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Chapter 32 : Human Lymphotropic Viruses: HTLV-1 and HTLV-2

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Abstract:

The discovery of the human T-cell lymphotropic virus type 1 (HTLV-1), in 1979 ushered in a new age of medical virology. The association of HTLV-1 with adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/ tropical spastic paraparesis (HAM/TSP), as well as other diseases, was established by clinical epidemiological studies, whereas links of human T-cell lymphotropic virus type 2 (HTLV-2) to diseases are less certain. Major structural and regulatory proteins of HTLV-1 are summarized in this chapter. The current standard of care involves antibody screening of donors and, if needed because of in-determinant Western blot results, molecular screening is also performed, an algorithm that has eliminated transplant-associated transmission. At the center of disease pathogenesis are the gene products of the pX reading frame which not only are engaged in promoting viral replication but also impact cellular functions that favor viral replication. The most important of these viral gene products coded for by pX IV is the p40 Tax viral regulatory protein, which, like its counterpart Tat from human immunodeficiency virus type 1 (HIV-1), plays an important role in promoting viral growth and disease pathogenesis. Tax represses transcription of the Bax gene, the product of which accelerates apoptosis. The Lymphoma Study Group in Japan has classified ATL into four clinical types based on clinical features and cell morphology: acute, chronic, smoldering, and lymphoma/leukemia types. Refinements of the PCR assay resulted in a highly sensitive and reproducible detection system with limits of detection at 10 molecules of DNA in 1 mg of human DNA.

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32

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Figures

Image of FIGURE 1
FIGURE 1

Phylogenetic relationship of HTLV-1, -2, and -3. Each type varies by approximately 60% from each other. STLV, simian T-lymphotropic virus. (Reprinted from reference with permission.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 2
FIGURE 2

Genomic structure of HTLV-1. The LTR is organized into three regions: (i) US, R, and U3, which house the polyadenylation site; (ii) (response element); and (iii) the 21-bp enhancer -activating response elements. The last two elements are involved in controlling virus expression. Shown are the gene (group-specific antigen), whose products form the skeleton of the virion (matrix, capsid, nucleocapsid, and nucleic acid binding protein); the / gene (the gene for reverse transcriptase, integrase, and protease), the gene (the envelope gene), the gene (the -activator gene), and the gene (the viral regulatory gene involved in promoting genomic RNA production). (Courtesy of Robert C. Gallo.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 3
FIGURE 3

Replication cycle of HTLV-1. Virus infection involves initial binding to the surface of the target CD4 cell, uncoating, and release of viral genetic material. Virally encoded reverse transcriptase creates a DNA copy that is integrated into the host genome under the influence of viral integrase. Viral replication involves the production of both genomic RNA and polyproteins that are cleaved by the viral protease, resulting in virion assembly at the cell surface. See the text for details. (Adapted from reference with permission of the publisher.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 4
FIGURE 4

HTLV-1 infection clusters with high rates in selected geographic areas.

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 5
FIGURE 5

Age-specific seroprevalence of HTLV-1 in Jamaica and Okinawa, Japan. There is a characteristic pattern of higher rates in females than in males, with an age-dependent increase in seroprevalence and a plateauing in males at age 50 years but an increase in females. (Reprinted from references and with permission of the publisher.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 6
FIGURE 6

Age distribution of ATL patients. Compared here are the age-specific prevalences of ATL in patients from Japan, Brazil, and the Caribbean. Age is given on the axis, and the number of cases is given on the axis. (Courtesy of Barry Haralad and Maria Pombo-Oliveira.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 7
FIGURE 7

HTLV lymphomagenesis: progression of T lymphocytes from immortalization and clonal expansion to transformation. Various changes in the cell during the different stages are listed in the shaded boxes. As shown, virus-infected cells can also go into apoptosis. (Reprinted from reference with permission of Macmillan Publishers Ltd.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 8
FIGURE 8

Cytoplasmic signaling of Tax-stimulated regulatory proteins. Tax by transactivation stimulates the gene expression of receptors OX40, IL-2Rα, and IL-15Rα1 and ligands OX40L, IL-13, and IL-15. IL-15, which is a close relative of IL-2 that shares a common backbone, is also up-regulated, as are the separate IL-4/IL-13R and IL-13 ligand and OX40 receptor and OX40 ligand. The activation of both ligand and receptor for OX40, a member of the tumor necrosis factor family, suggests that costimulatory signals delivered from OX40 contribute to a transformed phenotype. Receptor ligand binding results in the activation of growth- and survival-controlling signaling cascades and activation of transcription factors employing the Janus tyrosine kinase (JAK3) signal transducer of activated T cells (STAT5a and STAT5b) pathway to enter the nucleus and stimulate target gene transcription. Tax also stimulates transforming growth factor β1 to protect infected cells from cytotoxicity but employs transcription factors Smad 3 and Smad 4 to repress transforming growth factor β1, thus modulating this effect to the advantage of HTLV-induced cell proliferation. (Reprinted from reference with permission of Macmillan Publishers Ltd.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 9
FIGURE 9

Model of CD8 CTL-mediated control of HTLV-1 infection. HTLV-1 infects CD4 T lymphocytes, with expansion of infection primarily via cell replication. As HTLV-1-specific antigens, particularly Tax, are expressed, a robust CD8 CTL response is generated that results in killing of CD4-infected cells. The inability of some persons to control HTLV-1 expansion is thought to contribute to disease pathogenesis. In this model, the dynamic equilibrium between viral replication and immune destruction is mediated through Tax overexpression, causing CD4 target cell proliferation and a robust cell-mediated response to the antigen in particular, thereby leading to CTL-mediated lysis of these HTLV-1-infected CD4 cells ( ). As a consequence of ongoing Tax proliferation, there is a cell-associated expansion of HTLV-1 genome-containing CD4 cells and a compensatory expansion of CD8 CTL. As the number of CD4 cells containing the HTLV-1 genome expands, HTLV-1 antigens are expressed on the cell surface and become targets for CD8-mediated cytotoxic killing. (Reprinted from reference with permission of the publisher.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 10
FIGURE 10

Photomicrographs of typical peripheral blood leukemic cells from patients with acute ATL (A), chronic ATL (B), and smoldering ATL (C) and cutaneous manifestations (D). Details of the features are discussed in the text. (Panels A, B, and C are reprinted from reference and panel D is reprinted from reference with permission of the publisher.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Image of FIGURE 11
FIGURE 11

Survival patterns of patients with different ATL subtypes after polychemotherapy. Patients with acute and lymphoma-type ATL have the poorest prognosis after chemotherapy (see the text). (Reprinted from reference with permission of the publisher.)

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
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Tables

Generic image for table
TABLE 1

Major structural and regulatory proteins of HTLV-1

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
Generic image for table
TABLE 2

Transmission of HTLV-1 and HTLV-2

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32
Generic image for table
TABLE 3

HTLV-associated diseases

Citation: Blattner W, Charurat M. 2009. Human Lymphotropic Viruses: HTLV-1 and HTLV-2, p 709-736. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch32

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