Canine parvovirus NS1 induced apoptosis involves mitochondria, accumulation of reactive oxygen species and activation of caspases.

作者: A.K. Gupta , S.K. , Sahoo , A.P. , Rosh

DOI: 10.1016/J.VIRUSRES.2015.10.019

关键词: CaspaseHeLaProgrammed cell deathIntrinsic apoptosisBiologyCell cycleApoptosisCell biologyMitochondrionReactive oxygen species

摘要: The non-structural protein (NS1) of parvoviruses plays an important role in viral replication and is thought to be responsible for inducing cell death. However, the detailed mechanism pathways involved canine parvovirus type 2 NS1 (CPV2.NS1) induced apoptosis are not yet known. In present study, we report that expression CPV2.NS1 HeLa cells arrests G1 phase cycle mitochondria mediated as indicated by mitochondrial depolarization, release cytochrome-c activation caspase 9. Treatment with 9 inhibitor Z-LEHD-FMK reduced induction significantly. We also causes accumulation reactive oxygen species (ROS) treatment antioxidant reduces ROS levels extent apoptosis. Our results provide insight into apoptosis, which might prove valuable developing oncolytic agent.

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