TAILIEUCHUNG - Báo cáo y học: " Classic swine fever virus NS2 protein leads to the induction of cell cycle arrest at S-phase and endoplasmic reticulum stress"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Classic swine fever virus NS2 protein leads to the induction of cell cycle arrest at S-phase and endoplasmic reticulum stress | Tang et al. Virology Journal 2010 7 4 http content 7 1 4 VIROLOGY JOURNAL RESEARCH Open Access Classic swine fever virus NS2 protein leads to the induction of cell cycle arrest at S-phase and endoplasmic reticulum stress Qing-hai Tang Yan-ming Zhang Li Fan Gang Tong Lei He Chen Dai Abstract Background Classical swine fever CSF caused by virulent strains of Classical swine fever virus CSFV is a haemorrhagic disease of pigs characterized by disseminated intravascular coagulation thrombocytopoenia and immunosuppression and the swine endothelial vascular cell is one of the CSFV target cells. In this report we investigated the previously unknown subcellular localization and function of CSFV NS2 protein by examining its effects on cell growth and cell cycle progression. Results Stable swine umbilical vein endothelial cell line SUVEC expressing CSFV NS2 were established and showed that the protein localized to the endoplasmic reticulum ER . Cellular analysis revealed that replication of NS2-expressing cell lines was inhibited by 20-30 due to cell cycle arrest at S-phase. The NS2 protein also induced ER stress and activated the nuclear transcription factor kappa B NF-kB . a significant increase in cyclin A transcriptional levels was observed in NS2-expressing cells but was accompanied by a concomitant increase in the proteasomal degradation of cyclin A protein. Therefore the induction of cell cycle arrest at S-phase by CSFV NS2 protein is associated with increased turnover of cyclin A protein rather than the down-regulation of cyclin A transcription. Conclusions All the data suggest that CSFV NS2 protein modulate the cellular growth and cell cycle progression through inducing the S-phase arrest and provide a cellular environment that is advantageous for viral replication. These findings provide novel information on the function of the poorly characterized CSFV NS2 protein. Background Classical swine fever CSF is a highly contagious and often fatal disease

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