Abstract
Human T-cell lymphotropic virus type 1 (HTLV-1) is a human retrovirus that causes persistent infection in the host. While most infected persons remain asymptomatic carriers (ACs), 3–5% develop a T-cell malignancy termed adult T-cell leukemia (ATL) (Uchiyama et al., 1977), and another 0.25–3% develop a chronic progressive inflammatory neurologic disease known as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) (Gessain et al., 1985; Osame et al. 1986). Although HTLV-1-associated disorders have been extensively studied, the exact mechanism by which they are induced by HTLV-1 is not completely understood. The proviral load of HTLV-1 could contribute to the development of these disorders, since the circulating number of HTLV-1-infected T cells in the peripheral blood is associated with the risk of developing HAM/TSP and ATL (Iwanaga et al., 2010; Nagai et al. 1998). However, more detail on the precise immune mechanisms controlling HTLV-1-infected cells is still needed. HTLV-1 preferentially infects CD4+ T cells, the central regulators of the acquired immune system (Richardson et al., 1990). This is known to induce a variety of abnormalities, such as proliferation, cellular activation, and proinflammatory changes (Boxus et al., 2009; Satou et al., 2010; Yamano et al. 2009). These abnormalities, in turn, may deregulate the balance of the host immune system. HTLV-1 also causes abnormalities among uninfected immune cells. Patients with HTLV-1associated disorders demonstrate abnormalities in both the amount and function of CD8+ cytotoxic T lymphocytes (CTL), an important component of host immune response against HTLV-1 (Bangham 2009; Kannagi et al., 2011; Matsuura et al., 2010). Patients with ATL and HAM/TSP may also experience reductions in the amount and efficacy of cellular components of innate immunity, which is vital in regulating the immune response against general viral infections and cancers (Azakami et al., 2009; Matsuura et al., 2010). In this chapter, we have summarized the host immune system abnormalities that are associated with HTLV-1 infection.
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