Human T-Cell Lymphotropic Virus Type I (HTLV-I)-Associated Adult T-Cell Leukemia-Lymphoma in a Patient Infected with Human Immunodeficiency Virus Type 1 (HIV-1)

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).

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Interaction of human immunodeficiency virus type 1, human T-cell leukemia/lymphoma virus type I (HTLV-I), and HTLV-II with in vitro-generated dendritic cells.

Clinical and Diagnostic Laboratory Immunology ◽

10.1128/cdli.2.3.343-348.1995 ◽

1995 ◽

Vol 2 (3) ◽

pp. 343-348 ◽

Cited By ~ 6

Author(s):

D Zucker-Franklin ◽

M Fraig ◽

G Grusky

Keyword(s):

Human Immunodeficiency Virus ◽

Dendritic Cells ◽

T Cell ◽

Virus Type ◽

Type I ◽

Cell Leukemia ◽

Human T Cell ◽

Immunodeficiency Virus

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Oncogenic Human T-Cell Lymphotropic Virus Type 1 Tax Suppression of Primary Innate Immune Signaling Pathways

Journal of Virology ◽

10.1128/jvi.02493-14 ◽

2015 ◽

Vol 89 (9) ◽

pp. 4880-4893 ◽

Cited By ~ 13

Author(s):

Jinhee Hyun ◽

Juan Carlos Ramos ◽

Ngoc Toomey ◽

Siddharth Balachandran ◽

Alfonso Lavorgna ◽

...

Keyword(s):

T Cell ◽

Virus Type ◽

Host Defense ◽

Innate Immune ◽

Type I ◽

Type I Ifn ◽

Cell Leukemia ◽

Adult T Cell Leukemia ◽

Human T Cell

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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