tetano
Editor, Senior Moderator
J Virol. 2010 Sep 22. [Epub ahead of print]
Influenza A virus replication Induces Cell Cycle Arrest in G0/G1 Phase.
He Y, Xu K, Keiner B, Zhou J, Czudai V, Li T, Chen Z, Liu J, Klenk HD, Shu YL, Sun B.
Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai Institutes for Biological Sciences, 225 South Chongqing Road, Shanghai, 200025, China; Institut of Virology, Philipps University of Marburg, Hans-Meerwein-Str.2, Marburg, 35043, Germany; Chinese Center for Disease Control and Prevention, Yingxin Street 100, Xuanwu District, Beijing 100052, China; State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Science, Wuhan 430071, Hubei, China; Shanghai Institute of Biological Products, Shanghai 200052, China; Key Laboratory of Zoonosis of Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, 200031, China.
Abstract
Many viruses interact with the host cell division cycle to favor their own growth. In this study, we examined the ability of influenza A virus to manipulate cell cycle progression. Our results show that influenza A virus A/WSN/33 (H1N1) replication results in G0/G1 phase accumulation of infected cells, and this accumulation is caused by the prevention of cell cycle entry from G0/G1 phase to S phase. Consistent with the G0/G1 phase accumulation, the amount of hyperphosphorylated retinoblastoma protein, a necessary active form for cell cycle progression through late G1 into the S phase, decreased after the infection of A/WSN/33 (H1N1) virus. In addition, other key molecules in the regulation of the cell cycle, such as p21, cyclin E and D1, were also changed and showed a pattern of G0/G1 phase cell cycle arrest. It is interesting to note that an increased viral protein expression and progeny virus production in cells synchronized in the G0/G1 phase as compared to either unsynchronized cells or cells synchronized in the G2/M phase were observed. The G0/G1 phase cell cycle arrest is likely to be a common strategy since the effect was also observed in other strains such as H3N2, H9N2, PR8 H1N1 and pandemic swine H1N1 viruses. These findings, in all, suggest that influenza A virus may provide favorable conditions for viral protein accumulation and virus production by inducing a G0/G1 phase cell cycle arrest in infected cells.
PMID: 20861262 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/20861262
Influenza A virus replication Induces Cell Cycle Arrest in G0/G1 Phase.
He Y, Xu K, Keiner B, Zhou J, Czudai V, Li T, Chen Z, Liu J, Klenk HD, Shu YL, Sun B.
Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai Institutes for Biological Sciences, 225 South Chongqing Road, Shanghai, 200025, China; Institut of Virology, Philipps University of Marburg, Hans-Meerwein-Str.2, Marburg, 35043, Germany; Chinese Center for Disease Control and Prevention, Yingxin Street 100, Xuanwu District, Beijing 100052, China; State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Science, Wuhan 430071, Hubei, China; Shanghai Institute of Biological Products, Shanghai 200052, China; Key Laboratory of Zoonosis of Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, 200031, China.
Abstract
Many viruses interact with the host cell division cycle to favor their own growth. In this study, we examined the ability of influenza A virus to manipulate cell cycle progression. Our results show that influenza A virus A/WSN/33 (H1N1) replication results in G0/G1 phase accumulation of infected cells, and this accumulation is caused by the prevention of cell cycle entry from G0/G1 phase to S phase. Consistent with the G0/G1 phase accumulation, the amount of hyperphosphorylated retinoblastoma protein, a necessary active form for cell cycle progression through late G1 into the S phase, decreased after the infection of A/WSN/33 (H1N1) virus. In addition, other key molecules in the regulation of the cell cycle, such as p21, cyclin E and D1, were also changed and showed a pattern of G0/G1 phase cell cycle arrest. It is interesting to note that an increased viral protein expression and progeny virus production in cells synchronized in the G0/G1 phase as compared to either unsynchronized cells or cells synchronized in the G2/M phase were observed. The G0/G1 phase cell cycle arrest is likely to be a common strategy since the effect was also observed in other strains such as H3N2, H9N2, PR8 H1N1 and pandemic swine H1N1 viruses. These findings, in all, suggest that influenza A virus may provide favorable conditions for viral protein accumulation and virus production by inducing a G0/G1 phase cell cycle arrest in infected cells.
PMID: 20861262 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/20861262