Human T-Cell Lymphotropic Virus-Type I

1990 ◽  
Vol 11 (6) ◽  
pp. 314-318 ◽  
Author(s):  
Julie Larkin ◽  
John T. Sinnott ◽  
Joshua Weiss ◽  
Douglas A. Holt

Human T-cell lymphotropic virus type-1 (HTLV-I) is a recently recognized retrovirus identified as the cause of adult T-cell leukemia-lymphoma (ATLL) and HTLV-I-associated myelopathy (TSPI HAM). HTLV-I, a member of theRetroviridaefamily of viruses, was first described in 1980 after the isolation of the virus from a patient with a T-cell lymphoma. These pathogenic retroviruses are typically divided into theOncovirinaeandLentivirinae. The oncovirus group, including HTLV-I, HTLV-II and bovine leukemia virus (BLV), is generally associated with tumors. The lentiviruses are associated with immune deficiency and/or neurologic disease, and include agents such as the visna virus of sheep and the human immunodeficiency virus type-1 and -2 HIV-1 and HIV-2).

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.


2018 ◽  
Vol 6 (25) ◽  
Author(s):  
Takuro Fukumoto ◽  
Emi Ikebe ◽  
Masao Ogata ◽  
Kazuhiro Kohno ◽  
Madoka Kuramitsu ◽  
...  

ABSTRACT We report two complete proviral genome sequences of human T-cell leukemia virus type 1 (HTLV-1) isolated from the peripheral blood specimens of acute type adult T-cell leukemia (ATL) patients in Oita Prefecture, Japan.


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

2015 ◽  
Vol 89 (9) ◽  
pp. 4880-4893 ◽  
Author(s):  
Jinhee Hyun ◽  
Juan Carlos Ramos ◽  
Ngoc Toomey ◽  
Siddharth Balachandran ◽  
Alfonso Lavorgna ◽  
...  

ABSTRACTHuman T-cell lymphotropic virus type I (HTLV-1) is an oncogenic retrovirus considered to be the etiological agent of adult T-cell leukemia (ATL). The viral transactivator Tax is regarded as the oncoprotein responsible for contributing toward the transformation process. Here, we demonstrate that Tax potently inhibits the activity of DEx(D/H) box helicases RIG-I and MDA5 as well as Toll-dependent TIR-domain-containing adapter-inducing interferon-β (TRIF), which function as cellular sensors or mediators of viral RNA and facilitate innate immune responses, including the production of type I IFN. Tax manifested this function by binding to the RIP homotypic interaction motif (RHIM) domains of TRIF and RIP1 to disrupt interferon regulatory factor 7 (IRF7) activity, a critical type I IFN transcription factor. These data provide further mechanistic insight into HTLV-1-mediated subversion of cellular host defense responses, which may help explain HTLV-1-related pathogenesis and oncogenesis.IMPORTANCEIt is predicted that up to 15% of all human cancers may involve virus infection. For example, human T-cell lymphotropic virus type 1 (HTLV-1) has been reported to infect up to 25 million people worldwide and is the causative agent of adult T-cell leukemia (ATL). We show here that HTLV-1 may be able to successfully infect the T cells and remain latent due to the virally encoded product Tax inhibiting a key host defense pathway. Understanding the mechanisms by which Tax subverts the immune system may lead to the development of a therapeutic treatment for HTLV-1-mediated disease.


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