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Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective

DOI: 10.1155/2012/984754

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Abstract:

Cell type specificity of human T cell leukemia virus 1 has been proposed as a possible reason for differential viral outcome in primary target cells versus secondary. Through chromatin remodeling, the HTLV-1 transactivator protein Tax interacts with cellular factors at the chromosomally integrated viral promoter to activate downstream genes and control viral transcription. RNA interference is the host innate defense mechanism mediated by short RNA species (siRNA or miRNA) that regulate gene expression. There exists a close collaborative functioning of cellular transcription factors with miRNA in order to regulate the expression of a number of eukaryotic genes including those involved in suppression of cell growth, induction of apoptosis, as well as repressing viral replication and propagation. In addition, it has been suggested that retroviral latency is influenced by chromatin alterations brought about by miRNA. Since Tax requires the assembly of transcriptional cofactors to carry out viral gene expression, there might be a close association between miRNA influencing chromatin alterations and Tax-mediated LTR activation. Herein we explore the possible interplay between HTLV-1 infection and miRNA pathways resulting in chromatin reorganization as one of the mechanisms determining HTLV-1 cell specificity and viral fate in different cell types. 1. Introduction In the myriad interactions between viruses and host cells, there is a constant struggle for survival that causes both sides to adopt strategies counteracting each other’s effect. More often than not, the error-prone replication of viruses offers them an advantage of selective pressure enabling them to accumulate genetic mutations over time that helps evade host immune defense mechanisms. Most chronic viruses seem to have an edge in this struggle in that they evolve means to manipulate and exploit host molecular pathways to persist in the hostile cellular environment and remain hidden from immune surveillance [1]. In this regard, retroviruses have succeeded in establishing latent infection and developing drug resistance through escape mutants like very few other chronic viruses. One of the strategies utilized by retroviruses is the modulation of chromatin structure and regulation of the rate at which transcription occurs in the target cell. Chromatin remodeling in the context of retroviral infection is being explored as a potent means of long-term persistence. Many studies have shown that the exercise of chromatin modulation in retroviral infection begins with the proviral integration into the host

References

[1]  R. Easley, R. Van Duyne, W. Coley et al., “Chromatin dynamics associated with HIV-1 Tat-activated transcription,” Biochimica et Biophysica Acta, vol. 1799, no. 3-4, pp. 275–285, 2010.
[2]  L. Geeraert, G. Kraus, and R. J. Pomerantz, “Hide-and-seek: the challenge of viral persistence in HIV-1 infection,” Annual Review of Medicine, vol. 59, pp. 487–501, 2008.
[3]  R. Easley, L. Carpio, I. Guendel et al., “Human T-lymphotropic virus type 1 transcription and chromatin-remodeling complexes,” Journal of Virology, vol. 84, no. 9, pp. 4755–4768, 2010.
[4]  T. Koiwa, A. Hamano-Usami, T. Ishida et al., “ -long terminal repeat-selective CpG methylation of latent human T-cell leukemia virus type 1 provirus in vitro and in vivo,” Journal of Virology, vol. 76, no. 18, pp. 9389–9397, 2002.
[5]  A. Manns, M. Hisada, and L. La Grenade, “Human T-lymphotropic virus type I infection,” The Lancet, vol. 353, no. 9168, pp. 1951–1958, 1999.
[6]  J. H. Richardson, A. J. Edwards, J. K. Cruickshank, P. Rudge, and A. G. Dalgleish, “In vivo cellular tropism of human T-cell leukemia virus type 1,” Journal of Virology, vol. 64, no. 11, pp. 5682–5687, 1990.
[7]  M. Nagai, M. B. Brennan, J. A. Sakai, C. A. Mora, and S. Jacobson, “CD8+ T cells are an in vivo reservoir for human T-cell lymphotropic virus type I,” Blood, vol. 98, no. 6, pp. 1858–1861, 2001.
[8]  C. Grant, K. Barmak, T. Alefantis, J. Yao, S. Jacobson, and B. Wigdahl, “Human T cell leukemia virus type I and neurologic disease: events in bone marrow, peripheral blood, and central nervous system during normal immune surveillance and neuroinflammation,” Journal of Cellular Physiology, vol. 190, no. 2, pp. 133–159, 2002.
[9]  T. J. Lehky, C. H. Fox, S. Koenig et al., “Detection of human T-lymphotropic virus type I (HTLV-I) tax RNA in the central nervous system of HTLV-I-associated myelopathy/tropical spastic paraparesis patients by in situ hybridization,” Annals of Neurology, vol. 37, no. 2, pp. 167–175, 1995.
[10]  K. Doi, X. Wu, Y. Taniguchi et al., “Preferential selection of human T-cell leukemia virus type I provirus integration sites in leukemic versus carrier states,” Blood, vol. 106, no. 3, pp. 1048–1053, 2005.
[11]  T. Uchiyama, “Human T cell leukemia virus type I (HTLV-I) and human diseases,” Annual Review of Immunology, vol. 15, pp. 15–37, 1997.
[12]  I. Leclercq, F. Mortreux, M. Cavrois et al., “Host sequences flanking the human T-cell leukemia virus type 1 provirus in vivo,” Journal of Virology, vol. 74, no. 5, pp. 2305–2312, 2000.
[13]  D. Derse, B. Crise, Y. Li et al., “Human T-cell leukemia virus type 1 integration target sites in the human genome: comparison with those of other retroviruses,” Journal of Virology, vol. 81, no. 12, pp. 6731–6741, 2007.
[14]  S. J. Marriott and O. J. Semmes, “Impact of HTLV-I Tax on cell cycle progression and the cellular DNA damage repair response,” Oncogene, vol. 24, no. 39, pp. 5986–5995, 2005.
[15]  C. H. Lecellier, P. Dunoyer, K. Arar et al., “A cellular microRNA mediates antiviral defense in human cells,” Science, vol. 308, no. 5721, pp. 557–560, 2005.
[16]  Y. Bennasser, S. Y. Le, M. L. Yeung, and K. T. Jeang, “HIV-1 encoded candidate micro-RNAs and their cellular targets,” Retrovirology, vol. 1, p. 43, 2004.
[17]  L. Houzet and K. T. Jeang, “MicroRNAs and human retroviruses,” Biochimica et Biophysica Acta, vol. 1809, no. 11-12, pp. 686–693, 2011.
[18]  M. Bellon, Y. Lepelletier, O. Hermine, and C. Nicot, “Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia,” Blood, vol. 113, no. 20, pp. 4914–4917, 2009.
[19]  K. Pichler, G. Schneider, and R. Grassmann, “MicroRNA miR-146a and further oncogenesis-related cellular microRNAs are dysregulated in HTLV-1-transformed T lymphocytes,” Retrovirology, vol. 5, article 100, 2008.
[20]  L. Y. Man, J. I. Yasunaga, Y. Bennasser et al., “Roles for MicroRNAs, miR-93 and miR-130b, and tumor protein 53-induced nuclear protein 1 tumor suppressor in cell growth dysregulation by human T-cell lymphotrophic virus 1,” Cancer Research, vol. 68, no. 21, pp. 8976–8985, 2008.
[21]  K. T. Jeang, “Human T cell leukemia virus type 1 (HTLV-1) and oncogene or oncomiR addiction?” Oncotarget, vol. 1, no. 6, pp. 453–456, 2010.
[22]  H. Cerutti and J. A. Casas-Mollano, “On the origin and functions of RNA-mediated silencing: from protists to man,” Current Genetics, vol. 50, no. 2, pp. 81–99, 2006.
[23]  D. J. Obbard, K. H. J. Gordon, A. H. Buck, and F. M. Jiggins, “The evolution of RNAi as a defence against viruses and transposable elements,” Philosophical Transactions of the Royal Society B, vol. 364, no. 1513, pp. 99–115, 2009.
[24]  K. V. Morris, “siRNA-mediated transcriptional gene silencing: the potential mechanism and a possible role in the histone code,” Cellular and Molecular Life Sciences, vol. 62, no. 24, pp. 3057–3066, 2005.
[25]  A. Verdel, S. Jia, S. Gerber et al., “RNAi-mediated targeting of heterochromatin by the RITS complex,” Science, vol. 303, no. 5658, pp. 672–676, 2004.
[26]  G. Pichler, J. Heinzinger, P. Klaritsch, H. Zotter, W. Müller, and B. Urlesberger, “Impact of smoking during pregnancy on peripheral tissue oxygenation in term neonates,” Neonatology, vol. 93, no. 2, pp. 132–137, 2008.
[27]  D. H. Kim, L. M. Villeneuve, K. V. Morris, and J. J. Rossi, “Argonaute-1 directs siRNA-mediated transcriptional gene silencing in human cells,” Nature Structural and Molecular Biology, vol. 13, no. 9, pp. 793–797, 2006.
[28]  D. H. Kim, P. S?trom, J. O. Snove Jr., and J. J. Rossi, “MicroRNA-directed transcriptional gene silencing in mammalian cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 42, pp. 16230–16235, 2008.
[29]  J. Han, Y. Lee, K. H. Yeom et al., “Molecular basis for the recognition of primary microRNAs by the Drosha-DGCR8 complex,” Cell, vol. 125, no. 5, pp. 887–901, 2006.
[30]  Z. Klase, P. Kale, R. Winograd et al., “HIV-1 TAR element is processed by Dicer to yield a viral micro-RNA involved in chromatin remodeling of the viral LTR,” BMC Molecular Biology, vol. 8, article 63, 2007.
[31]  Z. Klase, R. Winograd, J. Davis et al., “HIV-1 TAR miRNA protects against apoptosis by altering cellular gene expression,” Retrovirology, vol. 6, article 18, 2009.
[32]  M. L. Yeung, Y. Bennasser, K. Watashi, S. Y. Le, L. Houzet, and K. T. Jeang, “Pyrosequencing of small non-coding RNAs in HIV-1 infected cells: evidence for the processing of a viral-cellular double-stranded RNA hybrid,” Nucleic Acids Research, vol. 37, no. 19, pp. 6575–6586, 2009.
[33]  D. L. Ouellet, I. Plante, P. Landry et al., “Identification of functional microRNAs released through asymmetrical processing of HIV-1 TAR element,” Nucleic Acids Research, vol. 36, no. 7, pp. 2353–2365, 2008.
[34]  Z. Liu, B. Xiao, B. Tang et al., “Up-regulated microRNA-146a negatively modulate Helicobacter pylori-induced inflammatory response in human gastric epithelial cells,” Microbes and Infection, vol. 12, no. 11, pp. 854–863, 2010.
[35]  M. Burton, C. D. Upadhyaya, B. Maier, T. J. Hope, and O. J. Semmes, “Human T-cell leukemia virus type 1 tax shuttles between functionally discrete subcellular targets,” Journal of Virology, vol. 74, no. 5, pp. 2351–2364, 2000.
[36]  I. Azran, K. T. Jeang, and M. Aboud, “High levels of cytoplasmic HTLV-1 Tax mutant proteins retain a Tax-NF-κB-CBP ternary complex in the cytoplasm,” Oncogene, vol. 24, no. 28, pp. 4521–4530, 2005.
[37]  M. Abe, H. Suzuki, H. Nishitsuji, H. Shida, and H. Takaku, “Interaction of human T-cell lymphotropic virus type I Rex protein with Dicer suppresses RNAi silencing,” FEBS Letters, vol. 584, no. 20, pp. 4313–4318, 2010.
[38]  T. Igakura, J. C. Stinchcombe, P. K. C. Goon et al., “Spread of HTLV-I between lymphocytes by virus-induced polarization of the cytoskeleton,” Science, vol. 299, no. 5613, pp. 1713–1716, 2003.
[39]  M. Matsuoka and K. T. Jeang, “Human T-cell leukaemia virus type 1 (HTLV-1) infectivity and cellular transformation,” Nature Reviews Cancer, vol. 7, no. 4, pp. 270–280, 2007.
[40]  M. Nejmeddine, A. L. Barnard, Y. Tanaka, G. P. Taylor, and C. R. M. Bangham, “Human T-lymphotropic virus, type 1, tax protein triggers microtubule reorientation in the virological synapse,” Journal of Biological Chemistry, vol. 280, no. 33, pp. 29653–29660, 2005.
[41]  N. Manel, F. J. Kim, S. Kinet, N. Taylor, M. Sitbon, and J. L. Battini, “The ubiquitous glucose transporter GLUT-1 is a receptor for HTLV,” Cell, vol. 115, no. 4, pp. 449–459, 2003.
[42]  D. Ghez, Y. Lepelletier, K. S. Jones, C. Pique, and O. Hermine, “Current concepts regarding the HTLV-1 receptor complex,” Retrovirology, vol. 7, article 99, 2010.
[43]  K. T. Jeang, C. Z. Giam, F. Majone, and M. Aboud, “Life, death, and tax: role of HTLV-I oncoprotein in genetic instability and cellular transformation,” Journal of Biological Chemistry, vol. 279, no. 31, pp. 31991–31994, 2004.
[44]  P. W. P. Ng, H. Iha, Y. Iwanaga et al., “Genome-wide expression changes induced by HTLV-1 Tax: evidence for MLK-3 mixed lineage kinase involvement in Tax-mediated NF-κB activation,” Oncogene, vol. 20, no. 33, pp. 4484–4496, 2001.
[45]  C. Neuveut and K. T. Jeang, “HTLV-I Tax and cell cycle progression,” Progress in Cell Cycle Research, vol. 4, pp. 157–162, 2000.
[46]  M. L. Gatza, J. C. Watt, and S. J. Marriott, “Cellular transformation by the HTLV-I Tax protein, a jack-of-all-trades,” Oncogene, vol. 22, no. 33, pp. 5141–5149, 2003.
[47]  P. Beimling and K. Moelling, “Direct interaction of CREB protein with 21 bp Tax-response elements of HTLV-I LTR,” Oncogene, vol. 7, no. 2, pp. 257–262, 1992.
[48]  S. Paca-Uccaralertkun, L. J. Zhao, N. Adya et al., “In vitro selection of DNA elements highly responsive to the human T-cell lymphotropic virus type I transcriptional activator, Tax,” Molecular and Cellular Biology, vol. 14, no. 1, pp. 456–462, 1994.
[49]  B. A. Lenzmeier, H. A. Giebler, and J. K. Nyborg, “Human T-cell leukemia virus type 1 tax requires direct access to DNA for recruitment of CREB binding protein to the vital promoter,” Molecular and Cellular Biology, vol. 18, no. 2, pp. 721–731, 1998.
[50]  N. Adya and C. Z. Giam, “Distinct regions in human T-cell lymphotropic virus type I tax mediate interactions with activator protein CREB and basal transcription factors,” Journal of Virology, vol. 69, no. 3, pp. 1834–1841, 1995.
[51]  T. Suzuki, H. Hirai, J. Fujisawa, T. Fujita, and M. Yoshida, “A trans-activator tax of human T-cell leukemia virus type 1 binds to NF-κB p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-κB site and CArG box,” Oncogene, vol. 8, no. 9, pp. 2391–2397, 1993.
[52]  D. Y. Jin and K. T. Jeang, “HTLV-I Tax self-association in optimal trans-activation function,” Nucleic Acids Research, vol. 25, no. 2, pp. 379–387, 1997.
[53]  K. T. Jeang, I. Boros, J. Brady, M. Radonovich, and G. Khoury, “Characterization of cellular factors that interact with the human T-cell leukemia virus type I p40x-responsive 21-base-pair sequence,” Journal of Virology, vol. 62, no. 12, pp. 4499–4509, 1988.
[54]  R. Harrod, Y. L. Kuo, Y. Tang et al., “p300 and p300/cAMP-responsive element-binding protein associated factor interact with human T-cell lymphotropic virus type-1 Tax in a multi-histone acetyltransferase/activator-enhancer complex,” Journal of Biological Chemistry, vol. 275, no. 16, pp. 11852–11857, 2000.
[55]  R. Harrod, Y. Tang, C. Nicot et al., “An exposed KID-like domain in human T-cell lymphotropic virus type 1 tax is responsible for the recruitment of coactivators CBP/p300,” Molecular and Cellular Biology, vol. 18, no. 9, pp. 5052–5061, 1998.
[56]  F. Tie, N. Adya, W. C. Greene, and C. Z. Giam, “Interaction of the human T-lymphotropic virus type 1 Tax dimer with CREB and the viral 21-base-pair repeat,” Journal of Virology, vol. 70, no. 12, pp. 8368–8374, 1996.
[57]  J. M. Bogenberger and P. J. Laybourn, “Human T lymphotropic virus type I protein tax reduces histone levels,” Retrovirology, vol. 5, article 9, 2008.
[58]  J. Inoue, M. Seiki, T. Taniguchi, S. Tsuru, and M. Yoshida, “Induction of interleukin 2 receptor gene expression by p40x encoded by human T-cell leukemia virus type 1,” EMBO Journal, vol. 5, no. 11, pp. 2883–2888, 1986.
[59]  S. L. Cross, M. B. Feinberg, J. B. Wolf, N. J. Holbrook, F. Wong-Staal, and W. J. Leonard, “Regulation of the human interleukin-2 receptor α chain promoter: activation of a nonfunctional promoter by the transactivator gene of HTLV-I,” Cell, vol. 49, no. 1, pp. 47–56, 1987.
[60]  M. Siekevitz, M. B. Feinberg, and N. Holbrook, “Activation of interleukin 2 and interleukin 2 receptor (Tac) promoter expression by the trans-activator (tat) gene product of human T-cell leukemia virus, type I,” Proceedings of the National Academy of Sciences of the United States of America, vol. 84, no. 15, pp. 5389–5393, 1987.
[61]  K. Nagata, K. Ohtani, M. Nakamura, and K. Sugamura, “Activation of endogenous c-fos proto-oncogene expression by human T-cell leukemia virus type I-encoded p40(tax) protein in the human T-cell line, Jurkat,” Journal of Virology, vol. 63, no. 8, pp. 3220–3226, 1989.
[62]  S. Miyatake, M. Seiki, M. Yoshida, and K. I. Arai, “T-cell activation signals and human T-cell leukemia virus type I-encoded p40x protein activate the mouse granulocyte-macrophage colony-stimulating factor gene through a common DNA element,” Molecular and Cellular Biology, vol. 8, no. 12, pp. 5581–5587, 1988.
[63]  N. Azimi, K. Brown, R. N. Bamford, Y. Tagaya, U. Siebenlist, and T. A. Waldmann, “Human T cell lymphotropic virus type I Tax protein trans-activates interleukin 15 gene transcription through an NF-κB site,” Proceedings of the National Academy of Sciences of the United States of America, vol. 95, no. 5, pp. 2452–2457, 1998.
[64]  J. M. Mesnard and C. Devaux, “Multiple control levels of cell proliferation by human T-cell leukemia virus type 1 Tax protein,” Virology, vol. 257, no. 2, pp. 277–284, 1999.
[65]  S. C. Sun and D. W. Ballard, “Persistent activation of NF-κB by the Tax transforming protein of HTLV-1: hijacking cellular IκB kinases,” Oncogene, vol. 18, no. 49, pp. 6948–6958, 1999.
[66]  K. T. Jeang, R. Chiu, E. Santos, and S. J. Kim, “Induction of the HTLV-I LTR by Jun occurs through the Tax-responsive 21-bp elements,” Virology, vol. 181, no. 1, pp. 218–227, 1991.
[67]  M. Fujii, H. Tsuchiya, T. Chuhjo, T. Akizawa, and M. Seiki, “Interaction of HTLV-1 Tax1 with p67(SRF) causes the aberrant induction of cellular immediate early genes through CArG boxes,” Genes and Development, vol. 6, no. 11, pp. 2066–2076, 1992.
[68]  K. T. Jeang, “Functional activities of the human T-cell leukemia virus type I Tax oncoprotein: cellular signaling through NF-κB,” Cytokine and Growth Factor Reviews, vol. 12, no. 2-3, pp. 207–217, 2001.
[69]  Y. Kamada, T. Iwamasa, M. Miyazato, K. Sunagawa, and N. Kunishima, “Kaposi sarcoma in Okinawa,” Cancer, vol. 70, no. 4, pp. 861–868, 1992.
[70]  Y. L. Kuo and C. Z. Giam, “Activation of the anaphase promoting complex by HTLV-1 tax leads to senescence,” EMBO Journal, vol. 25, no. 8, pp. 1741–1752, 2006.
[71]  M. Matsuoka and K. T. Jeang, “Human T-cell leukemia virus type I at age 25: a progress report,” Cancer Research, vol. 65, no. 11, pp. 4467–4470, 2005.
[72]  J. Yao, C. Grant, E. Harhaj et al., “Regulation of human T-cell leukemia virus type 1 gene expression by Sp1 and Sp3 interaction with TRE-1 repeat III,” DNA and Cell Biology, vol. 25, no. 5, pp. 262–276, 2006.
[73]  S. E. Adunyah, T. M. Unlap, F. Wagner, and A. S. Kraft, “Regulation of c-jun expression and AP-1 enhancer activity by granulocyte-macrophage colony-stimulating factor,” Journal of Biological Chemistry, vol. 266, no. 9, pp. 5670–5675, 1991.
[74]  D. A. Liebermann and B. Hoffman, “Differentiation primary response genes and proto-oncogenes as positive and negative regulators of terminal hematopoietic cell differentiation,” Stem Cells, vol. 12, no. 4, pp. 352–369, 1994.
[75]  C. Grant, P. Jain, M. Nonnemacher et al., “AP-1-directed human T cell leukemia virus type 1 viral gene expression during monocytic differentiation,” Journal of Leukocyte Biology, vol. 80, no. 3, pp. 640–650, 2006.
[76]  C. Grant, M. Nonnemacher, P. Jain et al., “CCAAT/enhancer-binding proteins modulate human T cell leukemia virus type 1 long terminal repeat activation,” Virology, vol. 348, no. 2, pp. 354–369, 2006.
[77]  T. Ego, Y. Ariumi, and K. Shimotohno, “The interaction of HTLV-1 tax with HDAC1 negatively regulates the viral gene expression,” Oncogene, vol. 21, no. 47, pp. 7241–7246, 2002.
[78]  A. El Kharroubi, G. Piras, R. Zensen, and M. A. Martin, “Transcriptional activation of the integrated chromatin-associated human immunodeficiency virus type 1 promoter,” Molecular and Cellular Biology, vol. 18, no. 5, pp. 2535–2544, 1998.
[79]  M. Okada and K. T. Jeang, “Differential requirements for activation of integrated and transiently transfected human T-cell leukemia virus type 1 long terminal repeat,” Journal of Virology, vol. 76, no. 24, pp. 12564–12573, 2002.
[80]  S. Jiang, T. Inada, M. Tanaka, R. A. Furuta, K. Shingu, and J. I. Fujisawa, “Involvement of TORC2, a CREB co-activator, in the in vivo-specific transcriptional control of HTLV-1,” Retrovirology, vol. 6, article 73, 2009.
[81]  Y. T. Siu, K. T. Chin, K. L. Siu, E. Y. W. Choy, K. T. Jeang, and D. Y. Jin, “TORC1 and TORC2 coactivators are required for tax activation of the human T-cell leukemia virus type 1 long terminal repeats,” Journal of Virology, vol. 80, no. 14, pp. 7052–7059, 2006.
[82]  F. Bantignies, R. Rousset, C. Desbois, and P. Jalinot, “Genetic characterization of transactivation of the human T-cell leukemia virus type 1 promoter: binding of tax to tax-responsive element 1 is mediated by the cyclic AMP-responsive members of the CREB/ATF family of transcription factors,” Molecular and Cellular Biology, vol. 16, no. 5, pp. 2174–2182, 1996.
[83]  J. Bodor, W. Walker, E. Flemington, A. L. Spetz, and J. F. Habener, “Modulation of Tax and PKA-mediated expression of HTLV-1 promoter via cAMP response element binding and modulator proteins CREB and CREM,” FEBS Letters, vol. 377, no. 3, pp. 413–418, 1995.
[84]  F. Kashanchi, J. F. Duvall, R. P. S. Kwok, J. R. Lundblad, R. H. Goodman, and J. N. Brady, “The coactivator CBP stimulates human T-cell lymphotrophic virus type I tax transactivation in vitro,” Journal of Biological Chemistry, vol. 273, no. 51, pp. 34646–34652, 1998.
[85]  R. P. S. Kwok, M. E. Laurance, J. R. Lundblad et al., “Control of cAMP-regulated enhancers by the viral transactivator tax through CREB and the co-activator CBP,” Nature, vol. 380, no. 6575, pp. 642–646, 1996.
[86]  H. Jiang, H. Lu, R. L. Schiltz et al., “PCAF interacts with Tax and stimulates Tax transactivation in a histone acetyltransferase-independent manner,” Molecular and Cellular Biology, vol. 19, no. 12, pp. 8136–8145, 1999.
[87]  K. E. S. Scoggin, A. Ulloa, and J. K. Nyborg, “The oncoprotein Tax binds the SRC-1-interacting domain of CBP/p300 to mediate transcriptional activation,” Molecular and Cellular Biology, vol. 21, no. 16, pp. 5520–5530, 2001.
[88]  M. Benkirane, R. F. Chun, H. Xiao et al., “Activation of integrated provirus requires histone acetyltransferase: p300 and P/CAF are coactivators for HIV-1 Tat,” Journal of Biological Chemistry, vol. 273, no. 38, pp. 24898–24905, 1998.
[89]  P. Hollsberg and D. A. Hafler, “Seminars in medicine of the beth Israel hospital, Boston: pathogenesis of diseases induced by human lymphotropic virus type I infection,” New England Journal of Medicine, vol. 328, no. 16, pp. 1173–1182, 1993.
[90]  G. Marzio, K. Verhoef, M. Vink, and B. Berkhout, “In vitro evolution of a highly replicating, doxycycline-dependent HIV for applications in vaccine studies,” Proceedings of the National Academy of Sciences of the United States of America, vol. 98, no. 11, pp. 6342–6347, 2001.
[91]  C. Rossi, D. Gibellini, G. Barbanti-Brodano et al., “Transiently transfected and stably integrated HIV-1 LTR responds differentially to the silencing activity of the Kruppel-associated box (KRAB) transcriptional repressor domain,” Journal of Medical Virology, vol. 58, no. 3, pp. 264–272, 1999.
[92]  D. Moazed, “Small RNAs in transcriptional gene silencing and genome defence,” Nature, vol. 457, no. 7228, pp. 413–420, 2009.
[93]  W. Filipowicz, L. Jaskiewicz, F. A. Kolb, and R. S. Pillai, “Post-transcriptional gene silencing by siRNAs and miRNAs,” Current Opinion in Structural Biology, vol. 15, no. 3, pp. 331–341, 2005.
[94]  J. C. Van Wolfswinkel and R. F. Ketting, “The role of small non-coding RNAs in genome stability and chromatin organization,” Journal of Cell Science, vol. 123, no. 11, pp. 1825–1839, 2010.
[95]  D. C. Baulcombe, “Molecular biology. Amplified silencing,” Science, vol. 315, no. 5809, pp. 199–200, 2007.
[96]  R. L. Skalsky and B. R. Cullen, “Viruses, microRNAs, and host interactions,” Annual Review of Microbiology, vol. 64, pp. 123–141, 2010.
[97]  T. P. Chendrimada, R. I. Gregory, E. Kumaraswamy et al., “TRBP recruits the Dicer complex to Ago2 for microRNA processing and gene silencing,” Nature, vol. 436, no. 7051, pp. 740–744, 2005.
[98]  G. Hutvagner, J. McLachlan, A. E. Pasquinelli, E. Balint, T. Tuschl, and P. D. Zamore, “A cellular function for the RNA-interference enzyme dicer in the maturation of the let-7 small temporal RNA,” Science, vol. 293, no. 5531, pp. 834–838, 2001.
[99]  J. Liu, M. A. Carmell, F. V. Rivas et al., “Argonaute2 is the catalytic engine of mammalian RNAi,” Science, vol. 305, no. 5689, pp. 1437–1441, 2004.
[100]  Y. Lorch, B. Maier-Davis, and R. D. Kornberg, “Chromatin remodeling by nucleosome disassembly in vitro,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 9, pp. 3090–3093, 2006.
[101]  A. Villagra, F. Cruzat, L. Carvallo et al., “Chromatin remodeling and transcriptional activity of the bone-specific osteocalcin gene require CCAAT/enhancer-binding protein β-dependent recruitment of SWI/SNF activity,” Journal of Biological Chemistry, vol. 281, no. 32, pp. 22695–22706, 2006.
[102]  J. F. Partridge, K. S. C. Scott, A. J. Bannister, T. Kouzarides, and R. C. Allshire, “cis-acting DNA from fission yeast centromeres mediates histone H3 methylation and recruitment of silencing factors and cohesin to an ectopic site,” Current Biology, vol. 12, no. 19, pp. 1652–1660, 2002.
[103]  K. Ekwall, “The RITS complex—a direct link between small RNA and heterochromatin,” Molecular Cell, vol. 13, no. 3, pp. 304–305, 2004.
[104]  V. Schramke and R. Allshire, “Hairpin RNAs and retrotransposon LTRs effect RNAi and chromatin-based gene silencing,” Science, vol. 301, no. 5636, pp. 1069–1074, 2003.
[105]  S. Pfeffer, M. Zavolan, F. A. Gr?sser et al., “Identification of virus-encoded microRNAs,” Science, vol. 304, no. 5671, pp. 734–736, 2004.
[106]  S. Tang, A. S. Bertke, A. Patel, K. Wang, J. I. Cohen, and P. R. Krause, “An acutely and latently expressed herpes simplex virus 2 viral microRNA inhibits expression of ICP34.5, a viral neurovirulence factor,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 31, pp. 10931–10936, 2008.
[107]  B. R. Cullen, “Viral and cellular messenger RNA targets of viral microRNAs,” Nature, vol. 457, no. 7228, pp. 421–425, 2009.
[108]  S. Omoto and Y. R. Fujii, “Regulation of human immunodeficiency virus 1 transcription by nef microRNA,” Journal of General Virology, vol. 86, no. 3, pp. 751–755, 2005.
[109]  S. C. Li, C. K. Shiau, and W. C. Lin, “Vir-Mir db: prediction of viral microRNA candidate hairpins,” Nucleic Acids Research, vol. 36, supplement 1, pp. D184–D189, 2008.
[110]  K. Ruggero, A. Corradin, P. Zanovello et al., “Role of microRNAs in HTLV-1 infection and transformation,” Molecular Aspects of Medicine, vol. 31, no. 5, pp. 367–382, 2010.
[111]  V. Scaria and V. Jadhav, “microRNAs in viral oncogenesis,” Retrovirology, vol. 4, article 82, 2007.
[112]  W. Tam, “Identification and characterization of human BIC, a gene on chromosome 21 that encodes a noncoding RNA,” Gene, vol. 274, no. 1-2, pp. 157–167, 2001.
[113]  A. M. Lum, B. B. Wang, L. Li, N. Channa, G. Bartha, and M. Wabl, “Retroviral activation of the mir-106a microRNA cistron in T lymphoma,” Retrovirology, vol. 4, article 5, 2007.
[114]  G. B. Beck-Engeser, A. M. Lum, K. Huppi, N. J. Caplen, B. B. Wang, and M. Wabl, “Pvt1-encoded microRNAs in oncogenesis,” Retrovirology, vol. 5, article 4, 2008.
[115]  D. M. Davis, T. Igakura, F. E. McCann et al., “The protean immune cell synapse: a supramolecular structure with many functions,” Seminars in Immunology, vol. 15, no. 6, pp. 317–324, 2003.
[116]  M. O. Delgadillo, P. Sáenz, B. Salvador, J. A. García, and C. Simón-Mateo, “Human influenza virus NS1 protein enhances viral pathogenicity and acts as an RNA silencing suppressor in plants,” Journal of General Virology, vol. 85, no. 4, pp. 993–999, 2004.
[117]  S. Bivalkar-Mehla, J. Vakharia, R. Mehla et al., “Viral RNA silencing suppressors (RSS): novel strategy of viruses to ablate the host RNA interference (RNAi) defense system,” Virus Research, vol. 155, no. 1, pp. 1–9, 2011.
[118]  G. L. Sen and H. M. Blau, “Argonaute 2/RISC resides in sites of mammalian mRNA decay known as cytoplasmic bodies,” Nature Cell Biology, vol. 7, no. 6, pp. 633–636, 2005.
[119]  S. Lu and B. R. Cullen, “Adenovirus VA1 noncoding RNA can inhibit small interfering RNA and microRNA biogenesis,” Journal of Virology, vol. 78, no. 23, pp. 12868–12876, 2004.
[120]  N. Mori, T. Matsuda, M. Tadano et al., “Apoptosis induced by the histone deacetylase inhibitor FR901228 in human T-cell leukemia virus type 1-infected T-cell lines and primary adult T-cell leukemia cells,” Journal of Virology, vol. 78, no. 9, pp. 4582–4590, 2004.
[121]  V. R. Sanghvi and L. F. Steel, “A re-examination of global suppression of RNA interference by HIV-1,” PLoS One, vol. 6, no. 2, Article ID e17246, 2011.
[122]  M. Lerner, J. Lundgren, S. Akhoondi et al., “MiRNA-27a controls FBW7/hCDC4-dependent cyclin E degradation and cell cycle progression,” Cell Cycle, vol. 10, no. 13, pp. 2172–2183, 2011.
[123]  G. Song, G. Ouyang, and S. Bao, “The activation of Akt/PKB signaling pathway and cell survival,” Journal of Cellular and Molecular Medicine, vol. 9, no. 1, pp. 59–71, 2005.
[124]  H. Iha, K. V. Kibler, V. R. K. Yedavalli et al., “Segregation of NF-κB activation through NEMO/IKKγ by Tax and TNFα: implications for stimulus-specific interruption of oncogenic signaling,” Oncogene, vol. 22, no. 55, pp. 8912–8923, 2003.
[125]  F. J. Lemoine and S. J. Marriott, “Accelerated G1 phase progression induced by the human T cell leukemia virus type I (HTLV-I) tax oncoprotein,” Journal of Biological Chemistry, vol. 276, no. 34, pp. 31851–31857, 2001.
[126]  Y. Huang, K. Ohtani, R. Iwanaga, Y. Matsumura, and M. Nakamura, “Direct trans-activation of the human cyclin D2 gene by the oncogene product Tax of human T-cell leukemia virus type I,” Oncogene, vol. 20, no. 9, pp. 1094–1102, 2001.
[127]  K. Haller, Y. Wu, E. Derow, I. Schmitt, K. T. Jeang, and R. Grassmann, “Physical interaction of human T-cell leukemia virus type 1 Tax with cyclin-dependent kinase 4 stimulates the phosphorylation of retinoblastoma protein,” Molecular and Cellular Biology, vol. 22, no. 10, pp. 3327–3338, 2002.
[128]  R. Iwanaga, K. Ohtani, T. Hayashi, and M. Nakamura, “Molecular mechanism of cell cycle progression induced by the oncogene product Tax of human T-cell leukemia virus type I,” Oncogene, vol. 20, no. 17, pp. 2055–2067, 2001.
[129]  T. Akagi, H. Ono, and K. Shimotohno, “Expression of cell-cycle regulatory genes in HTLV-I infected T-cell lines: possible involvement of Tax1 in the altered expression of cyclin D2, p18Ink4 and p21Waf1/Cip1/Sdi1,” Oncogene, vol. 12, no. 8, pp. 1645–1652, 1996.
[130]  K. V. Kibler and K. T. Jeang, “CREB/ATF-dependent repression of cyclin A by human T-cell leukemia virus type 1 tax protein,” Journal of Virology, vol. 75, no. 5, pp. 2161–2173, 2001.
[131]  D. H. Walker and J. L. Maller, “Role for cyclin A in the dependence of mitosis on completion of DNA replication,” Nature, vol. 354, no. 6351, pp. 314–317, 1991.
[132]  I. Lemasson, S. Thébault, C. Sardet, C. Devaux, and J. M. Mesnard, “Activation of E2F-mediated transcription by human T-cell leukemia virus type I tax protein in a p16(INK4A)-negative T-cell line,” Journal of Biological Chemistry, vol. 273, no. 36, pp. 23598–23604, 1998.
[133]  K. Ohtani, R. Iwanaga, M. Arai, Y. Huang, Y. Matsumura, and M. Nakamura, “Cell type-specific E2F activation and cell cycle progression induced by the oncogene product tax of human T-cell leukemia virus type I,” Journal of Biological Chemistry, vol. 275, no. 15, pp. 11154–11163, 2000.
[134]  K. Kehn, C. De La Fuente, K. Strouss et al., “The HTLV-I Tax oncoprotein targets the retinoblastoma protein for proteasomal degradation,” Oncogene, vol. 24, no. 4, pp. 525–540, 2005.
[135]  J. Whang-Peng, P. A. Bunn, and T. Knutsen, “Cytogenetic studies in human T-cell lymphoma virus (HTLV)-positive leukemia-lymphoma in the United States,” Journal of the National Cancer Institute, vol. 74, no. 2, pp. 357–369, 1985.
[136]  L. Chieco-Bianchi, D. Saggioro, A. Del Mistro, A. Montaldo, F. Majone, and A. G. Levis, “Chromosome damage induced in cord blood T-lymphocytes infected in vitro by HTLV-I,” Leukemia, vol. 2, supplement 12, pp. 223S–232S, 1988.
[137]  T. Itoyama, N. Sadamori, S. Tokunaga et al., “Cytogenetic studies of human T-cell leukemia virus type I carriers: a family study,” Cancer Genetics and Cytogenetics, vol. 49, no. 2, pp. 157–163, 1990.
[138]  A. Tanaka, C. Takahashi, S. Yamaoka, T. Nosaka, M. Maki, and M. Hatanaka, “Oncogenic transformation by the tax gene of human T-cell leukemia virus type I in vitro,” Proceedings of the National Academy of Sciences of the United States of America, vol. 87, no. 3, pp. 1071–1075, 1990.
[139]  K. Maruyama, T. Fukushima, K. Kawamura, and S. Mochizuki, “Chromosome and gene rearrangements in immortalized human lymphocytes infected with human T-lymphotropic virus type I,” Cancer Research, vol. 50, supplement 17, pp. 5697S–5702S, 1990.
[140]  T. Fujimoto, T. Hata, T. Itoyama et al., “High rate of chromosomal abnormalities in HTLV-I-infected T-cell colonies derived from prodromal phase of adult T-cell leukemia: a study of IL-2-stimulated colony formation in methylcellulose,” Cancer Genetics and Cytogenetics, vol. 109, no. 1, pp. 1–13, 1999.
[141]  F. Majone and K. T. Jeang, “Clastogenic effect of the human T-cell leukemia virus type I tax oncoprotein correlates with unstabilized DNA breaks,” Journal of Biological Chemistry, vol. 275, no. 42, pp. 32906–32910, 2000.
[142]  H. Miyake, T. Suzuki, H. Hirai, and M. Yoshida, “Trans-activator tax of human T-cell leukemia virus type 1 enhances mutation frequency of the cellular genome,” Virology, vol. 253, no. 2, pp. 155–161, 1999.
[143]  T. Okamoto, Y. Ohno, S. Tsugane et al., “Multi-step carcinogenesis model for adult T-cell leukemia,” Japanese Journal of Cancer Research, vol. 80, no. 3, pp. 191–195, 1989.
[144]  A. Sakashita, T. Hattori, C. W. Miller et al., “Mutations of the p53 gene in adult T-cell leukemia,” Blood, vol. 79, no. 2, pp. 477–480, 1992.
[145]  K. Yamato, T. Oka, M. Hiroi et al., “Aberrant expression of the p53 tumor suppressor gene in adult T-cell leukemia and HTLV-I-infected cells,” Japanese Journal of Cancer Research, vol. 84, no. 1, pp. 4–8, 1993.
[146]  Y. Hatta, K. Spirin, T. Tasaka et al., “Analysis of p18INK4C in adult T-cell leukaemia and non-Hodgkin's lymphoma,” British Journal of Haematology, vol. 99, no. 3, pp. 665–667, 1997.
[147]  T. Suzuki, T. Narita, M. Uchida-Toita, and M. Yoshida, “Down-regulation of the INK4 family of cyclin-dependent kinase inhibitors by tax protein of HTLV-1 through two distinct mechanisms,” Virology, vol. 259, no. 2, pp. 384–391, 1999.
[148]  Y. Hatta and H. P. Koeffler, “Role of tumor suppressor genes in the development of adult T cell leukemia/lymphoma (ATLL),” Leukemia, vol. 16, no. 6, pp. 1069–1085, 2002.
[149]  N. Takenouchi, K. S. Jones, I. Lisinski et al., “GLUT1 is not the primary binding receptor but is associated with cell-to-cell transmission of human T-cell leukemia virus type 1,” Journal of Virology, vol. 81, no. 3, pp. 1506–1510, 2007.
[150]  H. Lu, C. A. Pise-Masison, R. Linton et al., “Tax relieves transcriptional repression by promoting histone deacetylase 1 release from the human T-cell leukemia virus type 1 long terminal repeat,” Journal of Virology, vol. 78, no. 13, pp. 6735–6743, 2004.
[151]  K. Wu, M. E. Bottazzi, C. De La Fuente et al., “Protein profile of Tax-associated complexes,” Journal of Biological Chemistry, vol. 279, no. 1, pp. 495–508, 2004.
[152]  N. D. Collins, G. C. Newbound, B. Albrecht, J. L. Beard, L. Ratner, and M. D. Lairmore, “Selective ablation of human T-cell lymphotropic virus type 1 p12I reduces viral infectivity in vivo,” Blood, vol. 91, no. 12, pp. 4701–4707, 1998.
[153]  L. R. Silverman, A. J. Phipps, A. Montgomery, L. Ratner, and M. D. Lairmore, “Human T-cell lymphotropic virus type 1 open reading frame II-encoded p30II is required for in vivo replication: evidence of in vivo reversion,” Journal of Virology, vol. 78, no. 8, pp. 3837–3845, 2004.
[154]  I. Younis, B. Yamamoto, A. Phipps, and P. L. Green, “Human T-cell leukemia virus type 1 expressing nonoverlapping Tax and Rex genes replicates and immortalizes primary human T lymphocytes but fails to replicate and persist in vivo,” Journal of Virology, vol. 79, no. 23, pp. 14473–14481, 2005.
[155]  H. Hiraragi, B. Michael, A. Nair, M. Silic-Benussi, V. Ciminale, and M. Lairmore, “Human T-lymphotropic virus type 1 mitochondrion-localizing protein p13 II sensitizes Jurkat T cells to Ras-mediated apoptosis,” Journal of Virology, vol. 79, no. 15, pp. 9449–9457, 2005.
[156]  J. D. Rosenblatt, A. J. Cann, D. J. Slamon et al., “HTLV-II transactivation is regulated by the overlapping tax/rex nonstructural genes,” Science, vol. 240, no. 4854, pp. 916–919, 1988.
[157]  J. Ye, L. Xie, and P. L. Green, “Tax and overlapping rex sequences do not confer the distinct transformation tropisms of human T-cell leukemia virus types 1 and 2,” Journal of Virology, vol. 77, no. 14, pp. 7728–7735, 2003.
[158]  C. Nicot, M. Dundr, J. M. Johnson et al., “HTLV-1-encoded p30II is a post-transcriptional negative regulator of viral replication,” Nature Medicine, vol. 10, no. 2, pp. 197–201, 2004.
[159]  W. Zhang, J. W. Nisbet, J. T. Bartoe, W. Ding, and M. D. Lairmore, “Human T-lymphotropic virus type 1 p30II functions as a transcription factor and differentially modulates CREB-responsive promoters,” Journal of Virology, vol. 74, no. 23, pp. 11270–11277, 2000.

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