Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Host gene expression profiling in influenza A virus-infected lung epithelial (A549) cells: a comparative analysis between highly pathogenic and modified H5N1 viruses | Chakrabarti et al. Virology Journal 2010 7 219 http content 7 1 219 VIROLOGY JOURNAL RESEARCH Open Access Host gene expression profiling in influenza A virus-infected lung epithelial A549 cells a comparative analysis between highly pathogenic and modified H5N1 viruses Alok K Chakrabarti Veena C Vipat Sanjay Mukherjee Rashmi Singh Shailesh D Pawar Akhilesh C Mishra Abstract Background To understand the molecular mechanism of host responses to highly pathogenic avian influenza virus infection and to get an insight into the means through which virus overcomes host defense mechanism we studied global gene expression response of human lung carcinoma cells A549 at early and late stages of infection with highly pathogenic avian Influenza A H5N1 virus and compared it with a reverse genetics modified recombinant A H5N1 vaccine virus using microarray platform. Results The response was studied at time points 4 8 16 and 24 hours post infection hpi . Gene ontology analysis revealed that the genes affected by both the viruses were qualitatively similar but quantitatively different. Significant differences were observed in the expression of genes involved in apoptosis and immune responses specifically at 16 hpi. Conclusion We conclude that subtle differences in the ability to induce specific host responses like apoptotic mechanism and immune responses make the highly pathogenic viruses more virulent. Background Outbreaks of avian influenza A H5N1 virus a highly pathogenic avian influenza HPAI are considered as a public health risk with pandemic potential 1 . Understanding the pathology transmission clinical features and treatments has become necessary for the prevention and management of such outbreaks 2 3 . The mechanisms responsible for the virulence of HPAI viruses in humans are not completely understood. Viral factors are necessary for productive infection but are not sufficient to explain the pathogenesis of HPAI infection in humans 4 5 . It is well .
