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#4238 : Systemic and mucosal immune response variation during SARS-CoV-2 infection and recovery
Topics: Metagenomics (16s)
Origin: IP
Project type: Service

Name of Applicant: Pedro Goncalves
Date of application: 22-07-2020
Unit: Innate Immunity
Location: Metchnikoff Building
Phone: 0601080704
@ Mail: pedro.goncalves@pasteur.fr
@ PI-Mail: james.di-santo@pasteur.fr
Collaboration with:CHINA (HONG KONG)

Project context and summary:

Under normal conditions, the relationship between the nasopharynx microbiota and the host is symbiotic with many physiologic benefits. However, even in healthy individuals potentially pathogenic bacteria can also be found embedded in the community of nasopharynx commensals. Nasal-associated lymphoid tissue is strategically located to potential respiratory pathogens; in this context, B cell activation induces specific secretory IgA while T cells/ILCs produce cytokines. Previously we have established methods to characterize nasopharynx microbiota by 16S rRNA sequencing and assays are in place to analyze secretory antibodies, interferons (IFNs) and cytokines concentrations in nasopharyngeal secretions of healthy individuals. Coronavirus disease 2019 (COVID-19) is a newly emergent pandemic infectious disease caused by SARS-CoV-2. At present there are no biomarkers readily available to the physician at the time of hospital admission that are able to predict the likelihood of disease progression in COVID-19 patients. There is increasing evidence that suggest that the nasopharyngeal microbiome composition plays an important role in the pathogenesis of viral acute respiratory tract infections. One factor that has been poorly studied and needs to be integrated in SARS-CoV-2 pathogenesis models is the microbiome. We hypothesize that the nasopharynx microbiota at baseline affects the likelihood and density of successful SARS-CoV-2 colonization. At present there are no data regarding the potential role of bacterial co-infection in symptomatology and severity of COVID-19. We hypothesize that the increased bacterial pathobionts carriage in elderly and in some healthy augment microbiota dysbiosis caused by SARS-CoV-2 and is involved in severe and critical COVID-19 cases. Lastly, our capacity to quantitate antibodies, IFNs and cytokines should allow for the definition of biomarkers in nasopharyngeal secretions that can distinguish clinical outcomes in COVID-19 patients.


Related team publications:
Service Delivery
Manager: laurence.ma@pasteur.fr
Status: Closed


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