Mecanismos de morte utilizados pelas c?lulas epiteliais alveolares infectadas com o v?rus sincicial respirat?rio

• Main Author: Ferreira, Gabriela Acevedo
• Publication Date: 2016
• Format: Master thesis
• Language: por
• Source: Biblioteca Digital de Teses e Dissertações da PUC_RS
• Download full: http://tede2.pucrs.br/tede2/handle/tede/8402
• topic: Infec??es Respirat?rias; V?rus Sinciciais Respirat?rios; Morte Celular; Apoptose; CIENCIAS DA SAUDE::MEDICINA

Infection by respiratory syncytial virus (RSV) is the leading cause of childhood hospitalization as well as a major health and economic burden worldwide. RSV causes RTI in adults and lower respiratory tract illness (LRTI), including acute bronchiolitis and pneumonia, in infants and young children. Unfortunately, RSV infection provides only limited immune protection to reinfection, mostly due to inadequate immunological memory, which leads to an exacerbated inflammatory response in the respiratory tract promoting airway damage during virus clearance. Despite extensive research efforts, safe and effective vaccines against RSV are currently unavailable. Nevertheless, a prophylactic strategy based on a humanized neutralizing antibody against RSV is widely used in new born at high-risk, such as preterm infants and those suffering from cardiovascular diseases and immunosuppression. The alveolar epithelial cells are the first line of defense against the virus, most associated with the local inflammation in the disease. The entry of respiratory syncytial virus to alveolar epithelial cells (AECs) is an important step in the infection process involving binding of the RSV G and F protein molecules bound to the surface of the host cell. Infection with respiratory syncytial virus is associated with the epithelial cell death and vigorous inflammation, apoptotic death of infected cells is a mechanism to reduce virus replication. And this study showed infection induced by active respiratory syncytial virus in the epithelial cells of the A549 line showing the pathway of cell death induced by the host cells, our results show the pathway of apoptosis induced from the caspase-3 activation and no dependence production of the production of reactive oxygen species.