPIH24,andwas100-foldhigherintheF344andSD,comparedwiththeBNstrain.Alveolarmacrophages,LDactivity,andtotalproteinconcentrationwerehigherintheBNrats,whereasneutrophilnumbersandinterleukin6andtumornecrosisfactor-alphaactivitiesweregreatestinthebronchoalveolarlavagefluidofF344andSDrats.TheresultsindicatethatF344andSDratsrespondinsimilarmannertoviralinfection,whereasviralreplicationwasmorelimitedinBNratsandwasassociatedwithadifferentprofileofpulmonarycells.
机译:Influenzaisarespiratorytractdiseaseofviraloriginthatcancausemajorepidemicsinhumans.Theinfluenzavirusinfectsanddamagesepithelialcellsoftherespiratorytractandcausespneumonia.Lunglesionsofmiceinfectedwithinfluenzavirusresemblesthoseseeninhumanswithinfluenza,andcanresultinsevereandevenfatalpneumonia.Incontrast,experimentalinfectionofratswiththevirusinducesamilderformofthedisease,withnomortality.ThepurposeofthestudyreportedherewastodeterminethetimecourseofinfluenzainfectionandlunginjuryinBrownNorway(BN),费 - 344(F344),andSprague - 道(SD)ratstoascertainwhethergeneticbackgroundimpactssusceptibilitytoinfectionandhostresponses.Ratsofeachstrainwereinoculatedintranasallywith10,000plaque-formingunitsofrat-adaptedinfluenzavirus(RAIV),andlungswereassessedatpostinoculationhour(PIH)2 ,24、48、72和144分别代表PIH24的病毒滴度和较高的100倍,用于病毒,炎性细胞,促炎性细胞因子和生化指标,说明月球菌(蛋白质)和损伤(乳酸脱氢酶[LD]活性)。 DSD,comparedwiththeBNstrain.Alveolarmacrophages,LDactivity,andtotalproteinconcentrationwerehigherintheBNrats,whereasneutrophilnumbersandinterleukin6andtumornecrosisfactor-alphaactivitiesweregreatestinthebronchoalveolarlavagefluidofF344andSDrats.TheresultsindicatethatF344andSDratsrespondinsimilarmannertoviralinfection,whereasviralreplicationwasmorelimitedinBNratsandwasassociatedwithadifferentprofileofpulmonarycells。

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