Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
EPIDEMIOLOGY OF HUMAN T-CELL LEUKEMIA VIRUS TYPE I (HTLV-I)
The Human Retroviruses. Gallo RC and Jay G, eds. San Diego, Academic Press, p. 175-92, 1991.. Unique Identifier : AIDSLINE ICDB/92678727 Wiktor SZ; Blattner WA; Viral Epidemiology Section, Environmental Epidemiology Branch,; NCI, Bethesda, MD 20892
Abstract:
Since the discovery of HTLV-I, much has been learned about its epidemiology. Studies have linked the virus with two distinct clinical entities: adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic degenerative neurologic syndrome. The epidemiology of HTLV-I is reviewed, including diagnosis of infection, geographic distribution, demographic factors, modes of transmission, and disease associations. Despite improvements, serologic assays may underestimate the true prevalence of HTLV-I infection because they require the presence of an immune response to the virus. The global distribution of HTLV-I is marked by two sharply demarcated endemic areas, Japan and the Caribbean. After Japan and the Caribbean, parts of Africa appear to have large reservoirs of infection. Studies, mainly from southern Japan and the Caribbean basin, reveal that the distribution of HTLV-I is strongly influenced by age, race, and sex. Studies have documented transmission from parent to child and between spouses, especially from husband to wife. These early findings have been repeated and amplified. Patients with HAM/TSP have a higher HTLV-I antibody titer compared to patients with ATL. Researchers have looked for an association between HTLV-I and a number of illnesses, particularly autoimmune disorders, with limited success. Several lines of experimental data raise the possibility that HTLV-I may cause subtle immune dysfunction even among asymptomatic carriers. Several small studies indicate that HTLV-I carriers are more likely to acquire a number of infections, including tuberculosis, leprosy, and strongyloidosis. HTLV-I-associated lymphoproliferative disease probably results from infection in early life, with many decades between exposure and disease manifestation. In contrast, the latency period of HAM/TSP appears shorter, raising the possibility of a different natural history and pathogenesis, possibly involving indirect immunologic mechanisms. (93 Refs)
Keywords: Comparative Study Cross-Cultural Comparison Cross-Sectional Studies Human HIV Seroprevalence/TRENDS HTLV-I/ISOLATION & PURIF/*PATHOGENICITY Incidence Infant, Newborn Leukemia-Lymphoma, T-Cell, Acute, HTLV-I-Associated/DIAGNOSIS/ *EPIDEMIOLOGY/MICROBIOLOGY/TRANSMISSION Paraparesis, Tropical Spastic/EPIDEMIOLOGY/MICROBIOLOGY/ TRANSMISSION Pregnancy Risk Factors MONOGRAPH REVIEW 920430
M9240944
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Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
