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Host-pathogens interactions during RSV / S. pneumoniae infection immune response and p53 pathway

Abstract : Respiratory viruses play a leading role in the etiology of respiratory infections. Currently, respiratory syncytial virus (RSV) is generally considered to be the etiologic agent of respiratory disease in pediatric importance, as children can develop bronchiolitis and pneumonia when infected with the virus. The first RSV infection occurs in the first two years of life in about 95% of children, with the peak incidence occurring in the first few months of life. An important aspect of the prognosis of viral infections is the role of bacterial co-infection. The combination of viral and bacterial agents has been reported between RSV and Streptococcus pneumoniae bacteria. Because of the clinical importance of this co-infection and the high rate of RSV circulation, it is important to understand how the immune system is affected by the infection of both pathogens. Our study was designed to evaluate the immune response in macrophages, in addition to interactions between RSV and p53 transcription factor. The results show a particular profile of this mixed co-infection in macrophages and p53 regulation that implies several modifications in the innate immune response and that allowed us to better understand the mechanisms of pathogenesis of RSV in pulmonary epithelial cells. In the last part, we evaluated the direct impact of mixed co-infection in non-human primates and this model showed us the difficulties and complexities of establishing severe pneumonia.
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https://tel.archives-ouvertes.fr/tel-01837919
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Submitted on : Friday, July 13, 2018 - 1:01:13 AM
Last modification on : Wednesday, December 18, 2019 - 4:20:07 PM
Long-term archiving on: : Monday, October 15, 2018 - 9:43:18 PM

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  • HAL Id : tel-01837919, version 1

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Daniela Bandeira Brancante Machado. Host-pathogens interactions during RSV / S. pneumoniae infection immune response and p53 pathway. Virology. Université de Lyon, 2017. English. ⟨NNT : 2017LYSEN083⟩. ⟨tel-01837919⟩

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