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Article: Parvovirus infection-induced DNA damage response.

Luo, Yong / Qiu, Jianming

Future virology

2014 Volume 8, Issue 3, Page(s) 245–257

Abstract: ... for the study of the molecular mechanisms underlying viral infection-induced DNA damage response (DDR ... for efficient viral replication. Recent studies have shown that parvoviruses interact with the DNA damage ... This review aims to summarize recent advances in parvovirus-induced DDR, with a focus on the diverse DDR ...

Abstract	Parvoviruses are a group of small DNA viruses with ssDNA genomes flanked by two inverted terminal structures. Due to a limited genetic resource they require host cellular factors and sometimes a helper virus for efficient viral replication. Recent studies have shown that parvoviruses interact with the DNA damage machinery, which has a significant impact on the life cycle of the virus as well as the fate of infected cells. In addition, due to special DNA structures of the viral genomes, parvoviruses are useful tools for the study of the molecular mechanisms underlying viral infection-induced DNA damage response (DDR). This review aims to summarize recent advances in parvovirus-induced DDR, with a focus on the diverse DDR pathways triggered by different parvoviruses and the consequences of DDR on the viral life cycle as well as the fate of infected cells.
Language	English
Publishing date	2014-11-12
Publishing country	England
Document type	Journal Article
ISSN	1746-0794
ISSN	1746-0794
DOI	10.2217/fvl.13.5
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Article ; Online: Genomes of the autonomous parvovirus minute virus of mice induce replication stress through RPA exhaustion.

Haubold, MegAnn K / Aquino, Jessica N Pita / Rubin, Sarah R / Jones, Isabella K / Larsen, Clairine I S / Pham, Edward / Majumder, Kinjal

PLoS pathogens

2023 Volume 19, Issue 5, Page(s) e1011203

Abstract: ... replication induces a global cellular DNA Damage Response (DDR) that is dependent on signaling by the ATM ... environment by usurping host DNA damage signaling proteins in the vicinity of cellular DNA break sites. MVM ... for cellular stores of RPA. Overexpressing RPA in host cells prior to UV-MVM infection rescues DNA fiber ...

Abstract	The oncolytic autonomous parvovirus Minute Virus of Mice (MVM) establishes infection in the nuclear environment by usurping host DNA damage signaling proteins in the vicinity of cellular DNA break sites. MVM replication induces a global cellular DNA Damage Response (DDR) that is dependent on signaling by the ATM kinase and inactivates the cellular ATR-kinase pathway. However, the mechanism of how MVM generates cellular DNA breaks remains unknown. Using single molecule DNA Fiber Analysis, we have discovered that MVM infection leads to a shortening of host replication forks as infection progresses, as well as induction of replication stress prior to the initiation of virus replication. Ectopically expressed viral non-structural proteins NS1 and NS2 are sufficient to cause host-cell replication stress, as is the presence of UV-inactivated non-replicative MVM genomes. The host single-stranded DNA binding protein Replication Protein A (RPA) associates with the UV-inactivated MVM genomes, suggesting MVM genomes might serve as a sink for cellular stores of RPA. Overexpressing RPA in host cells prior to UV-MVM infection rescues DNA fiber lengths and increases MVM replication, confirming that MVM genomes deplete RPA stores to cause replication stress. Together, these results indicate that parvovirus genomes induce replication stress through RPA exhaustion, rendering the host genome vulnerable to additional DNA breaks.
MeSH term(s)	Animals ; Mice ; Minute Virus of Mice/genetics ; Replication Protein A/genetics ; Parvovirus/genetics ; Virus Replication/genetics ; Parvoviridae Infections/genetics ; DNA Replication/genetics
Chemical Substances	Replication Protein A
Language	English
Publishing date	2023-05-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1011203
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Article ; Online: New Insights of Human Parvovirus B19 in Modulating Erythroid Progenitor Cell Differentiation.

Feng, Shuwen / Zeng, Dongxin / Zheng, Junwen / Zhao, Dongchi

Viral immunology

2020 Volume 33, Issue 8, Page(s) 539–549

Abstract: ... maturation of EPCs through inducing viral DNA damage responses and cell cycle arrest. The time phase property ... Human parvovirus B19 (B19), a human pathogen of the erythroparvovirus genus, is responsible ... of NS1 activity during DNA replication and conformity to transient change of hemogram are suggestive ...

Abstract	Human parvovirus B19 (B19), a human pathogen of the erythroparvovirus genus, is responsible for a variety of diseases. B19 cause less symptoms in healthy individuals, also cause acute and chronic anemia in immunodeficiency patients. Transient aplastic crisis and pure red cell aplasia are two kinds of anemic hemogram, respectively, in acute and chronic B19 infection phase, especially occurring in patients with a shortened red cell survival or with immunodeficiency. In addition, B19-infected pregnant women may cause hydrops fetalis or fetal loss. B19 possesses high affinity to bone marrow and fetal liver due to its extremely restricted cytotoxicity to erythroid progenitor cells (EPCs) mediated by viral proteins. The nonstructural protein NS1 is considered to be the major pathogenic factor, which has been shown to inhibit the differentiation and maturation of EPCs through inducing viral DNA damage responses and cell cycle arrest. The time phase property of NS1 activity during DNA replication and conformity to transient change of hemogram are suggestive of its role in regulating differentiation of hematopoietic cells, which is not completely understood. In this review, we summarized the bridge between B19 NS1 and Notch signaling pathway or transcriptional factors GATA, which play an important role in erythroid cell proliferation and differentiation, to provide a new insight of the potential mechanism of B19-induced differential inhibition of EPCs.
MeSH term(s)	Animals ; Cell Differentiation ; DNA Replication ; Erythroid Precursor Cells/physiology ; Erythroid Precursor Cells/virology ; Female ; Humans ; Mice ; Parvoviridae Infections/virology ; Parvovirus B19, Human/pathogenicity ; Pregnancy ; Signal Transduction ; Viral Nonstructural Proteins/genetics ; Viral Nonstructural Proteins/metabolism ; Virus Replication
Chemical Substances	NS1 protein, parvovirus ; Viral Nonstructural Proteins
Language	English
Publishing date	2020-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639075-4
ISSN	1557-8976 ; 0882-8245
ISSN (online)	1557-8976
ISSN	0882-8245
DOI	10.1089/vim.2020.0013
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Article ; Online: Parvovirus B19 induces cellular senescence in human dermal fibroblasts: putative role in systemic sclerosis-associated fibrosis.

Arvia, Rosaria / Zakrzewska, Krystyna / Giovannelli, Lisa / Ristori, Sara / Frediani, Elena / Del Rosso, Mario / Mocali, Alessandra / Stincarelli, Maria A / Laurenzana, Anna / Fibbi, Gabriella / Margheri, Francesca

Rheumatology (Oxford, England)

2021 Volume 61, Issue 9, Page(s) 3864–3874

Abstract: ... such as morphological modifications, senescence-associated β-galactosidase (SA-β-gal) activity, DNA damage response and ... An increased level and nuclear localization of γH2AX, a hallmark of DNA damage response, were also found ... DNA damage with the comet assay: a subpopulation of fibroblasts from B19V-infected cultures showed ...

Abstract	Objective: Emerging evidence demonstrates that excessive accumulation of senescent cells is associated with some chronic diseases and suggests a pathogenic role of cellular senescence in fibrotic processes, such as that occurring in ageing or in SSc. Recently we demonstrated that parvovirus B19 (B19V) activates normal human dermal fibroblasts and induces expression of different profibrotic/pro-inflammatory genes. This observation prompted us to investigate whether it is also able to induce fibroblast senescence as a potential pathogenetic mechanism in B19V-induced fibrosis. Methods: Primary cultures of fibroblasts were infected with B19V and analysed for the acquisition of senescence markers, such as morphological modifications, senescence-associated β-galactosidase (SA-β-gal) activity, DNA damage response and expression of senescence-associated secretory phenotype (SASP)-related factors. Results: We demonstrated that B19V-infected fibroblasts develop typical senescence features such as enlarged and flat-shaped morphology and SA-β-gal activity similar to that observed in SSc skin fibroblasts. They also developed an SASP-like phenotype characterized by mRNA expression and release of some pro-inflammatory cytokines, along with activation of the transcription factor nuclear factor κB. Moreover, we observed B19V-induced DNA damage with the comet assay: a subpopulation of fibroblasts from B19V-infected cultures showed a significantly higher level of DNA strand breaks and oxidative damage compared with mock-infected cells. An increased level and nuclear localization of γH2AX, a hallmark of DNA damage response, were also found. Conclusions: B19V-induced senescence and production of SASP-like factors in normal dermal fibroblasts could represent a new pathogenic mechanism of non-productive B19V infection, which may have a role in the fibrotic process.
MeSH term(s)	Cellular Senescence ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Parvovirus B19, Human/genetics ; Scleroderma, Systemic/pathology
Language	English
Publishing date	2021-12-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1464822-2
ISSN	1462-0332 ; 1462-0324
ISSN (online)	1462-0332
ISSN	1462-0324
DOI	10.1093/rheumatology/keab904
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Article ; Online: Recent Advances in Replication and Infection of Human Parvovirus B19.

Ganaie, Safder S / Qiu, Jianming

Frontiers in cellular and infection microbiology

2018 Volume 8, Page(s) 166

Abstract: ... The B19V infection-induced DNA damage response (DDR) and cell cycle arrest at late S-phase are two key ... Parvovirus B19 (B19V) is pathogenic to humans and causes bone marrow failure diseases and various ... other inflammatory disorders. B19V infection exhibits high tropism for human erythroid progenitor cells (EPCs ...

Abstract	Parvovirus B19 (B19V) is pathogenic to humans and causes bone marrow failure diseases and various other inflammatory disorders. B19V infection exhibits high tropism for human erythroid progenitor cells (EPCs) in the bone marrow and fetal liver. The exclusive restriction of B19V replication to erythroid lineage cells is partly due to the expression of receptor and co-receptor(s) on the cell surface of human EPCs and partly depends on the intracellular factors essential for virus replication. We first summarize the latest developments in the viral entry process and the host cellular factors or pathways critical for B19V replication. We discuss the role of hypoxia, erythropoietin signaling and STAT5 activation in the virus replication. The B19V infection-induced DNA damage response (DDR) and cell cycle arrest at late S-phase are two key events that promote B19V replication. Lately, the virus infection causes G2 arrest, followed by the extensive cell death of EPCs that leads to anemia. We provide the current understanding of how B19V exploits the cellular resources and manipulate pathways for efficient virus replication. B19V encodes a single precursor mRNA (pre-mRNA), which undergoes alternate splicing and alternative polyadenylation to generate at least 12 different species of mRNA transcripts. The post-transcriptional processing of B19V pre-mRNA is tightly regulated through
MeSH term(s)	Cell Cycle Checkpoints ; DNA Damage ; Erythroid Precursor Cells/virology ; Gene Expression Regulation, Viral ; Humans ; Parvoviridae Infections/virology ; Parvovirus B19, Human/genetics ; Parvovirus B19, Human/pathogenicity ; Parvovirus B19, Human/physiology ; STAT5 Transcription Factor/metabolism ; Viral Proteins/metabolism ; Viral Tropism ; Virulence ; Virus Replication/physiology
Chemical Substances	STAT5 Transcription Factor ; Viral Proteins
Language	English
Publishing date	2018-06-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2018.00166
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Article ; Online: Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for Viral DNA Replication.

Zou, Wei / Wang, Zekun / Xiong, Min / Chen, Aaron Yun / Xu, Peng / Ganaie, Safder S / Badawi, Yomna / Kleiboeker, Steve / Nishimune, Hiroshi / Ye, Shui Qing / Qiu, Jianming

Journal of virology

2018 Volume 92, Issue 5

Abstract: ... damage response and cell cycle arrest at late S phase, which facilitates viral DNA ... We found that DNA metabolism, DNA replication, DNA repair, DNA damage response, cell cycle, and ... Human parvovirus B19 (B19V) infection of human erythroid progenitor cells (EPCs) induces a DNA ...

Abstract	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 δ and polymerase α 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.
MeSH term(s)	Bromodeoxyuridine/metabolism ; CD36 Antigens/analysis ; CD36 Antigens/metabolism ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Division ; Cell Line ; DNA Damage ; DNA Polymerase III ; DNA Polymerase beta ; DNA Repair ; DNA Replication ; DNA, Single-Stranded/metabolism ; DNA, Viral/genetics ; DNA, Viral/metabolism ; Erythroid Precursor Cells/cytology ; Erythroid Precursor Cells/virology ; Fetal Death ; Gene Expression Regulation, Viral/physiology ; Genome, Viral ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/physiology ; Humans ; Parvoviridae Infections/virology ; Parvovirus B19, Human/genetics ; Parvovirus B19, Human/metabolism ; Parvovirus B19, Human/pathogenicity ; Phosphorylation ; Protein Interaction Maps ; Red-Cell Aplasia, Pure/virology ; Replication Protein A/genetics ; S Phase ; Transcriptome ; Viremia/virology ; Virus Replication
Chemical Substances	CD36 Antigens ; DNA, Single-Stranded ; DNA, Viral ; Replication Protein A ; DNA Polymerase III (EC 2.7.7.7) ; DNA Polymerase beta (EC 2.7.7.7) ; RPA2 protein, human (EC 2.7.7.7) ; Bromodeoxyuridine (G34N38R2N1)
Language	English
Publishing date	2018-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01881-17
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Article ; Online: Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by activating the ATR-CDC25C-CDK1 pathway.

Xu, Peng / Zhou, Zhe / Xiong, Min / Zou, Wei / Deng, Xuefeng / Ganaie, Safder S / Kleiboeker, Steve / Peng, Jianxin / Liu, Kaiyu / Wang, Shengqi / Ye, Shui Qing / Qiu, Jianming

PLoS pathogens

2017 Volume 13, Issue 3, Page(s) e1006266

Abstract: ... infected cells at both late S-phase and G2-phase, which contain 4N DNA. B19V infection induces a DNA damage ... response (DDR) that facilitates viral DNA replication but is dispensable for cell cycle arrest at G2-phase ... role in B19V infection-induced G2-phase arrest. ...

Abstract	Human parvovirus B19 (B19V) infection of primary human erythroid progenitor cells (EPCs) arrests infected cells at both late S-phase and G2-phase, which contain 4N DNA. B19V infection induces a DNA damage response (DDR) that facilitates viral DNA replication but is dispensable for cell cycle arrest at G2-phase; however, a putative C-terminal transactivation domain (TAD2) within NS1 is responsible for G2-phase arrest. To fully understand the mechanism underlying B19V NS1-induced G2-phase arrest, we established two doxycycline-inducible B19V-permissive UT7/Epo-S1 cell lines that express NS1 or NS1mTAD2, and examined the function of the TAD2 domain during G2-phase arrest. The results confirm that the NS1 TAD2 domain plays a pivotal role in NS1-induced G2-phase arrest. Mechanistically, NS1 transactivated cellular gene expression through the TAD2 domain, which was itself responsible for ATR (ataxia-telangiectasia mutated and Rad3-related) activation. Activated ATR phosphorylated CDC25C at serine 216, which in turn inactivated the cyclin B/CDK1 complex without affecting nuclear import of the complex. Importantly, we found that the ATR-CHK1-CDC25C-CDK1 pathway was activated during B19V infection of EPCs, and that ATR activation played an important role in B19V infection-induced G2-phase arrest.
MeSH term(s)	Ataxia Telangiectasia Mutated Proteins/metabolism ; Blotting, Western ; CDC2 Protein Kinase ; Cell Line ; Cyclin-Dependent Kinases/metabolism ; Erythroid Precursor Cells/virology ; Flow Cytometry ; G2 Phase Cell Cycle Checkpoints/physiology ; Humans ; Immunoprecipitation ; Oligonucleotide Array Sequence Analysis ; Parvoviridae Infections/metabolism ; Parvovirus B19, Human ; Signal Transduction/physiology ; Viral Nonstructural Proteins/metabolism ; cdc25 Phosphatases/metabolism
Chemical Substances	NS1 protein, parvovirus ; Viral Nonstructural Proteins ; ATR protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; CDC2 Protein Kinase (EC 2.7.11.22) ; CDK1 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinases (EC 2.7.11.22) ; CDC25C protein, human (EC 3.1.3.48) ; cdc25 Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2017-03-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1006266
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Article ; Online: Parvovirus-induced depletion of cyclin B1 prevents mitotic entry of infected cells.

Adeyemi, Richard O / Pintel, David J

PLoS pathogens

2014 Volume 10, Issue 1, Page(s) e1003891

Abstract: ... minute virus of mice (MVM) induces a DNA damage response that is required for viral replication and induction of the S ... phase cell cycle arrest in response to diverse DNA damage stimuli, are either down-regulated, or ... cell cycle block proceeds via a two-step process unlike that seen in response to other DNA-damaging agents or ...

Abstract	Parvoviruses halt cell cycle progression following initiation of their replication during S-phase and continue to replicate their genomes for extended periods of time in arrested cells. The parvovirus minute virus of mice (MVM) induces a DNA damage response that is required for viral replication and induction of the S/G2 cell cycle block. However, p21 and Chk1, major effectors typically associated with S-phase and G2-phase cell cycle arrest in response to diverse DNA damage stimuli, are either down-regulated, or inactivated, respectively, during MVM infection. This suggested that parvoviruses can modulate cell cycle progression by another mechanism. In this work we show that the MVM-induced, p21- and Chk1-independent, cell cycle block proceeds via a two-step process unlike that seen in response to other DNA-damaging agents or virus infections. MVM infection induced Chk2 activation early in infection which led to a transient S-phase block associated with proteasome-mediated CDC25A degradation. This step was necessary for efficient viral replication; however, Chk2 activation and CDC25A loss were not sufficient to keep infected cells in the sustained G2-arrested state which characterizes this infection. Rather, although the phosphorylation of CDK1 that normally inhibits entry into mitosis was lost, the MVM induced DDR resulted first in a targeted mis-localization and then significant depletion of cyclin B1, thus directly inhibiting cyclin B1-CDK1 complex function and preventing mitotic entry. MVM infection thus uses a novel strategy to ensure a pseudo S-phase, pre-mitotic, nuclear environment for sustained viral replication.
MeSH term(s)	Animals ; CDC2 Protein Kinase ; Cell Line ; Checkpoint Kinase 2/genetics ; Checkpoint Kinase 2/metabolism ; Cyclin B1/genetics ; Cyclin B1/metabolism ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Enzyme Activation/genetics ; G2 Phase Cell Cycle Checkpoints/genetics ; Humans ; Mice ; Minute Virus of Mice/genetics ; Minute Virus of Mice/metabolism ; Mitosis ; Parvoviridae Infections/genetics ; Parvoviridae Infections/metabolism ; Parvoviridae Infections/pathology ; S Phase Cell Cycle Checkpoints/genetics ; cdc25 Phosphatases/genetics ; cdc25 Phosphatases/metabolism
Chemical Substances	CCNB1 protein, human ; Ccnb1 protein, mouse ; Cyclin B1 ; Checkpoint Kinase 2 (EC 2.7.1.11) ; CHEK2 protein, human (EC 2.7.11.1) ; Chek2 protein, mouse (EC 2.7.11.1) ; CDC2 Protein Kinase (EC 2.7.11.22) ; CDK1 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinases (EC 2.7.11.22) ; CDC25A protein, human (EC 3.1.3.48) ; Cdc25a protein, mouse (EC 3.1.3.48) ; cdc25 Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2014-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1003891
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Article ; Online: Parvovirus minute virus of mice interacts with sites of cellular DNA damage to establish and amplify its lytic infection

Kinjal Majumder / Juexin Wang / Maria Boftsi / Matthew S Fuller / Jordan E Rede / Trupti Joshi / David J Pintel

eLife, Vol

2018 Volume 7

Abstract: ... proceeded, new DNA damage sites were induced, and virus subsequently also associated with these. Sites ... to artificially induced sites of DNA damage. Thus, MVM established replication at cellular DNA damage sites ... that the parvovirus Minute Virus of Mice (MVM) genome initially associated with sites of cellular DNA damage ...

Abstract	We have developed a generally adaptable, novel high-throughput Viral Chromosome Conformation Capture assay (V3C-seq) for use in trans that allows genome-wide identification of the direct interactions of a lytic virus genome with distinct regions of the cellular chromosome. Upon infection, we found that the parvovirus Minute Virus of Mice (MVM) genome initially associated with sites of cellular DNA damage that in mock-infected cells also exhibited DNA damage as cells progressed through S-phase. As infection proceeded, new DNA damage sites were induced, and virus subsequently also associated with these. Sites of association identified biochemically were confirmed microscopically and MVM could be targeted specifically to artificially induced sites of DNA damage. Thus, MVM established replication at cellular DNA damage sites, which provide replication and expression machinery, and as cellular DNA damage accrued, virus spread additionally to newly damaged sites to amplify infection. MVM-associated sites overlap significantly with previously identified topologically-associated domains (TADs).
Keywords	Parvovirus ; DNA damage response ; chromosome conformation capture ; topologically associating domains ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2018-07-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
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Article ; Online: Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy.

Schmidt-Lucke, Caroline / Zobel, Thomas / Schrepfer, Sonja / Kuhl, Uwe / Wang, Dong / Klingel, Karin / Becher, Peter Moritz / Fechner, Henry / Pozzuto, Tanja / Van Linthout, Sophie / Lassner, Dirk / Spillmann, Frank / Escher, Felicitas / Holinski, Sebastian / Volk, Hans-Dieter / Schultheiss, Heinz-Peter / Tschope, Carsten

The Journal of infectious diseases

2015 Volume 212, Issue 7, Page(s) 1070–1081

Abstract: ... infection and damage to CACs result in dysfunctional endogenous vascular repair, supporting the emergence ... of primary bone marrow disease with secondary end-organ damage. ... we hypothesized that B19V is a perpetrator of impaired endogenous endothelial regeneration. B19V DNA and ...

Abstract	Human parvovirus B19 (B19V) is a common pathogen in microvascular disease and cardiomyopathy, owing to infection of endothelial cells. B19V replication, however, is almost restricted to erythroid progenitor cells (ErPCs). Endothelial regeneration attributable to bone marrow-derived circulating angiogenic cells (CACs) is a prerequisite for organ function. Because of many similarities of ErPCs and CACs, we hypothesized that B19V is a perpetrator of impaired endogenous endothelial regeneration. B19V DNA and messenger RNA from endomyocardial biopsy specimens, bone marrow specimens, and circulating progenitor cells were quantified by polymerase chain reaction analysis. The highest B19V DNA concentrations were found in CD34(+)KDR(+) cells from 17 patients with chronic B19V-associated cardiomyopathy. B19V replication intermediates could be detected in nearly half of the patients. Furthermore, chronic B19V infection was associated with impaired endothelial regenerative capacity. B19V infection of CACs in vitro resulted in expression of transcripts encoding B19V proteins. The capsid protein VP1 was identified as a novel inducer of apoptosis, as were nonstructural proteins. Inhibition studies identified so-called death receptor signaling with activation of caspase-8 and caspase-10 to be responsible for apoptosis induction. B19V causally impaired endothelial regeneration with spreading of B19V in CACs in an animal model in vivo. We thus conclude that B19V infection and damage to CACs result in dysfunctional endogenous vascular repair, supporting the emergence of primary bone marrow disease with secondary end-organ damage.
MeSH term(s)	Adult ; Aged ; Animals ; Apoptosis ; Capsid Proteins/genetics ; Capsid Proteins/metabolism ; Cardiomyopathies/complications ; Case-Control Studies ; Caspase 10/genetics ; Caspase 10/metabolism ; Cell Line ; Endothelial Cells/physiology ; Endothelial Cells/virology ; Erythema Infectiosum/virology ; Erythroid Precursor Cells/physiology ; Erythroid Precursor Cells/virology ; Female ; Humans ; Male ; Mice ; Middle Aged ; Parvovirus B19, Human/genetics ; Parvovirus B19, Human/physiology ; Regeneration ; Signal Transduction ; Virus Replication
Chemical Substances	Capsid Proteins ; Caspase 10 (EC 3.4.22.-) ; CASP10 protein, human (EC 3.4.22.63)
Language	English
Publishing date	2015-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiv178
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