https://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&feed=atom&action=historyHuman T-lymphotropic virus 1 - Revision history2024-03-28T18:10:22ZRevision history for this page on the wikiMediaWiki 1.39.6https://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=55094&oldid=prevBarichD at 15:07, 20 August 20102010-08-20T15:07:39Z<p></p>
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</table>BarichDhttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39507&oldid=prevKmagalhaes: /* References */2008-12-16T00:34:31Z<p><span dir="auto"><span class="autocomment">References</span></span></p>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">[Sample reference] [http://ijs</del>.<del style="font-weight: bold; text-decoration: none;">sgmjournals</del>.<del style="font-weight: bold; text-decoration: none;">org/cgi/reprint/50/2/489 Takai</del>, K., <del style="font-weight: bold; text-decoration: none;">Sugai</del>, <del style="font-weight: bold; text-decoration: none;">A</del>., <del style="font-weight: bold; text-decoration: none;">Itoh</del>, T., and <del style="font-weight: bold; text-decoration: none;">Horikoshi</del>, <del style="font-weight: bold; text-decoration: none;">K</del>. <del style="font-weight: bold; text-decoration: none;">"''Palaeococcus ferrophilus'' gen</del>. <del style="font-weight: bold; text-decoration: none;">nov</del>., <del style="font-weight: bold; text-decoration: none;">sp</del>. <del style="font-weight: bold; text-decoration: none;">nov</del>., <del style="font-weight: bold; text-decoration: none;">a barophilic</del>, <del style="font-weight: bold; text-decoration: none;">hyperthermophilic archaeon from a deep</del>-<del style="font-weight: bold; text-decoration: none;">sea hydrothermal vent chimney"</del>. <del style="font-weight: bold; text-decoration: none;">''International </del>Journal of <del style="font-weight: bold; text-decoration: none;">Systematic </del>and <del style="font-weight: bold; text-decoration: none;">Evolutionary Microbiology''</del>. <del style="font-weight: bold; text-decoration: none;">2000</del>. <del style="font-weight: bold; text-decoration: none;">Volume 50</del>. p. <del style="font-weight: bold; text-decoration: none;">489</del>-<del style="font-weight: bold; text-decoration: none;">500</del>.<del style="font-weight: bold; text-decoration: none;">]</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Aboud, M., Grassmann R, Jeang, KT., 2005, “Molecular mechanisms of cellular transformation by HTLV-1 Tax”. Oncogene, v. 24, p. 5976-5985.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Akizawa, T., Chuhjo, T., Fujii, M., Seiki, M., Fujii, M., 1992, “Interaction of HTLV-1 Taxl with p67 sRF causes the aberrant induction of cellular immediate early genes through CArG boxes”. Genes and Development, v. 6, p. 2066-2076.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Boxus, M., DeWolf, J., Legros, S., Kettmann, R., Twizere, J., Willems, L., 2008, “The HTLV-1 Tax</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Interactome”. Retrovirology, v. 5, p. 76.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Brady, J.,H., Chung, J.,H., Jeong, J.,H., Jeong, S.,J., Park, H.,U., 2006, “Human T-cell leukemia virus type 1 Tax attenuates c-irradiation-induced apoptosis through physical interaction with Chk2”. Oncogene, v. 25, p. 438-447.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"> </ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Brady, J</ins>.<ins style="font-weight: bold; text-decoration: none;">,N</ins>.<ins style="font-weight: bold; text-decoration: none;">, Clemens</ins>, K., <ins style="font-weight: bold; text-decoration: none;">Dittmer, J., Pise-Maison</ins>, <ins style="font-weight: bold; text-decoration: none;">C</ins>., <ins style="font-weight: bold; text-decoration: none;">1997</ins>, <ins style="font-weight: bold; text-decoration: none;">“Physical and Functional Interaction between the Human </ins>T<ins style="font-weight: bold; text-decoration: none;">-Cell Lymphotropic Virus Type 1 Tax1 Protein and the CCAAT Binding Protein NF-Y.” Molecular and Cellular Biology, v. 17, p. 1236-1243.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Feuer, G., Green, P.,L</ins>., <ins style="font-weight: bold; text-decoration: none;">2005, “Comparative biology of human T-cell lymphotropic virus type 1 (HTLV-1) </ins>and <ins style="font-weight: bold; text-decoration: none;">HTLV-2”. Oncogene, v. 24</ins>, <ins style="font-weight: bold; text-decoration: none;">p, 5996-6004.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Furukawa, Y</ins>.<ins style="font-weight: bold; text-decoration: none;">, Izumo, S</ins>.<ins style="font-weight: bold; text-decoration: none;">, Kubota, R</ins>., <ins style="font-weight: bold; text-decoration: none;">Mitsutoshi, T</ins>.<ins style="font-weight: bold; text-decoration: none;">, Osame, M</ins>., <ins style="font-weight: bold; text-decoration: none;">2001</ins>, <ins style="font-weight: bold; text-decoration: none;">“Existence of escape mutant in HTLV</ins>-<ins style="font-weight: bold; text-decoration: none;">I tax during the development of adult T-cell leukemia”. Blood, v. 97, p. 987-993</ins>.</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Jeang, K.,T., Kibler, K., 2001, “CREB/ATF-Dependent Repression of Cyclin A by Human T-Cell Leukemia Virus Type 1 Tax Protein”. </ins>Journal of <ins style="font-weight: bold; text-decoration: none;">Virology, v. 75, p. 2161-2173.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Matsuoka, M., Jeang, K.,T., 2007, “Human T-cell leukemia virus type 1(HTLV-1) infectivity </ins>and <ins style="font-weight: bold; text-decoration: none;">cellular transformation”. National Review Cancer, v. 7, p. 270-280.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Reddy, T</ins>.<ins style="font-weight: bold; text-decoration: none;">,R</ins>.<ins style="font-weight: bold; text-decoration: none;">, Tang, H</ins>.<ins style="font-weight: bold; text-decoration: none;">, Li, X., Wong-Staal, F., 1997, “Functional interaction of the HTLV-1 transactivator Tax with activating transcription factor-4 (ATF4)”. Oncogene, v. 14, </ins>p. <ins style="font-weight: bold; text-decoration: none;">2785</ins>-<ins style="font-weight: bold; text-decoration: none;">2792</ins>.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Edited by student of [mailto:elilly@umassd.edu Emily Lilly] at University of Massachusetts Dartmouth.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Edited by student of [mailto:elilly@umassd.edu Emily Lilly] at University of Massachusetts Dartmouth.</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39503&oldid=prevKmagalhaes: /* Current Research */2008-12-16T00:13:13Z<p><span dir="auto"><span class="autocomment">Current Research</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 00:13, 16 December 2008</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The first research topic of interest deals with the interaction between Tax1 and the CCAAT Binding protein NF-Y. Researchers at the National Institutes of Health in Bethesda, Maryland (1996) used a yeast two-hybrid system to screen for proteins that interact with Tax, by isolating the B subunit of the CCAAT binding protein NF-Y from a HeLa cDNA library. The specificity of the NF-YB-Tax interaction was examined by testing the ability of the NF-YB fused to an acidic activation domain to interact with a panel of different LexA fusion proteins. The interaction of Tax with NF-YB was found to be specific in that NF-YB did not interact with a variety of other transcription factors, including the human immunodeficiency virus Tat, and the human papillomavirus E6, but did interact with the C-terminal Tax1 mutants M22 and M47. It was also shown that in vitro-translated NF-YB specifically bound to a glutathione S-transferase-Tax fusion protein, and that Tax1 coimmunoprecipitated with NF-Y nuclear extracts of HTLV-1 transformed cells, providing evidence for the in vivo interacton of Tax1 and NF-YB. This data indicates that Tax1 interacts with NF-Y through the B subunit and that this interaction plays a critical role in causing cellular transformation and HTLV-1 pathogenesis.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The first research topic of interest deals with the interaction between Tax1 and the CCAAT Binding protein NF-Y. Researchers at the National Institutes of Health in Bethesda, Maryland (1996) used a yeast two-hybrid system to screen for proteins that interact with Tax, by isolating the B subunit of the CCAAT binding protein NF-Y from a HeLa cDNA library. The specificity of the NF-YB-Tax interaction was examined by testing the ability of the NF-YB fused to an acidic activation domain to interact with a panel of different LexA fusion proteins. The interaction of Tax with NF-YB was found to be specific in that NF-YB did not interact with a variety of other transcription factors, including the human immunodeficiency virus Tat, and the human papillomavirus E6, but did interact with the C-terminal Tax1 mutants M22 and M47. It was also shown that in vitro-translated NF-YB specifically bound to a glutathione S-transferase-Tax fusion protein, and that Tax1 coimmunoprecipitated with NF-Y nuclear extracts of HTLV-1 transformed cells, providing evidence for the in vivo interacton of Tax1 and NF-YB. This data indicates that Tax1 interacts with NF-Y through the B subunit and that this interaction plays a critical role in causing cellular transformation and HTLV-1 pathogenesis.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The second research topic of interest deals with evidence that HTLV-1 directly interacts with and inhibits the kinase activity of Chk2, which is known to contribute to the development of both hereditary and sporadic human cancers when defective. Researchers at the National Institutes of Health in Bethesda , Maryland observed the physical interaction of Chk2 and Tax by coimmunoprecipitation assays in HTLV-1 infected T-cells as well as GST pull-down assays using purified proteins. Binding and kinase activity inhibition studies were also completed using Tax deletion mutants, which indicated that at least two domains of Tax mediate the interaction with CHK2. Transient transfection and a TUNEL assay were also completed, which determined that γ-irradiation-induced apoptosis was decreased in 293T and HCT-116 cells expressing HTLV-1 Tax. The research demonstrated an important potential target of Tax in cellular transformation.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The second research topic of interest deals with evidence that HTLV-1 directly interacts with and inhibits the kinase activity of Chk2, which is known to contribute to the development of both hereditary and sporadic human cancers when defective. Researchers at the National Institutes of Health in Bethesda , Maryland <ins style="font-weight: bold; text-decoration: none;">(2005) </ins>observed the physical interaction of Chk2 and Tax by coimmunoprecipitation assays in HTLV-1 infected T-cells as well as GST pull-down assays using purified proteins. Binding and kinase activity inhibition studies were also completed using Tax deletion mutants, which indicated that at least two domains of Tax mediate the interaction with CHK2. Transient transfection and a TUNEL assay were also completed, which determined that γ-irradiation-induced apoptosis was decreased in 293T and HCT-116 cells expressing HTLV-1 Tax. The research demonstrated an important potential target of Tax in cellular transformation.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The third research topic of interest deals with</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The third research topic of interest deals with <ins style="font-weight: bold; text-decoration: none;">the repression of the CREB/ATF-Dependent Cyclin A by the HTLV-1 Tax Protein. Researchers at the National Institute of Allergy and Infectious diseases in Bethesda, Maryland (2000) observed that Tax altered the formation of a complex(es) at the cyclin A promoter-derived ATF site. Repression of the cyclin A promoter was seen in both ts13 adherent cells and Jurkat T lymphocytes along with two other TATA-less promoters, cyclin D3 and DNA polymerase a. This information led to the correlation between the removal of the CREB/ATF site from the promoter with the loss of repression by Tax. The researchers were also able to propose that the Tax repression occurred through protein-protein contact with CREB/ATF since a Tax mutant protein (which binds CREB) repressed the cyclin A promoter while another mutant protein (which does not bind CREB) did not.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39486&oldid=prevKmagalhaes: /* Current Research */2008-12-15T21:56:42Z<p><span dir="auto"><span class="autocomment">Current Research</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 21:56, 15 December 2008</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l40">Line 40:</td>
<td colspan="2" class="diff-lineno">Line 40:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The first research topic of interest deals with the interaction between Tax1 and the CCAAT Binding protein NF-Y. Researchers at the National Institutes of Health in Bethesda, Maryland (1996) used a yeast two-hybrid system to screen for proteins that interact with Tax, by isolating the B subunit of the CCAAT binding protein NF-Y from a HeLa cDNA library. The specificity of the NF-YB-Tax interaction was examined by testing the ability of the NF-YB fused to an acidic activation domain to interact with a panel of different LexA fusion proteins. The interaction of Tax with NF-YB was found to be specific in that NF-YB did not interact with a variety of other transcription factors, including the human immunodeficiency virus Tat, and the human papillomavirus E6, but did interact with the C-terminal Tax1 mutants M22 and M47. It was also shown that in vitro-translated NF-YB specifically bound to a glutathione S-transferase-Tax fusion protein, and that Tax1 coimmunoprecipitated with NF-Y nuclear extracts of HTLV-1 transformed cells, providing evidence for the in vivo interacton of Tax1 and NF-YB. This data indicates that Tax1 interacts with NF-Y through the B subunit and that this interaction plays a critical role in causing cellular transformation and HTLV-1 pathogenesis.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The first research topic of interest deals with the interaction between Tax1 and the CCAAT Binding protein NF-Y. Researchers at the National Institutes of Health in Bethesda, Maryland (1996) used a yeast two-hybrid system to screen for proteins that interact with Tax, by isolating the B subunit of the CCAAT binding protein NF-Y from a HeLa cDNA library. The specificity of the NF-YB-Tax interaction was examined by testing the ability of the NF-YB fused to an acidic activation domain to interact with a panel of different LexA fusion proteins. The interaction of Tax with NF-YB was found to be specific in that NF-YB did not interact with a variety of other transcription factors, including the human immunodeficiency virus Tat, and the human papillomavirus E6, but did interact with the C-terminal Tax1 mutants M22 and M47. It was also shown that in vitro-translated NF-YB specifically bound to a glutathione S-transferase-Tax fusion protein, and that Tax1 coimmunoprecipitated with NF-Y nuclear extracts of HTLV-1 transformed cells, providing evidence for the in vivo interacton of Tax1 and NF-YB. This data indicates that Tax1 interacts with NF-Y through the B subunit and that this interaction plays a critical role in causing cellular transformation and HTLV-1 pathogenesis.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The second research topic of interest deals with evidence that HTLV-1 directly interacts with and inhibits the kinase activity of Chk2, which is known to contribute to the development of both hereditary and sporadic human cancers when defective.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The second research topic of interest deals with evidence that HTLV-1 directly interacts with and inhibits the kinase activity of Chk2, which is known to contribute to the development of both hereditary and sporadic human cancers when defective. <ins style="font-weight: bold; text-decoration: none;"> Researchers at the National Institutes of Health in Bethesda , Maryland observed the physical interaction of Chk2 and Tax by coimmunoprecipitation assays in HTLV-1 infected T-cells as well as GST pull-down assays using purified proteins. Binding and kinase activity inhibition studies were also completed using Tax deletion mutants, which indicated that at least two domains of Tax mediate the interaction with CHK2. Transient transfection and a TUNEL assay were also completed, which determined that γ-irradiation-induced apoptosis was decreased in 293T and HCT-116 cells expressing HTLV-1 Tax. The research demonstrated an important potential target of Tax in cellular transformation.</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">The third research topic of interest deals with</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39485&oldid=prevKmagalhaes: /* Current Research */2008-12-15T21:29:04Z<p><span dir="auto"><span class="autocomment">Current Research</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 21:29, 15 December 2008</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">The first research topic of interest deals with the interaction between Tax1 and the CCAAT Binding protein NF-Y. Researchers at the National Institutes of Health in Bethesda, Maryland (1996) used a yeast two-hybrid system to screen for proteins that interact with Tax, by isolating the B subunit of the CCAAT binding protein NF-Y from a HeLa cDNA library. The specificity of the NF-YB-Tax interaction was examined by testing the ability of the NF-YB fused to an acidic activation domain to interact with a panel of different LexA fusion proteins. The interaction of Tax with NF-YB was found to be specific in that NF-YB did not interact with a variety of other transcription factors, including the human immunodeficiency virus Tat, and the human papillomavirus E6, but did interact with the C-terminal Tax1 mutants M22 and M47. It was also shown that in vitro-translated NF-YB specifically bound to a glutathione S-transferase-Tax fusion protein, and that Tax1 coimmunoprecipitated with NF-Y nuclear extracts of HTLV-1 transformed cells, providing evidence for the in vivo interacton of Tax1 and NF-YB. This data indicates that Tax1 interacts with NF-Y through the B subunit and that this interaction plays a critical role in causing cellular transformation and HTLV-1 pathogenesis.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">Enter summarries </del>of the <del style="font-weight: bold; text-decoration: none;">most rescent research here--at least three required</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">The second research topic of interest deals with evidence that HTLV-1 directly interacts with and inhibits the kinase activity </ins>of <ins style="font-weight: bold; text-decoration: none;">Chk2, which is known to contribute to </ins>the <ins style="font-weight: bold; text-decoration: none;">development of both hereditary and sporadic human cancers when defective.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==References==</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39484&oldid=prevKmagalhaes: /* Pathology */2008-12-15T20:06:33Z<p><span dir="auto"><span class="autocomment">Pathology</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 20:06, 15 December 2008</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Tax plays an important role in the pathogenesis of HTLV-1 by stimulating viral gene expression and by deregulating expression of cellular genes. Tax has also been shown to activate transcription of a number of cellular genes involved in cell proliferation, and the expression of these growth-related genes has been implicated in contributing to the establishment of HTLV-1 associated pathogenesis. While Tax does not bind directly to DNA, it appears to stimulate RNA synthesis through protein-protein interactions with host cell transcription factors. The most well-studied of these interactions is with the ATF/CREB family of transcription factors, which bind to cyclic AMP-responsive elements in the HTLV-1 long terminal repeats.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Tax plays an important role in the pathogenesis of HTLV-1 by stimulating viral gene expression and by deregulating expression of cellular genes. Tax has also been shown to activate transcription of a number of cellular genes involved in cell proliferation, and the expression of these growth-related genes has been implicated in contributing to the establishment of HTLV-1 associated pathogenesis. While Tax does not bind directly to DNA, it appears to stimulate RNA synthesis through protein-protein interactions with host cell transcription factors. The most well-studied of these interactions is with the ATF/CREB family of transcription factors, which bind to cyclic AMP-responsive elements in the HTLV-1 long terminal repeats.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). <del style="font-weight: bold; text-decoration: none;">The principle target cells for </del>HTLV-1 infection <del style="font-weight: bold; text-decoration: none;">in the lymphoid system are mature CD4+ T-lymphocytes</del>. Tax also plays an important role in the transformation of the virus, for its displays oncogenic potential in several experimental systems including the morphological transformation of rodent fibroblasts, induction of tumors in transgenic animals, and Herpes samiri vector immortalization of human T cells.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). <ins style="font-weight: bold; text-decoration: none;">A proportion of 1-3% of </ins>HTLV-1 <ins style="font-weight: bold; text-decoration: none;">infected individuals develop these diseases after prolonged viral persistance, usually after two decades of </ins>infection <ins style="font-weight: bold; text-decoration: none;">for ATL</ins>. Tax also plays an important role in the transformation of the virus, for its displays oncogenic potential in several experimental systems including the morphological transformation of rodent fibroblasts, induction of tumors in transgenic animals, and Herpes samiri vector immortalization of human T cells.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39483&oldid=prevKmagalhaes: /* Pathology */2008-12-15T19:47:46Z<p><span dir="auto"><span class="autocomment">Pathology</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 19:47, 15 December 2008</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Because of the long incubation period between viral exposure and disease onset, the exact mechanism of HTLV-1 pathogenesis remains unclear. Research has shown that the host cell's control of HTLV-1 replication is the primary determinant of virus expression and subsequent disease. It is also known that the transmission of HTLV-1 occurs through perinatal transmission by blood or breast milk, sexual transmission, or exposure to contaminated blood products, and that the infected cells must be passed from the infected individual or material because HTLV-1 transmits via cell to cell contact. </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Because of the long incubation period between viral exposure and disease onset, the exact mechanism of HTLV-1 pathogenesis remains unclear. Research has shown that the host cell's control of HTLV-1 replication is the primary determinant of virus expression and subsequent disease. It is also known that the transmission of HTLV-1 occurs through perinatal transmission by blood or breast milk, sexual transmission, or exposure to contaminated blood products, and that the infected cells must be passed from the infected individual or material because HTLV-1 transmits via cell to cell contact. </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The process begins when an infected cell contacts an uninfected cell, forming a microtubule-organizing center (MTOC) that is polarized at the cell-cell junction. A virological synapse is then formed at the interface. The HTLV-1 GAG-complex and viral genomic RNAs then accumulate at the synapse and are released into the uninfected cell. The engagement of intercellular adhesion molecule 1 (ICAM1) increases the polarization of the MTOC at the point of contact, indicating that the interaction of ICAM1 and lymphocyte function-associated antigen 1 (LFA1) is important for HTLV-1 infection.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The process begins when an infected cell contacts an uninfected cell, forming a microtubule-organizing center (MTOC) that is polarized at the cell-cell junction. A virological synapse is then formed at the interface<ins style="font-weight: bold; text-decoration: none;">, which is triggered by the Tax protein located in ORF IV</ins>. The HTLV-1 GAG-complex and viral genomic RNAs then accumulate at the synapse and are released into the uninfected cell. The engagement of intercellular adhesion molecule 1 (ICAM1) increases the polarization of the MTOC at the point of contact, indicating that the interaction of ICAM1 and lymphocyte function-associated antigen 1 (LFA1) is important for HTLV-1 infection.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">In addition </del>to cell to <del style="font-weight: bold; text-decoration: none;">cell contact, synapse formation is also triggered by </del>the HTLV-1 Tax protein, which <del style="font-weight: bold; text-decoration: none;">can be found </del>in <del style="font-weight: bold; text-decoration: none;">ORF IV</del>. <del style="font-weight: bold; text-decoration: none;"> Tax is also believed to exert its effect by stimulating viral gene expression</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Tax plays an important role in the pathogenesis of HTLV-1 by stimulating viral gene expression and by deregulating expression of cellular genes. Tax has also been shown </ins>to <ins style="font-weight: bold; text-decoration: none;">activate transcription of a number of cellular genes involved in </ins>cell <ins style="font-weight: bold; text-decoration: none;">proliferation, and the expression of these growth-related genes has been implicated in contributing </ins>to the <ins style="font-weight: bold; text-decoration: none;">establishment of </ins>HTLV-1 <ins style="font-weight: bold; text-decoration: none;">associated pathogenesis. While </ins>Tax <ins style="font-weight: bold; text-decoration: none;">does not bind directly to DNA, it appears to stimulate RNA synthesis through </ins>protein<ins style="font-weight: bold; text-decoration: none;">-protein interactions with host cell transcription factors. The most well-studied of these interactions is with the ATF/CREB family of transcription factors</ins>, which <ins style="font-weight: bold; text-decoration: none;">bind to cyclic AMP-responsive elements </ins>in <ins style="font-weight: bold; text-decoration: none;">the HTLV-1 long terminal repeats</ins>.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">Tax also displays oncogenic potential in several experimental systems including the morphological transformation of rodent fibroblasts, induction of tumors in transgenic animals, and Herpes samiri vector immortalization of human T cells.</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). The principle target cells for HTLV-1 infection in the lymphoid system are mature CD4+ T-lymphocytes<ins style="font-weight: bold; text-decoration: none;">. Tax also plays an important role in the transformation of the virus, for its displays oncogenic potential in several experimental systems including the morphological transformation of rodent fibroblasts, induction of tumors in transgenic animals, and Herpes samiri vector immortalization of human T cells</ins>.</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div> </div></td><td colspan="2" class="diff-side-added"></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). The principle target cells for HTLV-1 infection in the lymphoid system are mature CD4+ T-lymphocytes.</div></td><td colspan="2" class="diff-side-added"></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39482&oldid=prevKmagalhaes: /* Pathology */2008-12-15T19:33:15Z<p><span dir="auto"><span class="autocomment">Pathology</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 19:33, 15 December 2008</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Pathology==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Pathology==</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Because of the long incubation period between viral exposure and disease onset, the exact mechanism of HTLV-1 pathogenesis remains unclear. Research has shown that the host cell's control of HTLV-1 replication is the primary determinant of virus expression and subsequent disease. It is also known that the transmission of HTLV-1 occurs through perinatal transmission by blood or breast milk, sexual transmission, or exposure to contaminated blood products, and that the infected cells must be passed from the infected individual or material because HTLV-1 transmits via cell to cell contact. </ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">The process begins when an infected cell contacts an uninfected cell, forming a microtubule-organizing center (MTOC) that is polarized at the cell-cell junction. A virological synapse is then formed at the interface. The HTLV-1 GAG-complex and viral genomic RNAs then accumulate at the synapse and are released into the uninfected cell. The engagement of intercellular adhesion molecule 1 (ICAM1) increases the polarization of the MTOC at the point of contact, indicating that the interaction of ICAM1 and lymphocyte function-associated antigen 1 (LFA1) is important for HTLV-1 infection.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 <del style="font-weight: bold; text-decoration: none;">infects and transforms primary human T-lymphocytes (CD4+) </del>in <del style="font-weight: bold; text-decoration: none;">cell culture, and involves the viral transactivator protein Tax</del>. Tax displays oncogenic potential in several experimental systems including the morphological transformation of rodent fibroblasts, induction of tumors in transgenic animals, and Herpes samiri vector immortalization of human T cells.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">In addition to cell to cell contact, synapse formation is also triggered by the </ins>HTLV-1 <ins style="font-weight: bold; text-decoration: none;">Tax protein, which can be found </ins>in <ins style="font-weight: bold; text-decoration: none;">ORF IV</ins>. Tax <ins style="font-weight: bold; text-decoration: none;">is also believed to exert its effect by stimulating viral gene expression</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Tax also </ins>displays oncogenic potential in several experimental systems including the morphological transformation of rodent fibroblasts, induction of tumors in transgenic animals, and Herpes samiri vector immortalization of human T cells.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). The principle target cells for HTLV-1 infection in the lymphoid system are mature CD4+ T-lymphocytes.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). The principle target cells for HTLV-1 infection in the lymphoid system are mature CD4+ T-lymphocytes.</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39480&oldid=prevKmagalhaes: /* Pathology */2008-12-15T18:05:43Z<p><span dir="auto"><span class="autocomment">Pathology</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 18:05, 15 December 2008</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Pathology==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Pathology==</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">HTLV-1 infects and transforms primary human T-lymphocytes (CD4+) in cell culture, and involves the viral transactivator protein Tax. Tax displays oncogenic potential in several experimental systems including the morphological transformation of rodent fibroblasts, induction of tumors in transgenic animals, and Herpes samiri vector immortalization of human T cells.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). The principle target cells for HTLV-1 infection in the lymphoid system are mature CD4+ T-lymphocytes.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>HTLV-1 is the causative agent of at least two human diseases, namely adult T-cell leukemia (ATL), and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). The principle target cells for HTLV-1 infection in the lymphoid system are mature CD4+ T-lymphocytes.</div></td></tr>
</table>Kmagalhaeshttps://microbewiki.kenyon.edu/index.php?title=Human_T-lymphotropic_virus_1&diff=39479&oldid=prevKmagalhaes: /* Pathology */2008-12-15T17:37:34Z<p><span dir="auto"><span class="autocomment">Pathology</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:37, 15 December 2008</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l29">Line 29:</td>
<td colspan="2" class="diff-lineno">Line 29:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Pathology==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Pathology==</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">How does this organism cause disease? Human</del>, <del style="font-weight: bold; text-decoration: none;">animal</del>, <del style="font-weight: bold; text-decoration: none;">plant hosts? </del> <del style="font-weight: bold; text-decoration: none;">Virulence factors, as well as patient symptoms</del>.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">HTLV-1 is the causative agent of at least two human diseases</ins>, <ins style="font-weight: bold; text-decoration: none;">namely adult T-cell leukemia (ATL)</ins>, <ins style="font-weight: bold; text-decoration: none;">and a degenerative neurological disorder known as tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). </ins> <ins style="font-weight: bold; text-decoration: none;">The principle target cells for HTLV-1 infection in the lymphoid system are mature CD4+ T-lymphocytes</ins>.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Current Research==</div></td></tr>
</table>Kmagalhaes