T CD8 lymphocytes play critical role in controlling infection by some neurotrophic virus by dependent mechanisms of perforin and granzymes, FasL-Fas, or by the production of antiviral cytokines such as IFN-³ or TNF-±. Granzyme B induce apoptosis and DNA fragmentation into target cells. T CD8 cells participate in the eradication of infected cells by West Nile virus, whereas athymic mice exhibit susceptibility to Japanese encephalitis virus infection, which can be reversed by the adoptive transfer of cytolytic lymphocytes. In reinfection by Dengue virus, T CD8 cells can promote cross-reactivity of the memory about primary infection, resulting in high levels of degranulation, cytokine production, and altered cytolytic activity. So, contributing to the worsening of the disease and development of hemorrhagic fever. The Zika virus (ZIKV), Dengue virus and Yellow Fever are flavivirus well known as human pathogens, thus being of great importance to public health. According to WHO, the first cases of infection ZIKV in Brazil in 2015 was associated with increased cases of microcephaly. Despite the known part of the actions of the immune system to infection by certain flaviviruses, little is known about the pathogenesis of ZIKV infection. Thus, this project aims to elucidate the role of T CD8 cells in experimental ZIKV infection, and thus assist in the understanding of the pathogenesis of the disease caused by ZIK virus.
News published in Agência FAPESP Newsletter about the scholarship: