{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T22:13:16Z","timestamp":1791238396738,"version":"4.1.0"},"reference-count":207,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2001,12,17]],"date-time":"2001-12-17T00:00:00Z","timestamp":1008547200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2002,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Human T cell lymphotropic\/leukemia virus type I (HTLV\u2010I) has been identified as the causative agent of both adult T cell leukemia (ATL) and HTLV\u2010I\u2010associated myelopathy\/tropical spastic paraparesis (HAM\/TSP). Although the exact sequence of events that occur during the early stages of infection are not known in detail, the initial route of infection may predetermine, along with host, environmental, and viral factors, the subset of target cells and\/or the primary immune response encountered by HTLV\u2010I, and whether an HTLV\u2010I\u2010infected individual will remain asymptomatic, develop ATL, or progress to the neuroinflammatory disease, HAM\/TSP. Although a large number of studies have indicated that CD4<jats:sup>+<\/jats:sup> T cells represent an important target for HTLV\u2010I infection in the peripheral blood (PB), additional evidence has accumulated over the past several years demonstrating that HTLV\u2010I can infect several additional cellular compartments in vivo, including CD8<jats:sup>+<\/jats:sup> T lymphocytes, PB monocytes, dendritic cells, B lymphocytes, and resident central nervous system (CNS) astrocytes. More importantly, extensive latent viral infection of the bone marrow, including cells likely to be hematopoietic progenitor cells, has been observed in individuals with HAM\/TSP as well as some asymptomatic carriers, but to a much lesser extent in individuals with ATL. Furthermore, HTLV\u2010I<jats:sup>+<\/jats:sup> CD34<jats:sup>+<\/jats:sup> hematopoietic progenitor cells can maintain the intact proviral genome and initiate viral gene expression during the differentiation process. Introduction of HTLV\u2010I\u2010infected bone marrow progenitor cells into the PB, followed by genomic activation and low level viral gene expression may lead to an increase in proviral DNA load in the PB, resulting in a progressive state of immune dysregulation including the generation of a detrimental cytotoxic Tax\u2010specific CD8<jats:sup>+<\/jats:sup> T cell population, anti\u2010HTLV\u2010I antibodies, and neurotoxic cytokines involved in disruption of myelin\u2010producing cells and neuronal degradation characteristic of HAM\/TSP. J. Cell. Physiol. 190: 133\u2013159, 2002. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.10053","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T22:11:41Z","timestamp":1030313501000},"page":"133-159","source":"Crossref","is-referenced-by-count":87,"title":["Human T cell leukemia virus type I and neurologic disease: Events in bone marrow, peripheral blood, and central nervous system during normal immune surveillance and 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