Molecular and cellular aspects of HTLV-1 associated leukemogenesis in vivo

Mortreux, Frank; Gabet, As; Wattel, Éric

doi:10.1038/sj.leu.2402777

Cited by 116 publications

(127 citation statements)

References 97 publications

(106 reference statements)

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“…What determines whether an HTLV-1-infected individual will progress to develop ATL is unclear. In the early course of HTLV-1 infection, integration of the provirus into host cell chromatin is random and polyclonal (Mortreux et al, 2003). During the long premalignant phase, there is oligoclonal expansion of HTLV-1-infected cells (Wattel et al, 1995;Cavrois et al, 1996;Etoh et al, 1997).…”

Section: Adult T-cell Leukemia/lymphomamentioning

confidence: 99%

“…Somatic mutations are increased in peripheral blood mononuclear cell (PBMC) DNA from ATL patients compared to asymptomatic carriers (Mortreux et al, 2003). Somatic mutations are increased in both the provirus and within the proviral flanking sequences, and these mutations are thought to primarily arise during the clonal proliferative phase rather than during reverse transcription (Mortreux et al, 2001b).…”

Section: Adult T-cell Leukemia/lymphomamentioning

confidence: 99%

“…After infecting CD4 þ CD25 þ T cells, the HTLV-1 provirus is randomly integrated into the host genome, where it persists for years. Although HTLV-1 replicates via reverse transcription during the early stages of infection, the virus genome is effectively replicated during clonal expansion of infected cells (Mortreux et al, 2003). Typically, there is a progression from polyclonal to oligoclonal and then to monoclonal proliferation in vivo, which is achieved while the cells become interleukin 2 (IL-2) independent (Yoshida et al, 1984;Hollsberg et al, 1992;Franchini, 1995).…”

Section: Adult T-cell Leukemia/lymphomamentioning

confidence: 99%

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Animal models for human T-lymphotropic virus type 1 (HTLV-1) infection and transformation

2005

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Over the past 25 years, animal models of human T-lymphotropic virus type 1 (HTLV-1) infection and transformation have provided critical knowledge about viral and host factors in adult T-cell leukemia/lymphoma (ATL). The virus consistently infects rabbits, some non-human primates, and to a lesser extent rats. In addition to providing fundamental concepts in viral transmission and immune responses against HTLV-1 infection, these models have provided new information about the role of viral proteins in carcinogenesis. Mice and rats, in particular immunodeficient strains, are useful models to assess immunologic parameters mediating tumor outgrowth and therapeutic invention strategies against lymphoma. Genetically altered mice including both transgenic and knockout mice offer important models to test the role of specific viral and host genes in the development of HTLV-1-associated lymphoma. Novel approaches in genetic manipulation of both HTLV-1 and animal models are available to address the complex questions that remain about viral-mediated mechanisms of cell transformation and disease. Current progress in the understanding of the molecular events of HTLV-1 infection and transformation suggests that answers to these questions are approachable using animal models of HTLV-1-associated lymphoma Oncogene (2005) 24, 6005-6015.

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Section: Adult T-cell Leukemia/lymphomamentioning

confidence: 99%

Section: Adult T-cell Leukemia/lymphomamentioning

confidence: 99%

Section: Adult T-cell Leukemia/lymphomamentioning

confidence: 99%

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Animal models for human T-lymphotropic virus type 1 (HTLV-1) infection and transformation

2005

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“…6 These clonal expansions, at least early after infection, result from the expression of the viral transactivator protein Tax. Tax is a 40 kDa phosphoprotein that is encoded by the pX region of the viral genome.…”

Section: The Htlv-i Oncoprotein Taxmentioning

confidence: 99%

Proapoptotic regimes for HTLV-I-transformed cells: targeting Tax and the NF-κB pathway

Kfoury

Nasr²,

Hermine³

et al. 2005

Cell Death Differ

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“…Existing data suggest that oncogenic transformation caused by HTLV-1 is a complex event arising from a multistep process in which the virus, through the action of specific viral gene products acting on regulatory cellular genes, induces T-cell proliferation. This results both in the accumulation of genetic defects and in the dysregulation of growth and death in infected cells [Mortreux et al, 2003]. HTLV-1 encodes several regulatory proteins.…”

Section: Introductionmentioning

confidence: 99%

Modulation of apoptosis during HTLV‐1‐mediated immortalization process in vitro

Matteucci

Balestrieri

Macchi

et al. 2004

Journal of Medical Virology

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Suppression of apoptosis has been proposed as a mechanism involved in the transforming action of human T-cell leukemia/lymphotropic virus type-1 (HTLV-1). However, there is evidence that HTLV-1 and its protein Tax also induce apoptosis. To resolve this apparent paradox, apoptosis was monitored in primary cultures of peripheral blood lymphocytes (PBLs) from healthy donors, following HTLV-1 infection in vitro. High levels of apoptosis in HTLV-1 infected cultures during the first weeks after infection were detected. Apoptosis was not related to the presence of uninfected cells, as revealed by a fluorescence in situ hybridization assay. Successively, a progressive decrease in apoptosis in infected cultures going towards immortalization, was observed. When IL-2 in the medium was replaced by IL-4, allowing the cells to be efficiently infected by HTLV-1 but not immortalized, apoptosis levels tended to increase, instead of decreasing, with the ongoing time. The caspase cascade was remarkably activated in PBLs recently infected in vitro by HTLV-1, but apoptosis was only partly reduced by caspase inhibitors. Even if spontaneous apoptosis was relatively low in long-term cultures of PBLs immortalized by HTLV-1 in vitro, Fas death-receptor expression and function were well conserved. These observations provide a new rationale for explaining the dual effect of HTLV-1 in controlling apoptosis.

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Molecular and cellular aspects of HTLV-1 associated leukemogenesis in vivo

Cited by 116 publications

References 97 publications

Animal models for human T-lymphotropic virus type 1 (HTLV-1) infection and transformation

Animal models for human T-lymphotropic virus type 1 (HTLV-1) infection and transformation

Proapoptotic regimes for HTLV-I-transformed cells: targeting Tax and the NF-κB pathway

Modulation of apoptosis during HTLV‐1‐mediated immortalization process in vitro

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