Infection of human endothelial cells by human T-lymphotropic virus type I.

Ho, David D.; Rota, Teresa R.; Hirsch, Martin S.

doi:10.1073/pnas.81.23.7588

Cited by 119 publications

(60 citation statements)

References 30 publications

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“…Productive transmission of natural HTLV-1 isolates to primary human endothelial cell cultures (Ho et al, 1984;Hoxie et al, 1984), monocyte and microglial cells (Hoffman et al, 1992), as well as basal mammary epithelial cells (LeVasseur et al, 1998) has been reported.…”

Section: Htlv-1 Tropism: In Vitro or In Vivo Veritas?mentioning

confidence: 99%

HTLV-1 tropism and envelope receptor

et al. 2005

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The identification of CD4 as the primary receptor for HIV followed shortly after the discovery of the virus, but the HTLV receptor remained long elusive, until its recent identification as the GLUT1 glucose transporter. In the present review, we describe the status of the literature that surrounded this discovery as well as the in vitro and in vivo observations that led to the identification of GLUT1. Also, we will explore a few tracks to conciliate the in vitro and in vivo data on HTLV-1 tropism within the context of the HTLV literature that has accumulated over the past 25 years. A close examination of these data leads us to conclude that the preferential detection of HTLV-1 in CD4 þ T lymphocyte subsets in vivo, even in the absence of leukemia, is not likely to be directly related to envelope receptor interactions, but rather to an array of postentry selection bottlenecks in vivo. Furthermore, we propose that infection of other hematopoietic and nonhematopoietic cells is likely to take place during the lifetime of an individual, with a burst early during the infection. Oncogene (2005) 24, 6016-6025.

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Section: Htlv-1 Tropism: In Vitro or In Vivo Veritas?mentioning

confidence: 99%

HTLV-1 tropism and envelope receptor

et al. 2005

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“…First, cell-free infection by HTLV is very inefficient and efficient infection of cells requires cocultivation of peripheral blood mononuclear cells (PBMC) with irradiated HTLV-producer cells. Secondly, although HTLV has the capacity to infect a number of cell types including T cells, B cells, endothelial cells, glial cells, and monocytes of both human and nonhuman origin (Ho et al, 1984;Hoffman et al, 1984;Akagi et al, 1992;Koyanagi et al, 1993), the only cells susceptible to HTLV transformation are primary T lymphocytes. For the context of this article transformation is defined as continuous growth in the absence of exogenous IL-2; immortalization is defined as continuous IL-2-dependent growth.…”

Section: Htlv Experimental Systemmentioning

confidence: 99%

Comparative biology of human T-cell lymphotropic virus type 1 (HTLV-1) and HTLV-2

2005

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“…Evidence suggests that HTLV-1 and HTLV-2 have the same primary receptor, which is expressed ubiquitously on the surface of numerous cell types (11,45,68,69). In contrast to their restricted in vivo and in vitro transformation tropism, in vitro infection with both HTLV-1 and HTLV-2 can be established in many vertebrate cell lines, including T cells, B cells, endothelial cells, glial cells, and monocytes (1,(29)(30)(31). Therefore, it would seem unlikely that the HTLV Env would be responsible for the distinct cellular transformation tropism between HTLV-1 and HTLV-2.…”

Section: Discussionmentioning

confidence: 99%

Envelope Is a Major Viral Determinant of the Distinct In Vitro Cellular Transformation Tropism of Human T-Cell Leukemia Virus Type 1 (HTLV-1) and HTLV-2

Xie¹,

Green

2005

J Virol

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Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are related deltaretroviruses but are distinct in their disease-inducing capacity. These viruses can infect a variety of cell types, but only T lymphocytes become transformed, which is defined in vitro as showing indefinite interleukin-2-independent growth. Studies have indicated that HTLV-1 has a preferential tropism for CD4 ؉ T cells in vivo and is associated with the development of leukemia and neurological disease. Conversely, the in vivo T-cell tropism of HTLV-2 is less clear, although it appears that CD8 ؉ T cells preferentially harbor the provirus, with only a few cases of disease association. The difference in T-cell transformation tropism has been confirmed in vitro as shown by the preferential transformation of CD4 ؉ T cells by HTLV-1 versus the transformation of CD8 ؉ T cells by HTLV-2. Our previous studies showed that Tax and overlapping Rex do not confer the distinct T-cell transformation tropisms between HTLV-1 and HTLV-2. Therefore, for this study HTLV-1 and HTLV-2 recombinants were generated to assess the contribution of LTR and env sequences in T-cell transformation tropism. Both sets of proviral recombinants expressed p19 Gag following transfection into cells. Furthermore, recombinant viruses were replication competent and had the capacity to transform T lymphocytes. Our data showed that exchange of the env gene resulted in altered T-cell transformation tropism compared to wild-type virus, while exchange of long terminal repeat sequences had no significant effect. HTLV-2/Env1 preferentially transformed CD4 ؉ T cells similarly to wild-type HTLV-1 (wtHTLV-1), whereas HTLV-1/Env2 had a transformation tropism similar to that of wtHTLV-2 (CD8 ؉ T cells). These results indicate that env is a major viral determinant for HTLV T-cell transformation tropism in vitro and provides strong evidence implicating its contribution to the distinct pathogenesis resulting from HTLV-1 versus HTLV-2 infections.

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Infection of human endothelial cells by human T-lymphotropic virus type I.

Cited by 119 publications

References 30 publications

HTLV-1 tropism and envelope receptor

HTLV-1 tropism and envelope receptor

Comparative biology of human T-cell lymphotropic virus type 1 (HTLV-1) and HTLV-2

Envelope Is a Major Viral Determinant of the Distinct In Vitro Cellular Transformation Tropism of Human T-Cell Leukemia Virus Type 1 (HTLV-1) and HTLV-2

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