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Human T-Cell Leukemia Virus Type 1: Pathogenesis and Host Immune Response

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Viruses and Human Cancer

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is a pathogenic human retrovirus that induces a fatal T-cell malignancy, adult T-cell leukemia (ATL), and chronic inflammatory diseases, such as HTLV-1-associated myelopathy (HAM) and HTLV-1 uveitis (HU). HTLV-1 establishes a lifelong persistent infection mainly by clonal proliferation of infected cells and cell-to-cell viral transmission, instead of vigorous viral replication such as that observed in human immunodeficiency virus infection. Therefore, HTLV-1 needs to support cellular proliferation, inhibit apoptosis, and evade host immune surveillance by the functions of its regulatory/accessory proteins. HTLV-1-related diseases likely develop as a consequence of these viral strategies. The fact that only a small fraction of infected individuals develop these diseases after a long latent period suggests that host factors are implicated in their pathogenesis. In this chapter, our accumulating knowledge about the molecular basis of HTLV-1 infection and latency, its association with host factors/pathways, and its oncogenic mechanisms will be summarized.

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Abbreviations

AP1:

Activator protein 1

ATL:

Adult T-cell leukemia

CREB:

Cyclic AMP response element-binding protein

CTL:

Cytotoxic T lymphocyte

HAM/TSP:

HTLV-1-associated myelopathy/tropical spastic paraparesis

HBZ:

HTLV-1 bZIP factor

HTLV-1:

Human T-cell leukemia virus type 1

LTR:

Long terminal repeat

NF-κB:

Nuclear factor kappa B

ORF:

Open reading frame

SRF:

Serum responsive factor

TGF-β:

Transforming growth factor β

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Yasunaga, Ji., Matsuoka, M. (2014). Human T-Cell Leukemia Virus Type 1: Pathogenesis and Host Immune Response. In: Hudnall, S. (eds) Viruses and Human Cancer. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-0870-7_10

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