Detection of HTLV1 in Patients with B and T-Cell Malignancies Which Are Different to Adult T-Cell Leukemia-Lymphoma: A Prospective Study.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3869-3869
Author(s):  
Jose J.M. Marquez ◽  
Natalia N.O. Ortiz ◽  
Ramon R.C. Cisterna ◽  
Jose Maria J.B. Beltran de Heredia

Abstract Human T-lymphotropic virus type I (HTLV-I), is the pathogenic agent of adult T-cell leukemia-lymphoma (ATLL), which always shows monoclonal HTLV-I provirus DNA integration. HTLV-I is rarely associated with B-cell disorders. The gen Tax of a human T-cell leukemia virus type I (HTLV-I) induces the expression of several cellular genes that are involved in T cell activation and proliferation. In the current study was to analyze prospectively HTLV-I proviral DNA presence in peripheral blood mononuclear cells (PBMCs) in patients with leukemia or lymphoma which are different to ATLL. Following this pattern we have studied in 61 patients with T and B-cell malignancies the presence of the virus HTLV-I on the during our service between April 2004 and May 2006. A real time PCR assay using SYBR Green intercalation was established. Primer and hybridization probes targeting tax region were standardized against MT2 cell line DNA for HTLV-I. The assay reliably detected a single copy of HTLV-I proviral genome in DNA from 1X106 PBMCs. Also included for each sample the HLA-DQ alpha gene (a measure of genomic DNA), We have detected the presence of HTLV-I in five patients: 2 patients with B-CLL (lymphocytes count: 1.3 x 109/L and 16,8 respectly), one patient with T-ALL CD4 and CD8 positive; other with NHL and one with B-ALL Ph+. As an interesting data, one of the patients with B-CLL presented as complication a immune thrombocytopenia after Fludarabine therapy. Two patients were died and the two cases with B-CLL show stable sickness. Only the patient with T-ALL achieved complete remission after chemotherapy. In conclusion, we have detected on our series, in a unsuspected way, the presence of HTLV-I on some of the patients with lymphoid malignancies, which are different to the ATLL, showing in these cases an atypical clinic course. After knowing the repercussion of HTLV-I over the immune competition of the infected patients it seems suggestive speculate on the possible implication of the virus in a deterioration of the immunity favouring the progress of neoplasia and/or a greater propensity to infections and immunological upheavals, like the observed ones in our series.

1986 ◽  
Vol 83 (12) ◽  
pp. 4524-4528 ◽  
Author(s):  
M. Shimoyama ◽  
Y. Kagami ◽  
K. Shimotohno ◽  
M. Miwa ◽  
K. Minato ◽  
...  

Blood ◽  
1990 ◽  
Vol 76 (5) ◽  
pp. 971-976 ◽  
Author(s):  
SJ Greenberg ◽  
ES Jaffe ◽  
GD Ehrlich ◽  
NJ Korman ◽  
BJ Poiesz ◽  
...  

Abstract Kaposi's sarcoma (KS) developed in a patient with human T-cell leukemia virus type I (HTLV-I)-associated adult T-cell leukemia who was treated with a short-term course of monoclonal antibody immunotherapy. The presentation was transient and temporally related to the underlying clinical course. The association of KS in an HTLV-I infected, but not human immunodeficiency virus (HIV)-infected, individual should alert investigators to the occurrence of KS in retroviral-associated diseases other than acquired immunodeficiency disease syndrome. Recognition of the similarities and differences between HTLV-I and HIV infections may provide insights concerning the angiopathogenesis of KS.


2000 ◽  
Vol 24 (4) ◽  
pp. 353-358 ◽  
Author(s):  
Vincenzo Ciminale ◽  
Maria Hatziyanni ◽  
Barbara K Felber ◽  
Jenifer Bear ◽  
Angelos Hatzakis ◽  
...  

Blood ◽  
1990 ◽  
Vol 76 (5) ◽  
pp. 971-976 ◽  
Author(s):  
SJ Greenberg ◽  
ES Jaffe ◽  
GD Ehrlich ◽  
NJ Korman ◽  
BJ Poiesz ◽  
...  

Kaposi's sarcoma (KS) developed in a patient with human T-cell leukemia virus type I (HTLV-I)-associated adult T-cell leukemia who was treated with a short-term course of monoclonal antibody immunotherapy. The presentation was transient and temporally related to the underlying clinical course. The association of KS in an HTLV-I infected, but not human immunodeficiency virus (HIV)-infected, individual should alert investigators to the occurrence of KS in retroviral-associated diseases other than acquired immunodeficiency disease syndrome. Recognition of the similarities and differences between HTLV-I and HIV infections may provide insights concerning the angiopathogenesis of KS.


1994 ◽  
Vol 14 (2) ◽  
pp. 1374-1382
Author(s):  
C Béraud ◽  
S C Sun ◽  
P Ganchi ◽  
D W Ballard ◽  
W C Greene

Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent of the adult T-cell leukemia, an aggressive and often fatal malignancy of activated human CD4 T cells. HTLV-I encodes an essential 40-kDa protein termed Tax that not only transactivates the long terminal repeat of this retrovirus but also induces an array of cellular genes. Tax-mediated transformation of T cells likely involves the deregulated expression of various cellular genes that normally regulate lymphocyte growth produced by altered activity of various endogenous host transcription factors. In particular, Tax is capable of modulating the expression or activity of various host transcription factors, including members of the NF-kappa B/Rel and CREB/ATF families, as well as the cellular factors HEB-1 and p67SRF. An additional distinguishing characteristic of HTLV-I infection is the profound state of viral latency that is present in circulating primary leukemic T cells. In this study, we demonstrate that HTLV-I Tax can physically associate with p100, the product of the Rel-related NF-kappa B2 gene, both in transfected cells and in HTLV-I-infected leukemic T-cell lines. Furthermore, the physical interaction of Tax with p100 leads to the inhibition of Tax-induced activation of the HTLV-I and human immunodeficiency virus type 1 long terminal repeats, reflecting p100-mediated cytoplasmic sequestration of the normally nuclearly expressed Tax protein. In contrast, a mutant of Tax that selectively fails to activate nuclear NF-kappa B expression does not associate with p100. Together, these results suggest that the cytoplasmic interplay of Tax and p100 may play an important role in the initiation and maintenance of HTLV-1 latency observed in adult T-cell leukemia.


1990 ◽  
Vol 81 (9) ◽  
pp. 884-889 ◽  
Author(s):  
Saburo Momita ◽  
Shuichi Ikeda ◽  
Tatsuhiko Amagasaki ◽  
Hisashi Soda ◽  
Yasuaki Yamada ◽  
...  

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