Virology & Mycology
Open Access
ISSN: 2161-0517
+44 1223 790975
ISSN: 2161-0517
+44 1223 790975
Rafael Polidoro Alves Barbosa
Posters-Accepted Abstracts: Virol-mycol
Vaccines are considered one of the most successful and effective medical interventions to prevent infectious diseases. It is estimated that up to 3 million human lives are spared through vaccination per year. The use of recombinant viruses as vectors is one of the most viable strategies for the development of new vaccines. In 2010, our group has demonstrated the feasibility of the generation and use of recombinant influenza (Flu) viruses in combination with recombinant adenoviruses (Ad) to protect against Toxoplasma gondii infection in mice. The potential of Flu-Ad protocol led us to the search of an experimental model in which the CD8 T cell response has a pivotal role in protection. In this context, an important model is the mice infection by Trypanosoma cruzi. This protozoan parasite is responsible for the Chagas disease in humans. The treatment has higher efficacy in the acute phase of the disease, yet causes undesired side effects. There are currently no vaccines against Chagas disease in humans, which makes the study and development of an optimized vaccination protocol an important research subject. Using reverse genetics we generated recombinant influenza viruses encoding the C-terminus and Medial portions of the T. cruzia mastigote surface protein (ASP2) and further characterized the phenotype and genotype of those viruses. Immunization using Influenza-ASP2 as prime and Ad-ASP2 as boost induced a potent CD8+ polyfunctional T cell response, which was mostly immunodominant. This immune response was able to protect C57BL/6 and C3H/He mice challenged with Y strain of T. cruzi. Despite the level of protection reached in the effector phase of immune response, a significant reduction of survival was observed when vaccinated mice were challenged 130 days after boost dose. Accordingly, the production of cytokines and number of immunodominant cells in splenocytes of vaccinated mice dropped in this time point, explaining the reduced memory protection.