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dc.contributor.authorDanz, Hillary Rose
dc.description.abstractApproximately three billion people in the world are infected with helminth parasites. Schistosoma mansoni is a blood fluke that accounts for over 85 million infections across sub-Saharan Africa, Middle East, and parts of Brazil. S. mansoni is often found in areas with high rates of viral infections such as dengue, rotavirus, HCV, and HIV, and this co-endimicity greatly increases the risk of coinfection. Chronic S. mansoni infection biases the immune system to a CD4+ Th2 and anti-inflammatory phenotype. In contrast, a robust pro-inflammatory response is needed to effectively resolve most viral infections. Therefore, it is important to understand how a Th2/anti-inflammatory biased immune system influences a secondary viral infection requiring a pro-inflammatory response. Several studies have evaluated helminth, influenza coinfections, with varied results dependent on the helminth species. We hypothesize that this variation is related to the ability of the helminth to induce localized immune biasing, in particular in the lung, during subsequent infection with influenza. During chronic S. mansoni infection, schistosome eggs travel to the pulmonary vasculature, become embedded in pulmonary tissue, and secrete products that induce localized immune biasing. Here we show that mice chronically infected with S. mansoni had significantly reduced morbidity and mortality to influenza infection. Coinfected mice also had significantly reduced pro-inflammatory responses from influenza-specific CD8+ T cells in the lung milieu. Additionally, histopathology showed lungs of S. mansoni infected mice had smaller lesions of alveolitis and pneumonitis as a result of influenza infection. Together, these data indicate chronic S. mansoni infection is beneficial for influenza infection due to decreased pro-inflammatory responses that limit cellular infiltration to the lungs resulting in decreased pneumonitis. Additionally, this study adds to the literature suggesting a relationship between the location(s) of localized helminth biasing and location of viral infections.
dc.subjectSchistosoma mansoni
dc.subjectInfluenza A
dc.subjectlung granuloma
dc.subjectalternative activation
dc.titleAnalysis of immune interactions, histopathology, and viral load during Schistosoma mansoni and Influenza A coinfection
dc.description.departmentInfectious Diseases
dc.description.majorInfectious Diseases
dc.description.advisorDonald Harn
dc.description.committeeDonald Harn
dc.description.committeeWendy Watford
dc.description.committeeKimberly Klonowski
dc.description.committeeRay Kaplan
dc.description.committeeR. Jeff Hogan

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