Artículos de revistas
Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression
Fecha
2010Registro en:
VIRUS RESEARCH, v.149, n.1, p.56-63, 2010
0168-1702
10.1016/j.virusres.2009.12.013
Autor
ACRANI, Gustavo Olszanski
GOMES, Rogerio
PROENCA-MODENA, Jose Luiz
SILVA, Andrei Furlan da
CARMINATI, Patricia Oliveira
SILVA, Maria Lucia
SANTOS, Rodrigo Ivo Marques
ARRUDA, Eurico
Institución
Resumen
Oropouche (OROV) is a single-stranded RNA arbovirus of the family Bunyaviridae, genus Orthobunyavirus, which has caused over half a million cases of febrile illness in Brazil in the past 30 years. OROV fever has been registered almost exclusively in the Amazon region, but global warming, deforestation and redistribution of vectors and animal reservoirs increases the risk of Oropouche virus emergence in other areas. OROV causes a cytolytical infection in cultured cells with characteristic cytopathic effect 48 h post-infection. We have studied the mechanisms of apoptosis induced by OROV in HeLa cells and found that OROV causes DNA fragmentation detectable by gel electrophoresis and by flow cytometric analysis of the Sub-G1 population at 36 h post-infection. Mitochondrial release of cytochrome C and activation of caspases 9 and 3 were also detected by western blot analysis. Lack of apoptosis induced by UV-inactivated OROV reveals that virus-receptor binding is not sufficient to induce cell death. Results obtained in cells treated with chloroquine and cycloheximide indicated that viral uncoating and replication are required for apoptosis induction by OROV. Furthermore, treatment of the cells with pan-caspase inhibitor prevented OROV-induced apoptosis without affecting virus progeny production. The results show that OROV infection in vitro causes apoptosis by an intracellular pathway involving mitochondria, and activated by a mechanism dependent on viral replication and protein synthesis. (C) 2010 Elsevier B.V. All rights reserved.