期刊
JOURNAL OF NEUROIMMUNE PHARMACOLOGY
卷 5, 期 3, 页码 310-325出版社
SPRINGER
DOI: 10.1007/s11481-010-9216-9
关键词
HTLV; HTLV-1; HAM/TSP; myelopathy; uveitis; myositis; alveolitis; neuropathy; cytotoxic T lymphocyte; CTL; proviral load; pathology; immunology
资金
- Intramural NIH HHS [Z01 NS002817-18, Z01 NS002817-19, Z01 NS003040-01] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [ZIANS003040, ZIANS002817] Funding Source: NIH RePORTER
Human T-lymphotrophic virus type I (HTLV-I) is an oncogenic retrovirus and its infection is associated with a variety of human diseases including HTLV-I-associated myelopathy/tropic spastic paraparesis (HAM/TSP). Large numbers of epidemiological, virological, immunological, and clinical studies on HTLV-I- and HTLV-I-associated diseases have been published, although the pathogenesis of HAM/TSP remains to be fully understood. In the last several years, researchers have shown that several key factors are important in HTLV-I-associated neurologic disease including high HTLV-I proviral load and a strong immune response to HTLV-I. Here, we review pathophysiological findings on HAM/TSP and focus on viral-host immune responses to the virus in HTLV-I infected individuals. In particular, the role of HTLV-I-specific CD8+ T cell response is highlighted.
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