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Influenza A Virus Replication Induces Cell Cycle
, 2010
"... 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 cel ..."
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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 G0/G1-phase accumulation of infected cells and that this accumulation is caused by the prevention of cell cycle entry from G0/G1 phase into 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 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 G0/G1-phase cell cycle arrest. It is interesting that increased viral protein expression and progeny virus production in cells synchronized in the G0/G1 phase were observed compared to
Review The Coronavirus Nucleocapsid Is a Multifunctional Protein
, 2014
"... All in-text references underlined in blue are linked to publications on ResearchGate, letting you access and read them immediately. ..."
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All in-text references underlined in blue are linked to publications on ResearchGate, letting you access and read them immediately.
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, 1993
"... Murine AIDS is initiated in the lymph nodes draining the site of inoculation, and the infected B cells influence T cells located at distance, in noninfected organs. ..."
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Murine AIDS is initiated in the lymph nodes draining the site of inoculation, and the infected B cells influence T cells located at distance, in noninfected organs.
Nonstructural Protein 1s Mediates Reovirus-Induced Cell Cycle Arrest and Apoptosis
"... Reovirus nonstructural protein1s is implicated in cell cycle arrest at the G2/M boundary and induction of apoptosis. However, the contribution of1s to these effects in an otherwise isogenic viral background has not been defined. To evaluate the role of 1s in cell cycle arrest and apoptosis, we used ..."
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Reovirus nonstructural protein1s is implicated in cell cycle arrest at the G2/M boundary and induction of apoptosis. However, the contribution of1s to these effects in an otherwise isogenic viral background has not been defined. To evaluate the role of 1s in cell cycle arrest and apoptosis, we used reverse genetics to generate a1s-null reovirus. Following infection with wild-type virus, we observed an increase in the percentage of cells in G2/M, whereas the proportion of cells in G2/M following infec-tion with the1s-null mutant was unaffected. Similarly, we found that the wild-type virus induced substantially greater levels of apoptosis than the1s-null mutant. These data indicate that1s is required for both reovirus-induced cell cycle arrest and apoptosis. To define sequences in1s that mediate these effects, we engineered viruses encoding C-terminal1s truncations by introducing stop codons in the1s open reading frame.We also generated viruses in which charged residues near the1s amino terminus were replaced individually or as a cluster with nonpolar residues. Analysis of these mutants revealed that amino acids 1 to 59 and the amino-terminal basic cluster are required for induction of both cell cycle arrest and apoptosis. Remarkably, viruses that fail to induce cell cycle arrest and apoptosis also are attenuated in vivo. Thus, identical sequences in1s are required for reovirus-induced cell cycle arrest, apoptosis, and pathogenesis. Collectively, these findings provide evidence that the1s-medi-ated properties are genetically linked and suggest that these effects are mechanistically related. Apoptosis is a critical host response to viral infection. Induc-tion of apoptotic cell death limits production of viral progeny from infected cells (1) and provides signals that activate adaptive
Murine Norovirus Replication Induces G0/G1 Cell Cycle Arrest in Asynchronously Growing Cells
"... Many viruses replicate most efficiently in specific phases of the cell cycle, establishing or exploiting favorable conditions for viral replication, although little is known about the relationship between caliciviruses and the cell cycle. Microarray andWestern blot analysis of murine norovirus 1 (MN ..."
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Many viruses replicate most efficiently in specific phases of the cell cycle, establishing or exploiting favorable conditions for viral replication, although little is known about the relationship between caliciviruses and the cell cycle. Microarray andWestern blot analysis of murine norovirus 1 (MNV-1)-infected cells showed changes in cyclin transcript and protein levels indicative of a G1 phase arrest. Cell cycle analysis confirmed that MNV-1 infection caused a prolonging of the G1 phase and an accumulation of cells in the G0/G1 phase. The accumulation in G0/G1 phase was caused by a reduction in cell cycle progression through the G1/S restriction point, withMNV-1-infected cells released from a G1 arrest showing reduced cell cycle progression compared to mock-infected cells. MNV-1 replication was compared in populations of cells synchronized into specific cell cycle phases and in asyn-chronously growing cells. Cells actively progressing through the G1 phase had a 2-fold or higher increase in virus progeny and capsid protein expression over cells in other phases of the cell cycle or in unsynchronized populations. These findings suggest that MNV-1 infection leads to prolonging of the G1 phase and a reduction in S phase entry in host cells, establishing favorable conditions for viral protein production and viral replication. There is limited information on the interactions between norovi-ruses and the cell cycle, and this observation of increased replication in the G1 phase may be representative of other members of the Caliciviridae. IMPORTANCE
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, 2004
"... This article cites 90 articles, 46 of which can be accessed free ..."
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, 2001
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, 2008
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, 2003
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