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10.1128/JVI.01881-17 http://scihub22266oqcxt.onion/10.1128/JVI.01881-17 29237843!5809726!29237843     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Virol 2018 ; 92 (5): ä Nephropedia Template TP {{tp|p=29237843|t=2018. Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for Viral DNA Replication |pdf=|usr=}}{{29237843}} gab.com Text Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for Viral DNA Replication JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=29237843 #FOAvip Human parvovirus B19 (B19V) infection of human erythroid progenitor cells (EPCs) induces a DNA damage response and cell cycle arrest at late S phase, which facilitates viral DNA replication. However, it is not clear exactly which cellular factors are employed by this single-stranded DNA virus. Here, we used microarrays to systematically analyze the dynamic transcriptome of EPCs infected with B19V. We found that DNA metabolism, DNA replication, DNA repair, DNA damage response, cell cycle, and cell cycle arrest pathways were significantly regulated after B19V infection. Confocal microscopy analyses revealed that most cellular DNA replication proteins were recruited to the centers of viral DNA replication, but not the DNA repair DNA polymerases. Our results suggest that DNA replication polymerase delta and polymerase alpha are responsible for B19V DNA replication by knocking down its expression in EPCs. We further showed that although RPA32 is essential for B19V DNA replication and the phosphorylated forms of RPA32 colocalized with the replicating viral genomes, RPA32 phosphorylation was not necessary for B19V DNA replication. Thus, this report provides evidence that B19V uses the cellular DNA replication machinery for viral DNA replication.IMPORTANCE Human parvovirus B19 (B19V) infection can cause transient aplastic crisis, persistent viremia, and pure red cell aplasia. In fetuses, B19V infection can result in nonimmune hydrops fetalis and fetal death. These clinical manifestations of B19V infection are a direct outcome of the death of human erythroid progenitors that host B19V replication. B19V infection induces a DNA damage response that is important for cell cycle arrest at late S phase. Here, we analyzed dynamic changes in cellular gene expression and found that DNA metabolic processes are tightly regulated during B19V infection. Although genes involved in cellular DNA replication were downregulated overall, the cellular DNA replication machinery was tightly associated with the replicating single-stranded DNA viral genome and played a critical role in viral DNA replication. In contrast, the DNA damage response-induced phosphorylated forms of RPA32 were dispensable for viral DNA replication. Twit Text FOAVip Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for Viral DNA Replication ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=29237843 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29237843 #FOAvip English Wikipedia <ref>{{Cite pmid|29237843}}</ref> Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for Viral DNA Replication #MMPMID29237843 Zou W; Wang Z; Xiong M; Chen AY; Xu P; Ganaie SS; Badawi Y; Kleiboeker S; Nishimune H; Ye SQ; Qiu J J Virol 2018[Mar]; 92 (5): ä PMID29237843show ga Human parvovirus B19 (B19V) infection of human erythroid progenitor cells (EPCs) induces a DNA damage response and cell cycle arrest at late S phase, which facilitates viral DNA replication. However, it is not clear exactly which cellular factors are employed by this single-stranded DNA virus. Here, we used microarrays to systematically analyze the dynamic transcriptome of EPCs infected with B19V. We found that DNA metabolism, DNA replication, DNA repair, DNA damage response, cell cycle, and cell cycle arrest pathways were significantly regulated after B19V infection. Confocal microscopy analyses revealed that most cellular DNA replication proteins were recruited to the centers of viral DNA replication, but not the DNA repair DNA polymerases. Our results suggest that DNA replication polymerase delta and polymerase alpha are responsible for B19V DNA replication by knocking down its expression in EPCs. We further showed that although RPA32 is essential for B19V DNA replication and the phosphorylated forms of RPA32 colocalized with the replicating viral genomes, RPA32 phosphorylation was not necessary for B19V DNA replication. Thus, this report provides evidence that B19V uses the cellular DNA replication machinery for viral DNA replication.IMPORTANCE Human parvovirus B19 (B19V) infection can cause transient aplastic crisis, persistent viremia, and pure red cell aplasia. In fetuses, B19V infection can result in nonimmune hydrops fetalis and fetal death. These clinical manifestations of B19V infection are a direct outcome of the death of human erythroid progenitors that host B19V replication. B19V infection induces a DNA damage response that is important for cell cycle arrest at late S phase. Here, we analyzed dynamic changes in cellular gene expression and found that DNA metabolic processes are tightly regulated during B19V infection. Although genes involved in cellular DNA replication were downregulated overall, the cellular DNA replication machinery was tightly associated with the replicating single-stranded DNA viral genome and played a critical role in viral DNA replication. In contrast, the DNA damage response-induced phosphorylated forms of RPA32 were dispensable for viral DNA replication. |*Cell Division[MESH] |*DNA Replication[MESH] |*Host-Pathogen Interactions/genetics/physiology[MESH] |*Virus Replication[MESH] |Bromodeoxyuridine/metabolism[MESH] |CD36 Antigens/analysis/metabolism[MESH] |Cell Cycle[MESH] |Cell Cycle Checkpoints[MESH] |Cell Line[MESH] |DNA Damage[MESH] |DNA Polymerase III[MESH] |DNA Polymerase beta[MESH] |DNA Repair[MESH] |DNA, Single-Stranded/metabolism[MESH] |DNA, Viral/genetics/metabolism[MESH] |Erythroid Precursor Cells/cytology/virology[MESH] |Fetal Death[MESH] |Gene Expression Regulation, Viral/physiology[MESH] |Genome, Viral[MESH] |Humans[MESH] |Parvoviridae Infections/*virology[MESH] |Parvovirus B19, Human/*genetics/*metabolism/pathogenicity[MESH] |Phosphorylation[MESH] |Protein Interaction Maps[MESH] |Red-Cell Aplasia, Pure/virology[MESH] |Replication Protein A/genetics[MESH] |S Phase[MESH] |Transcriptome[MESH]Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for V(epmc).pdf DeepDyve Pubget Overpricing