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Characterization of the cellular immune response induced in individuals infected with the Yellow fever virus and vaccinated with the formulation YF17DD

Grant number: 19/11462-1
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): September 01, 2019
Effective date (End): August 31, 2020
Field of knowledge:Health Sciences - Medicine
Principal Investigator:Esper Georges Kallás
Grantee:Clara Quitete Rabahi
Home Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Yellow fever (YF) is an arbovirus disease, caused by a virus and transmitted by an infected mosquito. The incubation period is from 3 to 6 days. The disease progresses with fever, malaise, chills, headache and low back pain, in addition to generalized myalgia, nausea and dizziness. YF does not have specific treatment, and its management is only carried out with clinical care. To date, the unique protection is a single dose of the anti-yellow fever vaccine, which has its immunogenic power proven by the production of neutralizing antibodies and confer about 98% protection. Although there are some studies reporting the important role of neutralizing antibodies after vaccination by the 17DD vaccine strain, few of them are related to the activation of TCD4+ and TCD8+. The most of them are restricted to the analysis of the immunological response conferred by the vaccine virus strain yellow fever (YFV) and not by the wild type virus. Thus, this study aims to identify and compare the antigen-specific response of CD4+ and CD8+ T cells from individuals vaccinated by the 17DD strain and in individuals naturally infected by YFV. To this end, 10 vaccinated patients and 20 patients infected with the wild virus will be evaluated for the activation of CD4 + and CD8+ T lymphocytes, using pools of peptides specific for YFV proteins, in order to identify the memory profile and production of cytokines which may be associated with the form of immunity induced by vaccination or by natural infection.