Journal
JOURNAL OF VIROLOGY
Volume 84, Issue 24, Pages 12832-12840Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01216-10
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Funding
- European Union [SP5B-CT-2006-044161]
- Deutsche Forschungsgemeinschaft [SFB 593, TP B2]
- CAS [KSCX2-YW-R-161]
- National Ministry of Science and Technology [20072714]
- National Natural Science Foundation of China [30950002, 30623003, 30721065, 30801011, 30870126, 90713044]
- Technology Commission of Shanghai Municipality [08DZ2291703, 088014199]
- National Science and Technology Major Project [2008ZX10002-014, 2009ZX10004-016]
- National 973 key project [2007CB512404]
- SPHRF [SPHRF2008001, SPHRF2009001]
- Li Kha Shing Foundation
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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 G(0)/G(1)-phase accumulation of infected cells and that this accumulation is caused by the prevention of cell cycle entry from G(0)/G(1) phase into S phase. Consistent with the G(0)/G(1)-phase accumulation, the amount of hyperphosphorylated retinoblastoma protein, a necessary active form for cell cycle progression through late G(1) into S phase, decreased after infection with A/WSN/33 ( H1N1) virus. In addition, other key molecules in the regulation of the cell cycle, such as p21, cyclin E, and cyclin D1, were also changed and showed a pattern of G(0)/G(1)-phase cell cycle arrest. It is interesting that increased viral protein expression and progeny virus production in cells synchronized in the G(0)/G(1) phase were observed compared to those in either unsynchronized cells or cells synchronized in the G(2)/M phase. G(0)/G(1)-phase cell cycle arrest is likely 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 G(0)/G(1)-phase cell cycle arrest in infected cells.
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