Otros
O papel de IRF-5 em macrófagos e linfócitos B para o controle da infecção pelo vírus oropouche em modelo murino
Fecha
2021-06-17Registro en:
Autor
Simeoni, Camila Lopes
Institución
Resumen
Emerging viruses can cause great impacts in a susceptible population. For instance, virusestransmitted by arthropod vectors can widely spread in wild landscapes and in urban areas. This is the case of Oropouche virus. This emerging arbovirus can be transmitted in urban areas through Culicoides paraensis’ prick. The Culicoides paraensis is a hematophagous midge, which circulates in Brazilian north and northeast. The Oropouche virus cause an exanthematic febrile illness in humans, which in some cases, can evolve to neurological complications. Although, the pathogenetics details and the role of key transcription factors of the innate immune response on control of this viral infection are not completely understood. Furthermore, IRF-5, a transcription factor activated after the recognition of pathogen-associate molecular patterns, is essential to control neuroinvasion by Oropouche virus. Thus, the aim of this study was to characterize how the absence of this gene in essential cells of the immunological response, such as macrophages and B lymphocytes, could affect the disease progression caused by Oropouche in a murine model. To achieve this goal, a recombination system known as Cre Lox has been taken. As a result, the virus has achieved the central nervous system of both lineages. Oropouche has caused meningitis, encephalitis and conditional mutants’ death. Highlighting the IRF5’s importance in these leucocytes in front of neuropathogenesis induced by this virus. In conclusion, there is a requirement to investigate how Oropouche virus gain access to Central Nervous System. This project has been approved by the Ethics Committee on Animal Experimentation at Unicamp (CEUA) under number 5423-1/2019. It has conducted in the Animal Facility NB2 of the Biology Institute of the State University of Campinas CTNBio CIBIO 2018 / type2- 02 (01250.017340 / 2018-28).