DNA content distribution of mouse cells following infection with polyoma virus

Lehman, John M.; Laffin, Judith; Friedrich, Thomas

doi:10.1002/cyto.990160207

Cited by 9 publications

(7 citation statements)

References 15 publications

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“…This synthesis, however, may occur out of normal cell cycle control, and it does not involve a full round of the cell cycle since mitosis does not follow the S phase (197,198). However, in vivo studies in our laboratory have provided no evidence for DNA synthesis following Py infection in vivo (233).…”

Section: Dna Synthesismentioning

confidence: 86%

Natural Biology of Polyomavirus Middle T Antigen

Gottlieb

Villarreal

2001

Microbiol Mol Biol Rev

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“It has been commented by someone that ‘polyoma’ is an adjective composed of a prefix and suffix, with no root between—a meatless linguistic sandwich” (C. J. Dawe). The very name “polyomavirus” is a vague mantel: a name given before our understanding of these viral agents was clear but implying a clear tumor life-style, as noted by the late C. J. Dawe. However, polyomavirus are not by nature tumor-inducing agents. Since it is the purpose of this review to consider the natural function of middle T antigen (MT), encoded by one of the seemingly crucial transforming genes of polyomavirus, we will reconsider and redefine the virus and its MT gene in the context of its natural biology and function. This review was motivated by our recent in vivo analysis of MT function. Using intranasal inoculation of adult SCID mice, we have shown that polyomavirus can replicate with an MT lacking all functions associated with transformation to similar levels to wild-type virus. These observations, along with an almost indistinguishable replication of all MT mutants with respect to wild-type viruses in adult competent mice, illustrate that MT can have a play subtle role in acute replication and persistence. The most notable effect of MT mutants was in infections of newborns, indicating that polyomavirus may be highly adapted to replication in newborn lungs. It is from this context that our current understanding of this well-studied virus and gene is presented

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Section: Dna Synthesismentioning

confidence: 86%

Natural Biology of Polyomavirus Middle T Antigen

Gottlieb

Villarreal

2001

Microbiol Mol Biol Rev

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“…For instance, HIV Vpr-mediated arrest at G2/M can benefit the early infection stages by increasing the number of integrated proviruses (Groschel and Bushman, 2005). In turn, adenovirus and SV40 polyomavirus infection induces the cell to remain in a pseudo-S phase state, during which normal cellular DNA replication is complete, but the cell still remains competent for viral DNA replication (Lehman et al, 1994, 2000; Ben-Israel and Kleinberger, 2002). …”

Section: Baculovirus Infection: Impact On the Host Cellmentioning

confidence: 99%

Toward system-level understanding of baculovirus–host cell interactions: from molecular fundamental studies to large-scale proteomics approaches

Monteiro¹,

Carinhas²,

Carrondo³

et al. 2012

Front. Microbio.

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Baculoviruses are insect viruses extensively exploited as eukaryotic protein expression vectors. Molecular biology studies have provided exciting discoveries on virus–host interactions, but the application of omic high-throughput techniques on the baculovirus–insect cell system has been hampered by the lack of host genome sequencing. While a broader, systems-level analysis of biological responses to infection is urgently needed, recent advances on proteomic studies have yielded new insights on the impact of infection on the host cell. These works are reviewed and critically assessed in the light of current biological knowledge of the molecular biology of baculoviruses and insect cells.

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“…Moreover, polyomaviruses are thought to take advantage of the DNA damage response to enhance viral replication. SV40 lytic infection thus triggers the DNA damage checkpoint, resulting in a bypass of mitosis and additional replication of cellular and viral DNA (9), and murine polyomavirus-infected cells accumulate in S and G 2 phases (10). Replication of viral DNA in cells infected with SV40 or murine polyomavirus has also been recently shown to activate the ataxia telangiectasia mutated (ATM)-mediated signaling pathway and thereby promote viral replication (11,12).…”

mentioning

confidence: 99%

Large T Antigen Promotes JC Virus Replication in G2-arrested Cells by Inducing ATM- and ATR-mediated G2 Checkpoint Signaling

Orba

Suzuki

Makino

et al. 2010

Journal of Biological Chemistry

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The human polyomavirus JC virus (JCV) 2 is the causative agent of progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease of the central nervous system. JCV infection usually occurs during childhood, but remains subclinical. However, opportunistic reactivation of JCV results in the development of PML in individuals with a compromised immune system, such as those with acquired immunodeficiency syndrome (AIDS) or advanced-stage malignant tumors, or those recently having undergone organ transplantation with immunosuppressive therapy (1). There is currently no effective or specific therapy for PML, even though the incidence of this condition is increasing with the growing number of individuals with AIDS.JCV is a small virus with a double-stranded DNA genome that encodes early proteins (large T antigen, small t antigen, and TЈ antigen) and late proteins (VP1, VP2, VP3, and agnoprotein) (2). The entry of JCV into the nucleus of an infected cell is followed by transcription of the early genes and the production of large T antigen (TAg). The replication of JCV DNA progresses in association with the accumulation of TAg, which subsequently stimulates transcription of late genes and represses that of the early genes (3). JCV TAg shares 72% amino acid sequence identity with TAg of simian virus 40 (SV40), another primate polyomavirus, and, like SV40 TAg, it is necessary for replication of the viral genome as a result of its DNA binding and helicase activities. The replication of polyomaviruses also requires DNA replication proteins of the host cell, such as DNA polymerase ␣, topoisomerases, and replication protein A (RPA) (4, 5), with such host cell factors being thought to serve as determinants of host specificity (6).The utilization of such cellular proteins requires that polyomaviruses replicate in a phase of the cell cycle in which they are available. Polyomavirus TAg thus modulates cellular signaling pathways to induce quiescent cells to enter S phase, in which cellular DNA is replicated (7). A key event in this process is the interaction of TAg with members of the retinoblastoma protein family, which results in inactivation of retinoblastoma protein and in consequent progression of the cell cycle (8). Moreover, polyomaviruses are thought to take advantage of the DNA damage response to enhance viral replication. SV40 lytic infection thus triggers the DNA damage checkpoint, resulting in a bypass of mitosis and additional replication of cellular and viral DNA (9), and murine polyomavirus-infected cells accumulate in S and G 2 phases (10). Replication of viral DNA in cells *

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DNA content distribution of mouse cells following infection with polyoma virus

Cited by 9 publications

References 15 publications

Natural Biology of Polyomavirus Middle T Antigen

Natural Biology of Polyomavirus Middle T Antigen

Toward system-level understanding of baculovirus–host cell interactions: from molecular fundamental studies to large-scale proteomics approaches

Large T Antigen Promotes JC Virus Replication in G2-arrested Cells by Inducing ATM- and ATR-mediated G2 Checkpoint Signaling

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