Strategies in subversion: de‐regulation of the mammalian cell cycle by viral gene products

Swanton, Charles; Jones, Nic

doi:10.1046/j.1365-2613.2001.00165.x

Cited by 45 publications

(46 citation statements)

References 100 publications

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“…The third model proposes a Ras-independent activation of ERK by integrins (13,33). (15,57). However, a HHV-8 envelope association of these proteins has not been shown; v-cyclin and kaposin are expressed during the latent infection, and v-GPCR, K1, K15, and ORF 74 are expressed in the lytic cycle (50).…”

Section: Discussionmentioning

confidence: 99%

“…Despite the expression of these powerful viral proteins that can modulate cell growth (6,53,57), cells cultured from KS tumors grow for a limited number of passages, contain a mixture of cell types, depend upon growth factors, fail to grow in soft agar, and do not induce tumors in immunodeficient mice (21). The factors driving the KS tumor spindle cell growth, the inability of KS cells latently infected with HHV-8 to grow in cell culture, and the reasons for the loss of HHV-8 DNA within a few passages of KS cells are not known.…”

Section: Discussionmentioning

confidence: 99%

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Kaposi's Sarcoma-Associated Herpesvirus Induces the Phosphatidylinositol 3-Kinase-PKC-ζ-MEK-ERK Signaling Pathway in Target Cells Early during Infection: Implications for Infectivity

Naranatt¹,

Akula²,

Zien

et al. 2003

J Virol

170

290

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Kaposi's Sarcoma-Associated Herpesvirus Induces the Phosphatidylinositol 3-Kinase-PKC-ζ-MEK-ERK Signaling Pathway in Target Cells Early during Infection: Implications for Infectivity

Naranatt¹,

Akula²,

Zien

et al. 2003

J Virol

170

290

View full text Add to dashboard Cite

show abstract

“…Many animal viruses can exploit these regulatory pathways to their own advantage, by either promoting or blocking cell cycle progression via the action of virus-encoded proteins [Op De Beeck and Caillet-Fauquet, 1997;Swanton and Jones, 2001;Schang, 2003]. As cellular components fluctuate during the cell cycle, these manipulations can force the cell into a phase that is favorable for virus replication.…”

Section: Viruses and The Cell Cyclementioning

confidence: 99%

Effects of cell cycle status on early events in retroviral replication

Katz

Greger

Skalka

2005

J of Cellular Biochemistry

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The study of retroviruses over the last century has revealed a wide variety of disease-producing mechanisms, as well as apparently harmless interactions with animal hosts. Despite their potential pathogenic properties, the intrinsic features of retroviruses have been harnessed to create gene transfer vectors that may be useful for the treatment of disease. Retroviruses, as all viruses, have evolved to infect specific cells within the host, and such specificities are relevant to both pathogenesis and retrovirus-based vector design. The majority of cells of an animal host are not progressing rapidly through the cell cycle, and such a cellular environment appears to be suboptimal for replication of all retroviruses. Retrovirus-based vectors can therefore be restricted in many important target cells, such as post-mitotic differentiated cells or stem cells that may divide only infrequently. Despite intense interest, our understanding of how cell cycle status influences retroviral infection is still quite limited. In this review, we focus on the importance of the cell cycle as it relates to the early steps in retroviral replication. Retroviruses have been categorized based on their abilities to complete these early steps in non-cycling cells. However, all retroviruses are subject to a variety of cell cycle restrictions. Here, we discuss such restrictions, and how they may block retroviral replication, be tolerated, or overcome. J. Cell. Biochem. 94: 880-889, 2005. ß 2005 Wiley-Liss, Inc.

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“…It causes infectious mononucleosis and is also associated with nasopharyngeal carcinoma, Burkitt's lymphoma, Hodgkin's disease, gastric cancer and post-transplant lymphoproliferative disease (Cohen, 2000;Swanton and Jones, 2001;Young and Murray, 2003;Dolcetti, 2007;Brady et al, 2008). EBV displays two distinct phases in its life cycle: latency and lytic replication.…”

Section: Introductionmentioning

confidence: 99%

Effect of Rta protein of Epstein-Barr virus on the cell cycle in HeLa cells

Guo¹,

Sun²,

Yuan³

et al. 2012

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Summary. -Epstein-Barr virus (EBV) replication and transcription activator (Rta) is an immediate-early transcription factor that mediates the switch from latent to lytic infection. DNA viruses often modulate the function of critical cell cycle proteins to maximize the efficiency of virus replication. Here we have examined the effect of Rta on cell cycle progression. Cell cycle analysis revealed that Rta induced HeLa cells in G0/G1-phase to reenter the S-phase. Analysis of the expression pattern of a key set of cell cycle regulators revealed that expression of Rta inhibited the expression of Rb and p53 and induced the expression of E 2 F 1 . These findings suggest that Rta plays an active role in redirecting HeLa cell physiology through an Rta-mediated cell cycle transformation.

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Strategies in subversion: de‐regulation of the mammalian cell cycle by viral gene products

Cited by 45 publications

References 100 publications

Kaposi's Sarcoma-Associated Herpesvirus Induces the Phosphatidylinositol 3-Kinase-PKC-ζ-MEK-ERK Signaling Pathway in Target Cells Early during Infection: Implications for Infectivity

Kaposi's Sarcoma-Associated Herpesvirus Induces the Phosphatidylinositol 3-Kinase-PKC-ζ-MEK-ERK Signaling Pathway in Target Cells Early during Infection: Implications for Infectivity

Effects of cell cycle status on early events in retroviral replication

Effect of Rta protein of Epstein-Barr virus on the cell cycle in HeLa cells

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