Abstract
This chapter reviews the epidemiology, disease associations, molecular biology, and pathogenic mechanisms of human T‐cell lymphotropic virus (HTLV) types I and II. Association of HTLV‐I with two distinct disease processes, a malignancy and a chronic neurologic disorder, spurred worldwide surveys for prevalence of HTLV‐I and associated diseases. Transmission of HTLV‐I seems to require prolonged, close contact between individuals. Transfer of infected T cells is likely required. The three major reported routes of HTLV‐I transmission include sexual intercourse, blood product transmission, and mother‐to‐child transfer. The most commonly used screening test for HTLV‐I/HTLV‐II is an enzyme‐linked immunosorbent assay (ELISA) which uses a viral lysate‐based antigen derived from HTLV‐I infection of human T cells. Unlike human immunodeficiency virus (HIV), which has significant genetic differences between isolates, the various HTLV‐I strains show a high degree of genetic conservation. There are two major hypotheses for pathogenesis in HTLV‐I associated myelopathy (HAM)/tropical spastic paresis (TSP). The first hypothesis is that HTLV‐I infects glial cells in the CNS and subsequently induces a cytotoxic immune response against these cells, leading to demyelination. The second hypothesis is that HTLV‐I infection activates autoreactive T cells which then cause autoimmune destruction within the CNS (and perhaps in other areas). The molecular biology of HTLV‐II is strikingly similar to that of HTLV‐I. HTLV‐I infection, however, has been linked to several disorders, especially adult T‐cell leukemia/lymphoma (ATL) and HAM/TSP. HTLV‐I and HTLVII have a similar genetic organization and regulation and share several unique transregulatory proteins.