Human T ‐cell leukemia virus type I associated lymphadenitis

Ohshima, Kohichi; Kikuchi, Masahiro; Y, Masuda; Sumiyoshi, Yoshiaki; Eguchi, Fuyuki; Mohtai, Hidehito; Takeshita, Morishige; Kimura, Norbuhiro

doi:10.1002/1097-0142(19920101)69:1<239::aid-cncr2820690139>3.0.co;2-#

Cited by 46 publications

(19 citation statements)

References 19 publications

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“…Although some failure during the PCR process could be responsible for a remote possible mistaken interpretation of results; however another real explanation is that defective proviruses would be generated during the infection process to oral keratinocytes. In order to support the last explanation, previous studies report the existence of defective HTLV-1 provirus in lymphocytic infections not only in ATL (9,20,11,15) but also in HAM/TSP patients (29,30,16,14). In this sense our results would be the first to document the existence of defective HTLV-1 provirus in infected oral keratinocytes.…”

Section: Immunophenotyping Of Oral Epithelium Cells Culturedsupporting

confidence: 83%

Human T-Lymphotropic virus (HTLV) type I in vivo integration in oral keratinocytes

Domínguez¹,

González.²,

Sánchez³

et al. 2011

Braz. J. Microbiol.

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Section: Immunophenotyping Of Oral Epithelium Cells Culturedsupporting

confidence: 83%

Human T-Lymphotropic virus (HTLV) type I in vivo integration in oral keratinocytes

Domínguez¹,

González.²,

Sánchez³

et al. 2011

Braz. J. Microbiol.

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“…Deletions of the HTLV-1 proviral sequence are frequently observed in PBMC samples derived from asymptomatic or symptomatic carriers (Ohshima et al, 1991;Shimamoto et al, 1994;Tamiya et al, 1996;Tsukasaki et al, 1997). However, all these defective proviruses retain the 3' Px region that encodes the regulatory viral proteins.…”

Section: High Proviral Load In Htlv-1 Carriers With Strongyloidiasismentioning

confidence: 99%

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

et al. 2000

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Adult T cell leukemia (ATLL) develops in 3 ± 5% of HTLV-1 carriers after a long period of latency during which a persistent polyclonal expansion of HTLV-1 infected lymphocytes is observed in all individuals. This incubation period is signi®cantly shortened in HTLV-1 carrier with Strongyloides stercoralis (Ss) infection, suggesting that Ss could be a cofactor of ATLL. As an increased T cell proliferation at the asymptomatic stage of HTLV-1 infection could increase the risk of malignant transformation, the e ect of Ss infection on infected T lymphocytes was assessed in vivo in HTLV-1 asymptomatic carriers. After real-time quantitative PCR, the mean circulating HTLV-1 proviral load was more than ®ve times higher in HTLV-1 carriers with stongyloidiasis than in HTLV-1+ individuals without Ss infection (P50.009). This increased proviral load was found to result from the extensive proliferation of a restricted number of infected clones, i.e. from oligoclonal expansion, as evidenced by the semiquantitative ampli®-cation of HTLV-1¯anking sequences. The positive e ect of Ss on clonal expansion was reversible under e ective treatment of strongyloidiasis in one patient with parasitological cure whereas no signi®cant modi®cation of the HTLV-1 replication pattern was observed in an additional case with strongyloidiasis treatment failure. Therefore, Ss stimulates the oligoclonal proliferation of HTLV-1 infected cells in HTLV-1 asymptomatic carriers in vivo. This is thought to account for the shortened period of latency observed in ATLL patients with strongyloidiasis. Oncogene (2000) 19, 4954 ± 4960.

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“…It is this activity of Tax that has been postulated to lead to the proliferation and transformation of T cells in ATLL (7)(8)(9). Additional support for the role of Tax in leukemogenesis comes from studies of malignant cells from ATLL patients, which have defective HTLV proviral genomes that preferentially retain the 3' end of the proviral genome encoding the Tax protein (10,11). Transgenic models have been described in which Tax was expressed with a variety of different promoters; however, none of these models resulted in the development of lymphomas and/or leukemia (12)(13)(14)(15)(16)(17).…”

mentioning

confidence: 99%

Development of leukemia in mice transgenic for the tax gene of human T-cell leukemia virus type I.

Grossman

Kimata

Wong

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

350

302

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The human T-cell leukemia virus type I Tax protein trans-activates several cellular genes implicated in T-cell replication and activation. To investigate its leukemogenic potential, Tax was targeted to the mature T-lymphocyte compartment in transgenic mice by using the human granzyme B promoter. These mice developed large granular lymphocytic leukemia, demonstrating that expression of Tax in the lymphocyte compartment is sufficient for the development of leukemia. Furthermore, these observations suggest that human T-cell leukemia virus infection may be involved in the development of large granular lymphocytic leukemia.

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Human T ‐cell leukemia virus type I associated lymphadenitis

Cited by 46 publications

References 19 publications

Human T-Lymphotropic virus (HTLV) type I in vivo integration in oral keratinocytes

Human T-Lymphotropic virus (HTLV) type I in vivo integration in oral keratinocytes

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

Development of leukemia in mice transgenic for the tax gene of human T-cell leukemia virus type I.

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