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The human T-cell lymphotropic virus type I (HTLV-I) is the first retrovirus identified in humans. It has been responsible for a number of clinical syndromes, most notably adult T-cell leukemia or lymphoma and tropical spastic paraparesis. In the United States, infection with this virus is most frequently found in specific subsets of our population, particularly in those who live in the southeastern states, have southern Japanese ancestry, or share intravenous drug paraphernalia. Understanding the epidemiology and clinical manifestations of this virus is necessary to properly diagnose and care for patients with HTLV-I infection. 相似文献
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E L Murphy K F Varney N T Miyasaki R J Moore J I Umekubo A N Watanabe H Khayam-Bashi 《The Western journal of medicine》1993,158(5):480-483
The epidemiology of human T-lymphotropic virus type I (HTLV-I) infection is not well defined in Japanese Americans. This impairs using approaches that could reduce viral transmission and monitor carriers for the disease. Using enzyme-linked immunosorbent assay and p21e recombinant Western blot testing, HTLV-I antibody was measured in unlinked samples from Japanese-American patients at 4 physicians'' offices in San Francisco, California. Of 442 patients, 4 (0.9%; 95% confidence interval 0.25%, 2.3%) were confirmed seropositive, all with an HTLV-I rather than an HTLV-II pattern on Western blot. Seroprevalence was highest among the issei or immigrant generation (3/230 or 1.3%) compared with the second-generation nisei (1/191 or 0.5%) or third-generation sansei (0 of 17). Prevalence did not differ by age or sex, although the number of positive subjects in each subgroup was small. Of 88 patients with familial origins in endemic areas of southern Japan, none were seropositive. In this sample of Japanese Americans, HTLV-I seroprevalence was lower than in residents of endemic southern Japan but higher than among American blood donors. The prevalence was most similar to that in nonendemic areas of Japan. The public health implications of HTLV-I infection among Japanese Americans are discussed. 相似文献
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Inactivation of human T-lymphotropic virus type III/lymphadenopathy-associated virus by formaldehyde-based reagents. 总被引:1,自引:0,他引:1
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Neutral buffered Formalin, a fixative used in most pathology laboratories, was found to inactivate human T-lymphotropic virus type III/lymphadenopathy-associated virus. Preparations containing this virus with infectivity titers of greater than 10(5) were treated with 1% or greater neutral buffered Formalin; after treatment, virus was undetectable (titer, less than 10(1)). In addition, when infected phytohemagglutinin-stimulated lymphocytes were treated with paraformaldehyde, transmission of the virus to other such lymphocytes was eliminated. 相似文献
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Isolation,characterization, and transmission of human T-lymphotropic virus types I and II in culture
Katsuhiko Kitamura Donna L. Rudolph Cynthia Goldsmith Thomas M. Folks Renu B. Lal Ph.D. 《Current microbiology》1993,27(6):355-360
Highly sensitive coculture methods were developed both for isolation of human T-lymphotropic virus types I and II (HTLV-1 and HTLV-II) from infected individuals and for productive infection of lymphoid cells. Mitogen-activated peripheral blood mononuclear cells (PBMC) from 13 HTLV-I- and 20 HTLV-II-positive specimens were cocultured with an equal number of mitogen-activated PBMC from HTLV-seronegative individuals, and culture supernatants were tested for the presence of soluble p24gag antigens at weekly intervals for 4 weeks. Eleven of 13 (85%) HTLV-I and 14 of 20 (70%) HTLV-II cultures were positive for p24 antigens. None of the 17 HTLV-seroindeterminate or six HTLV-seronegative specimens were positive for the presence of p24 antigen. The isolation rates for HTLV-I and HTLV-II by an alternative whole-blood lysis procedure were comparable to those obtained by standard PBMC cultures. Furthermore, cocultivation of PHA-stimulated PBMC from healthy donors with lethally irradiated HTLV-I- and HTLV-II-infected cell lines (SP and Mo-T, respectively) resulted in productive viral infection, as reflected by the appearance of p24gag antigens concomitant with specific genomic amplification of HTLV proviral DNA after 3 weeks of cocultivation. Thus, the cocultivation technique provides a highly sensitive and specific procedure both for HTLV isolation and for infection of target cells. 相似文献
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Hasegawa H Sawa H Lewis MJ Orba Y Sheehy N Yamamoto Y Ichinohe T Tsunetsugu-Yokota Y Katano H Takahashi H Matsuda J Sata T Kurata T Nagashima K Hall WW 《Nature medicine》2006,12(4):466-472
Adult T-cell leukemia-lymphoma (ATLL) is a group of T-cell malignancies caused by infection with human T-lymphotropic virus type I (HTLV-I). Although the pathogenesis of ATLL remains incompletely understood, the viral regulatory protein Tax is centrally involved in cellular transformation. Here we describe the generation of HTLV-I Tax transgenic mice using the Lck proximal promoter to restrict transgene expression to developing thymocytes. After prolonged latency periods, transgenic mice developed diffuse large-cell lymphomas and leukemia with clinical, pathological and immunological features characteristic of acute ATLL. Transgenic mice were functionally immunocompromised and they developed opportunistic infections. Fulminant disease also developed rapidly in SCID mice after engraftment of lymphomatous cells from transgenic mice. Flow cytometry showed that the cells were CD4(-) and CD8(-), but CD44(+), CD25(+) and cytoplasmic CD3(+). This phenotype is indicative of a thymus-derived pre-T-cell phenotype, and disease development was associated with the constitutive activation of NF-kappaB. Our model accurately reproduces human disease and will provide a tool for analysis of the molecular events in transformation and for the development of new therapeutics. 相似文献
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J D Rosenblatt 《The Western journal of medicine》1993,158(4):379
Human T-lymphotropic virus types I (HTLV-I) and II (HTLV-II) are members of a family of four known retroviruses that are oncogenic as opposed to cytopathic. This family includes HTLV-I and -II, bovine leukemia virus, and simian T-cell leukemia virus. The two types of HTLV are closely related, and for more than a decade we have been aware of the presence of these viruses in humans. In the first part of this article I summarize recent epidemiologic and clinical findings related to the presence of HTLV-I and -II in the Americas. In the second part, I discuss how these viruses may regulate themselves and how in turn they might cause leukemia and neurologic disease in humans. 相似文献
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Neutral buffered Formalin, a fixative used in most pathology laboratories, was found to inactivate human T-lymphotropic virus type III/lymphadenopathy-associated virus. Preparations containing this virus with infectivity titers of greater than 10(5) were treated with 1% or greater neutral buffered Formalin; after treatment, virus was undetectable (titer, less than 10(1)). In addition, when infected phytohemagglutinin-stimulated lymphocytes were treated with paraformaldehyde, transmission of the virus to other such lymphocytes was eliminated. 相似文献
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S Wakamatsu M Makino C Tei M Baba 《Journal of immunology (Baltimore, Md. : 1950)》1999,163(7):3914-3919
We attempted apoptotic cell death induction of T cells infected with human T lymphotropic virus type I (HTLV-I) which induces HTLV-I-associated myelopathy/tropical spastic paraparesis and adult T cell leukemia. T cells acutely infected and expressing HTLV-Igag Ags were killed by cross-linking their TCR with anti-CD3 mAb. Cells in apoptotic process were found by staining with annexin V. The apoptosis was not affected by costimulation through CD28 molecules and was resistant to ligation of Fas molecules. Whereas the virus-infected T cells expressed higher levels of HLA-DR, CD25, CD80, and CD86 Ags than apoptosis-resistant PHA-blasts, the T cell apoptosis was enhanced by addition of exogenous IL-2. Furthermore, in this apoptosis, monocytes played an important role because T cells infected in the absence of monocytes were resistant to the death signals. The apoptosis-sensitive T cells responded to TCR signaling more strongly by proliferating than those apoptosis-resistant cells. Monocytes weakly affected the expression levels of viral Ags on T cells. However, HTLV-I-infected monocytes primed T cells to die by subsequent TCR signaling. T cells primed with the monocytes, subsequently infected in the absence of monocytes, were killed by TCR signaling. These observations suggest that primed and infected T cells could be killed by activation-induced cell death. 相似文献
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M Ogata M Iwasaki S Kubo I Nakasono H Suyama K Kinoshita S Ikeda S Momida M Ichimaru 《Human heredity》1990,40(5):253-256
The serum Gc, Hp and alpha 2HS phenotypes were examined in 64 subjects known to have the human T-lymphotropic leukemia virus type I (HTLV-I) infection and in 60 uninfected subjects. There were no significant differences in the distributions of Gc, Hp and alpha 2HS phenotype and allele frequencies between any grouping of HTLV-I-infected subjects and the controls. No association between the Gc, Hp and alpha 2HS genotypes and susceptibility to adult T-cell leukemia was found. 相似文献
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The human T-lymphotropic virus type I tax gene can cooperate with the ras oncogene to induce neoplastic transformation of cells. 总被引:23,自引:6,他引:17
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Epidemiologic studies have linked infection by the human T-lymphotropic virus type I (HTLV-I) with the development of adult T-cell leukemia. The low penetrance of the virus and the long latency for disease manifestation are factors that obscure the role of HTLV-I infection in oncogenesis. We have used an in vitro transformation assay system to determine directly whether the HTLV-I tax gene has transformation potential. Transfection of the tax gene alone into early-passage rat embryo fibroblasts did not induce morphological alterations. However, cotransfection of tax with the selectable marker plasmid pRSVneo gave rise to G418-resistant colonies that could be established as immortalized cell lines. Cotransfection of tax with the ras oncogene into rat embryo fibroblasts gave rise to foci of transformed cells that were highly tumorigenic in nude mice. These data represent a direct demonstration of the oncogenic potential of the tax gene in nonlymphoid cells and establish HTLV-I as a transforming virus. 相似文献
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van Tienen C de Silva TI Alcantara LC Onyango CO Jarju S Gonçalves N Vincent T Aaby P Whittle H Schim van der Loeff M Cotten M 《PLoS neglected tropical diseases》2012,6(6):e1690