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1

Lin, Jennifer, and Bryan R. Cullen. "Analysis of the Interaction of Primate Retroviruses with the Human RNA Interference Machinery." Journal of Virology 81, no. 22 (2007): 12218–26. http://dx.doi.org/10.1128/jvi.01390-07.

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ABSTRACT The question of whether retroviruses, including human immunodeficiency virus type 1 (HIV-1), interact with the cellular RNA interference machinery has been controversial. Here, we present data showing that neither HIV-1 nor human T-cell leukemia virus type 1 (HTLV-1) expresses significant levels of either small interfering RNAs or microRNAs in persistently infected T cells. We also demonstrate that the retroviral nuclear transcription factors HIV-1 Tat and HTLV-1 Tax, as well as the Tas transactivator encoded by primate foamy virus, fail to inhibit RNA interference in human cells. Mor
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2

Cleveland, Susan M., and Utpal P. Dave. "Insertional Activation of GLI2 in Adult T-Cell Leukemia/Lymphoma." Blood 110, no. 11 (2007): 4149. http://dx.doi.org/10.1182/blood.v110.11.4149.4149.

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Abstract Retroviruses induce cancer by integrating into the cellular genome and activating oncogenes or inactivating tumor suppressor genes. Human T-cell Leukemia Virus type 1 (HTLV-1), a complex retrovirus, induces Adult T-cell Leukemia/Lymphoma (ATLL) after a latency of over 30 years and in only 5% of carriers. The long latency and incomplete penetrance is similar to how slow transforming retroviruses induce cancer in mice and imply multiple oncogenic “hits” need to accumulate for clinically apparent disease. Insertional mutagenesis may be one mechanism by which ATLL develops. We used splink
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3

Lemasson, Isabelle, Nicholas J. Polakowski, Paul J. Laybourn, and Jennifer K. Nyborg. "Transcription Regulatory Complexes Bind the Human T-Cell Leukemia Virus 5′ and 3′ Long Terminal Repeats To Control Gene Expression." Molecular and Cellular Biology 24, no. 14 (2004): 6117–26. http://dx.doi.org/10.1128/mcb.24.14.6117-6126.2004.

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ABSTRACT The human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that integrates randomly into the T-cell genome. Two long terminal repeats (LTRs) flank the integrated provirus. The upstream and downstream LTRs carry identical promoter sequences. Studies with other retroviruses suggest that the downstream promoter is silent and that RNA polymerases initiating at the upstream promoter proceed through the 3′ LTR. In this study, we used the chromatin immunoprecipitation assay to compare the binding of transcription regulatory proteins at both the upstream and downstream promoters in HTLV-
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4

Ghosh, SK, JT Abrams, H. Terunuma, EC Vonderheid, and E. DeFreitas. "Human T-cell leukemia virus type I tax/rex DNA and RNA in cutaneous T- cell lymphoma." Blood 84, no. 8 (1994): 2663–71. http://dx.doi.org/10.1182/blood.v84.8.2663.2663.

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Abstract Peripheral blood mononuclear cells (PBMCs) and T-cell lines from patients with Sezary syndrome (SS) and skin lesions from patients with mycosis fungoides (MF) were examined by polymerase chain reaction (PCR) for DNA sequences homologous to the human retroviruses human T- lymphotropic virus (HTLV)-I and -II. Results obtained using primers and probes from the tax/rex region of HTLV-I indicate that 72% (18/25) of SS patients PBMCs, 80% (20/25) of T-cell lines established from SS- PBMC, and 30% (3/10) of skin lesions from MF patients were positive for HTLV-I tax/rex region DNA. Sequence a
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5

Ghosh, SK, JT Abrams, H. Terunuma, EC Vonderheid, and E. DeFreitas. "Human T-cell leukemia virus type I tax/rex DNA and RNA in cutaneous T- cell lymphoma." Blood 84, no. 8 (1994): 2663–71. http://dx.doi.org/10.1182/blood.v84.8.2663.bloodjournal8482663.

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Peripheral blood mononuclear cells (PBMCs) and T-cell lines from patients with Sezary syndrome (SS) and skin lesions from patients with mycosis fungoides (MF) were examined by polymerase chain reaction (PCR) for DNA sequences homologous to the human retroviruses human T- lymphotropic virus (HTLV)-I and -II. Results obtained using primers and probes from the tax/rex region of HTLV-I indicate that 72% (18/25) of SS patients PBMCs, 80% (20/25) of T-cell lines established from SS- PBMC, and 30% (3/10) of skin lesions from MF patients were positive for HTLV-I tax/rex region DNA. Sequence analysis o
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6

Younis, Ihab, Lyne Khair, Miroslav Dundr, Michael D. Lairmore, Genoveffa Franchini, and Patrick L. Green. "Repression of Human T-Cell Leukemia Virus Type 1 and Type 2 Replication by a Viral mRNA-Encoded Posttranscriptional Regulator." Journal of Virology 78, no. 20 (2004): 11077–83. http://dx.doi.org/10.1128/jvi.78.20.11077-11083.2004.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are complex retroviruses that persist in the host, eventually causing leukemia and neurological disease in a small percentage of infected individuals. In addition to structural and enzymatic proteins, HTLV encodes regulatory (Tax and Rex) and accessory (open reading frame I and II) proteins. The viral Tax and Rex proteins positively regulate virus production. Tax activates viral and cellular transcription to promote T-cell growth and, ultimately, malignant transformation. Rex acts posttranscriptionally to facilitate cytoplasmic ex
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7

Endo, Keiichi, Akira Hirata, Kousuke Iwai, et al. "Human T-Cell Leukemia Virus Type 2 (HTLV-2) Tax Protein Transforms a Rat Fibroblast Cell Line but Less Efficiently than HTLV-1 Tax." Journal of Virology 76, no. 6 (2002): 2648–53. http://dx.doi.org/10.1128/jvi.76.6.2648-2653.2002.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are retroviruses with similar biological properties. Whereas HTLV-1 is the causative agent of an aggressive T-cell leukemia, HTLV-2 has been associated with only a few cases of lymphoproliferative disorders. Tax1 and Tax2 are the transcriptional activators of HTLV-1 and HTLV-2, respectively. Here we show that Tax2 transformed a Rat-1 fibroblast cell line to form colonies in soft agar, but the size and number of the colonies were lower than those of Tax1. Use of a chimeric Tax protein showed that the C-terminal amino acids 300 to 3
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8

Kucerova, Lucia, Veronika Altanerova, Cestmir Altaner, and Kathleen Boris-Lawrie. "Bovine Leukemia Virus Structural Gene Vectors Are Immunogenic and Lack Pathogenicity in a Rabbit Model." Journal of Virology 73, no. 10 (1999): 8160–66. http://dx.doi.org/10.1128/jvi.73.10.8160-8166.1999.

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ABSTRACT Infection with a replication-competent bovine leukemia virus structural gene vector (BLV SGV) is an innovative vaccination approach to prevent disease by complex retroviruses. Previously we developed BLV SGV that constitutively expresses BLV gag, pol, and env and related cis-acting sequences but lacks tax, rex, RIII, andGIV and most of the BLV long terminal repeat sequences, including the cis-acting Tax and Rex response elements. The novel SGV virus is replication competent and replicates a selectable vector to a titer similar to that of the parental BLV in cell culture. The overall g
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9

Arnold, Joshua, Brenda Yamamoto, Min Li, et al. "Enhancement of infectivity and persistence in vivo by HBZ, a natural antisense coded protein of HTLV-1." Blood 107, no. 10 (2006): 3976–82. http://dx.doi.org/10.1182/blood-2005-11-4551.

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Natural antisense viral transcripts have been recognized in retroviruses, including human T-cell leukemia virus type 1 (HTLV-1), HIV-1, and feline immunodeficiency virus (FIV), and have been postulated to encode proteins important for the infection cycle and/or pathogenesis of the virus. The antisense strand of the HTLV-1 genome encodes HBZ, a novel nuclear basic region leucine zipper (b-ZIP) protein that in overexpression assays down-regulates Tax oncoprotein-induced viral transcription. Herein, we investigated the contribution of HBZ to HTLV-1–mediated immortalization of primary T lymphocyte
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10

Goldberg, Tony L., David M. Sintasath, Colin A. Chapman, et al. "Coinfection of Ugandan Red Colobus (Procolobus [Piliocolobus] rufomitratus tephrosceles) with Novel, Divergent Delta-, Lenti-, and Spumaretroviruses." Journal of Virology 83, no. 21 (2009): 11318–29. http://dx.doi.org/10.1128/jvi.02616-08.

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ABSTRACT Nonhuman primates host a plethora of potentially zoonotic microbes, with simian retroviruses receiving heightened attention due to their roles in the origins of human immunodeficiency viruses type 1 (HIV-1) and HIV-2. However, incomplete taxonomic and geographic sampling of potential hosts, especially the African colobines, has left the full range of primate retrovirus diversity unexplored. Blood samples collected from 31 wild-living red colobus monkeys (Procolobus [Piliocolobus] rufomitratus tephrosceles) from Kibale National Park, Uganda, were tested for antibodies to simian immunod
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11

Easley, Rebecca, Lawrence Carpio, Irene Guendel, et al. "Human T-Lymphotropic Virus Type 1 Transcription and Chromatin-Remodeling Complexes." Journal of Virology 84, no. 9 (2010): 4755–68. http://dx.doi.org/10.1128/jvi.00851-09.

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ABSTRACT Human T-lymphotropic virus type 1 (HTLV-1) encodes the viral protein Tax, which is believed to act as a viral transactivator through its interactions with a variety of transcription factors, including CREB and NF-κB. As is the case for all retroviruses, the provirus is inserted into the host DNA, where nucleosomes are deposited to ensure efficient packaging. Nucleosomes act as roadblocks in transcription, making it difficult for RNA polymerase II (Pol II) to proceed toward the 3′ end of the genome. Because of this, a variety of chromatin remodelers can act to modify nucleosomes, allow
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12

Ye, Jianxin, Li Xie, and Patrick 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 77, no. 14 (2003): 7728–35. http://dx.doi.org/10.1128/jvi.77.14.7728-7735.2003.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are distinct oncogenic retroviruses that infect several cell types but display their biological and pathogenic activity only in T cells. Previous studies have indicated that in vivo HTLV-1 has a preferential tropism for CD4+ T cells, whereas HTLV-2 in vivo tropism is less clear but appears to favor CD8+ T cells. Both CD4+ and CD8+ T cells are susceptible to HTLV-1 and HTLV-2 infection in vitro, and HTLV-1 has a preferential immortalization and transformation tropism of CD4+ T cells, whereas HTLV-2 immortalizes and transforms prima
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13

Yin, Han, Priya Kannian, Nathan Dissinger, Robyn Haines, Stefan Niewiesk, and Patrick L. Green. "Human T-Cell Leukemia Virus Type 2 Antisense Viral Protein 2 Is Dispensable forIn VitroImmortalization but Functions To Repress Early Virus ReplicationIn Vivo." Journal of Virology 86, no. 16 (2012): 8412–21. http://dx.doi.org/10.1128/jvi.00717-12.

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Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are closely related but pathogenically distinct human retroviruses. The antisense strand of the HTLV-1 genome encodes HTLV-1 basic leucine zipper (b-ZIP) protein (HBZ), a protein that inhibits Tax-mediated viral transcription, enhances T-cell proliferation, and promotes viral persistence. Recently, an HTLV-2 antisense viral protein (APH-2) was identified. Despite its lack of a typical b-ZIP domain, APH-2, like HBZ, interacts with cyclic AMP response element binding protein (CREB) and downregulates Tax-mediated viral transcription. Here, we
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14

Panfil, Amanda R., Nathan J. Dissinger, Cory M. Howard, et al. "Functional Comparison of HBZ and the Related APH-2 Protein Provides Insight into Human T-Cell Leukemia Virus Type 1 Pathogenesis." Journal of Virology 90, no. 7 (2016): 3760–72. http://dx.doi.org/10.1128/jvi.03113-15.

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ABSTRACTHuman T-cell leukemia virus type 1 (HTLV-1) and type 2 (HTLV-2) are highly related retroviruses that transform T cellsin vitrobut have distinct pathological outcomesin vivo. HTLV-1 encodes a protein from the antisense strand of its proviral genome, the HTLV-1 basic leucine zipper factor (HBZ), which inhibits Tax-1-mediated viral transcription and promotes cell proliferation, a high proviral load, and persistencein vivo. In adult T-cell leukemia/lymphoma (ATL) cell lines and patient T cells,hbzis often the only viral gene expressed. The antisense strand of the HTLV-2 proviral genome als
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15

Albrecht, Björn, and Michael D. Lairmore. "Critical Role of Human T-Lymphotropic Virus Type 1 Accessory Proteins in Viral Replication and Pathogenesis." Microbiology and Molecular Biology Reviews 66, no. 3 (2002): 396–406. http://dx.doi.org/10.1128/mmbr.66.3.396-406.2002.

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SUMMARY Human T-cell lymphotropic virus type 1 (HTLV-1) infection is associated with a diverse range of lymphoproliferative and neurodegenerative diseases, yet pathogenic mechanisms induced by the virus remain obscure. This complex retrovirus contains typical structural and enzymatic genes but also unique regulatory and accessory genes in four open reading frames (ORFs) of the pX region of the viral genome (pX ORFs I to IV). The regulatory proteins encoded by pX ORFs III and IV, Tax and Rex, respectively, have been extensively characterized. In contrast the contribution of the four accessory p
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16

Xiao, Jianqiao, and Gertrude C. Buehring. "In Vivo Protein Binding and Functional Analysis ofcis-Acting Elements in the U3 Region of the Bovine Leukemia Virus Long Terminal Repeat." Journal of Virology 72, no. 7 (1998): 5994–6003. http://dx.doi.org/10.1128/jvi.72.7.5994-6003.1998.

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ABSTRACT Bovine leukemia virus (BLV) is a member of the human T-cell leukemia virus (HTLV)/BLV group of retroviruses. These viruses regulate their own transcription by producing Tax, a protein which activates the virus promoter region, the long terminal repeat (LTR). To explore the molecular mechanisms involved in the transactivation, we identified protein binding elements by in vivo footprinting and analyzed their function by site- directed mutagenesis. We used in vivo dimethyl sulfate footprinting by ligation-mediated PCR to detect constitutive in vivo protein-DNA interactions in a BLV-produ
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17

Halbrook, Megan, Adva Gadoth, Anupama Shankar, et al. "Human T-cell lymphotropic virus type 1 transmission dynamics in rural villages in the Democratic Republic of the Congo with high nonhuman primate exposure." PLOS Neglected Tropical Diseases 15, no. 1 (2021): e0008923. http://dx.doi.org/10.1371/journal.pntd.0008923.

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The Democratic Republic of the Congo (DRC) has a history of nonhuman primate (NHP) consumption and exposure to simian retroviruses yet little is known about the extent of zoonotic simian retroviral infections in DRC. We examined the prevalence of human T-lymphotropic viruses (HTLV), a retrovirus group of simian origin, in a large population of persons with frequent NHP exposures and a history of simian foamy virus infection. We screened plasma from 3,051 persons living in rural villages in central DRC using HTLV EIA and western blot (WB). PCR amplification of HTLV tax and LTR sequences from bu
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18

Palker, T. J. "Human T-cell Lymphotropic Viruses: Review and Prospects for Antiviral Therapy." Antiviral Chemistry and Chemotherapy 3, no. 3 (1992): 127–39. http://dx.doi.org/10.1177/095632029200300301.

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The human T-cell lymphotropic viruses types I and II (HTLV-I, II) pose challenges to researchers and clinicians who seek to unveil mechanisms of viral transformation and pathogenesis. HTLV-I infection in humans is associated with a wide array of primary and secondary diseases ranging from mild immunosuppression to adult T-cell leukaemia/lymphoma and HTLV-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a neurological degenerative syndrome. As retroviruses, HTLV-I and II share similar replicative cycles with human immunodeficiency virus (HIV), the causative agent of acquired immuno
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19

Paca, Robert E., Robert A. Ogert, Catherine S. Hibbert, Elisa Izaurralde, and Karen L. Beemon. "Rous Sarcoma Virus DR Posttranscriptional Elements Use a Novel RNA Export Pathway." Journal of Virology 74, no. 20 (2000): 9507–14. http://dx.doi.org/10.1128/jvi.74.20.9507-9514.2000.

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ABSTRACT Rous sarcoma virus (RSV), a simple retrovirus, needs to export unspliced viral RNA from the nucleus to the cytoplasm, circumventing the host cell restriction on cytoplasmic expression of intron-containing RNA. The cytoplasmic accumulation of full-length viral RNA is promoted by two cis-acting direct repeat (DR) elements that flank the src gene; at least one copy of the DR sequence is necessary for viral replication. We show here that the DR mediates export of a reporter construct from the nucleus, suggesting it is a constitutive transport element (CTE). In contrast, human immunodefici
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20

Merezak, C., C. Pierreux, E. Adam, et al. "Suboptimal Enhancer Sequences Are Required for Efficient Bovine Leukemia Virus Propagation In Vivo: Implications for Viral Latency." Journal of Virology 75, no. 15 (2001): 6977–88. http://dx.doi.org/10.1128/jvi.75.15.6977-6988.2001.

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ABSTRACT Repression of viral expression is a major strategy developed by retroviruses to escape from the host immune response. The absence of viral proteins (or derived peptides) at the surface of an infected cell does not permit the establishment of an efficient immune attack. Such a strategy appears to have been adopted by animal oncoviruses such as bovine leukemia virus (BLV) and human T-cell leukemia virus (HTLV). In BLV-infected animals, only a small fraction of the infected lymphocytes (between 1 in 5,000 and 1 in 50,000) express large amounts of viral proteins; the vast majority of the
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21

Elaiw, A. M., and N. H. AlShamrani. "Modeling and stability analysis of HIV/HTLV-I co-infection." International Journal of Biomathematics 14, no. 05 (2021): 2150030. http://dx.doi.org/10.1142/s1793524521500303.

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Human immunodeficiency virus (HIV) and human T-lymphotropic virus type I (HTLV-I) are two retroviruses that infect the susceptible CD[Formula: see text]T cells. It is known that HIV and HTLV-I have in common a way of transmission through direct contact with certain body fluids related to infected individuals. Therefore, it is not surprising that a mono-infected person with one of these viruses can be co-infected with the other virus. In the literature, a great number of mathematical models has been presented to describe the within-host dynamics of HIV or HTLV-I mono-infection. However, the wit
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Cockerell, GL, J. Rovnak, PL Green, and IS Chen. "A deletion in the proximal untranslated pX region of human T-cell leukemia virus type II decreases viral replication but not infectivity in vivo." Blood 87, no. 3 (1996): 1030–35. http://dx.doi.org/10.1182/blood.v87.3.1030.bloodjournal8731030.

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The function of untranslated (UT) nucleotide sequences in the proximal portion of the pX region of the human T-cell leukemia virus (HTLV) family of retroviruses remains enigmatic. Previous studies have shown that these sequences are not necessary for the expression of viral proteins or for the induction, transmission, or maintenance of the transformed cell type in vitro. To determine the effect of the UT region in vivo, separate groups of rabbits were inoculated with lethally irradiated, stable clones of the human B-lymphoblastoid cell line, 729, transfected with either a full-length wild-type
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23

Lecellier, Charles-Henri, Manuel Neves, Marie-Lou Giron, Joelle Tobaly-Tapiero, and Ali Saïb. "Further Characterization of Equine Foamy Virus Reveals Unusual Features among the Foamy Viruses." Journal of Virology 76, no. 14 (2002): 7220–27. http://dx.doi.org/10.1128/jvi.76.14.7220-7227.2002.

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ABSTRACT Foamy viruses (FVs) are nonpathogenic, widely spread complex retroviruses which have been isolated in nonhuman primates, cattle, cats, and more recently in horses. The equine foamy virus (EFV) was isolated from healthy horses and was characterized by molecular cloning and nucleotide sequence analysis. Here, to further characterize this new FV isolate, the location of the transcriptional cap and poly(A) addition sites as well as the main splice donor and acceptor sites were determined, demonstrating the existence of the specific subgenomic pol mRNA, one specific feature of FVs. Moreove
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24

Peloponese, Jean-Marie, Junichiro Yasunaga, Takao Kinjo, Koichi Watashi та Kuan-Teh Jeang. "Peptidylproline cis-trans-Isomerase Pin1 Interacts with Human T-Cell Leukemia Virus Type 1 Tax and Modulates Its Activation of NF-κB". Journal of Virology 83, № 7 (2009): 3238–48. http://dx.doi.org/10.1128/jvi.01824-08.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus etiologically causal of adult T-cell leukemia (ATL). The virus encodes a Tax oncoprotein that functions in transcriptional regulation, cell cycle control, and transformation. ATL is a highly virulent cancer that is resistant to chemotherapeutic treatments. To understand this disease better, it is important to comprehend how HTLV-1 promotes cellular growth and survival. Tax activation of NF-κB is important for the proliferation and transformation of virus-infected cells. We show here that prolyl isomerase Pin1 is ov
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Sheleg, Sergey V., Jean-Marie Peloponese, Ya-Hui Chi, Yan Li, Michael Eckhaus, and Kuan-Teh Jeang. "Evidence for Cooperative Transforming Activity of the Human Pituitary Tumor Transforming Gene and Human T-Cell Leukemia Virus Type 1 Tax." Journal of Virology 81, no. 15 (2007): 7894–901. http://dx.doi.org/10.1128/jvi.00555-07.

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ABSTRACT Aneuploidy is frequent in cancers. Recently it was found that pituitary tumor transforming gene (PTTG; also called Pds1p or securin) is overexpressed in many different tumors. Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that primarily infects CD4+ T lymphocytes and causes adult T-cell leukemia. Here, we report that overexpression of human PTTG cooperated with the HTLV-I Tax oncoprotein in cellular transformation. Coexpression of Tax and PTTG enhanced chromosomal instability and neoplastic changes to levels greater than overexpression of either factor singularly. Cells
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Asbury, Sarah, Seung Mi Yoo, and Jonathan Bramson. "101 Engineering gamma/delta T cells with the T-Cell antigen coupler receptor effectively induces antigen-specific tumor cytotoxicity in vitro and in vivo." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A112. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0101.

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BackgroundEngineered T cell therapies have revolutionized treatment of relapsed refractory haematological malignancies, however the cost of treatment for autologous products remains a significant challenge to their widespread use. The high cost is driven largely by the need for personalized manufacturing of autologous cell products. A non-conventional class of T cells, the gamma/delta T cell, can be safely transplanted into an unrelated recipient without inducing graft-versus host disease,1 making them an ideal candidate for mass-manufactured off-the-shelf T cell therapies. We have previously
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Sandrock, Robert W., Isaac Peterson, Cameron Evans, William Wheatley, and Alexander Kamb. "Enhanced expression of exogenous genes from retroviruses using HIV2/Tat." Journal of Biotechnology 97, no. 1 (2002): 41–50. http://dx.doi.org/10.1016/s0168-1656(02)00054-8.

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Foskett, Shannon M., Romi Ghose, Derek Ng Tang, Dorothy E. Lewis, and Andrew P. Rice. "Antiapoptotic Function of Cdk9 (TAK/P-TEFb) in U937 Promonocytic Cells." Journal of Virology 75, no. 3 (2001): 1220–28. http://dx.doi.org/10.1128/jvi.75.3.1220-1228.2001.

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ABSTRACT Cdk9 is the catalytic subunit of TAK (cyclinT1/P-TEFb), a cellular protein kinase that mediates human immunodeficiency virus type 1 (HIV-1) Tat transcriptional activation function. To examine Cdk9 function in cells relevant to HIV-1 infection, we used a murine leukemia virus retrovirus vector to transduce and overexpress the cDNA of a dominant negative mutant Cdk9 protein (Cdk9-dn) in Jurkat T cells and U937 promonocytic cells. In Jurkat cells, overexpression of Cdk9-dn specifically inhibited Tat transactivation and HIV-1 replication but had no inhibitory effect on induction of CD69,
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Arya, Suresh K., Barbara Beaver, Linda Jagodzinski, et al. "New human and simian HIV-related retroviruses possess functional transactivator (tat) gene." Nature 328, no. 6130 (1987): 548–50. http://dx.doi.org/10.1038/328548a0.

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Chiari, Estelle, Isabelle Lamsoul, Julie Lodewick, Cécile Chopin, Françoise Bex, and Claudine Pique. "Stable Ubiquitination of Human T-Cell Leukemia Virus Type 1 Tax Is Required for Proteasome Binding." Journal of Virology 78, no. 21 (2004): 11823–32. http://dx.doi.org/10.1128/jvi.78.21.11823-11832.2004.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) is the retrovirus responsible for adult T-cell leukemia and HTLV-1-associated myelopathy. Adult T-cell leukemia development is mainly due to the ability of the viral oncoprotein Tax to promote T-cell proliferation, whereas the appearance of HTLV-1-associated myelopathy involves the antigenic properties of Tax. Understanding the events regulating the intracellular level of Tax is therefore an important issue. How Tax is degraded has not been determined, but it is known that Tax binds to proteasomes, the major sites for degradation of intracel
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Lefèbvre, Laurent, Vincenzo Ciminale, Alain Vanderplasschen, et al. "Subcellular Localization of the Bovine Leukemia Virus R3 and G4 Accessory Proteins." Journal of Virology 76, no. 15 (2002): 7843–54. http://dx.doi.org/10.1128/jvi.76.15.7843-7854.2002.

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ABSTRACT Bovine leukemia virus (BLV) is a complex retrovirus that belongs to the Deltaretrovirus genus, which also includes Human T-cell leukemia virus type 1 (HTLV-1). Both viruses contain an X region coding for at least four proteins: Tax and Rex, which are involved in transcriptional and posttranscriptional regulation, respectively, and the accessory proteins R3 and G4 (for BLV) and p12I, p13II, and p30II (for HTLV-1). The present study was aimed at characterizing the subcellular localization of BLV R3 and G4. The results of immunofluorescence experiments on transfected HeLa Tat cells demon
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Laverdure, Sylvain, Nicholas Polakowski, Kimson Hoang, and Isabelle Lemasson. "Permissive Sense and Antisense Transcription from the 5′ and 3′ Long Terminal Repeats of Human T-Cell Leukemia Virus Type 1." Journal of Virology 90, no. 7 (2016): 3600–3610. http://dx.doi.org/10.1128/jvi.02634-15.

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ABSTRACTHuman T-cell leukemia virus type 1 (HTLV-1) is a retrovirus, and, as such, its genome becomes chromosomally integrated following infection. The resulting provirus contains identical 5′ and 3′ peripheral long terminal repeats (LTRs) containing bidirectional promoters. Antisense transcription from the 3′ LTR regulates expression of a single gene,hbz, while sense transcription from the 5′ LTR controls expression of all other viral genes, includingtax. Both the HBZ and Tax proteins are implicated in the development of adult T-cell leukemia (ATL), a T-cell malignancy caused by HTLV-1 infect
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Doucas, V., and R. M. Evans. "Human T-cell leukemia retrovirus-Tax protein is a repressor of nuclear receptor signaling." Proceedings of the National Academy of Sciences 96, no. 6 (1999): 2633–38. http://dx.doi.org/10.1073/pnas.96.6.2633.

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34

Bazarbachi, Ali, Hiba El Hajj, Marwan El-Sabban, et al. "The Combination of Arsenic Trioxide and Interferon-Alpha Eradicates Leukemia Initiating Cells in TAX-Driven Murine Adult T Cell Leukemia/Lymphoma." Blood 114, no. 22 (2009): 2714. http://dx.doi.org/10.1182/blood.v114.22.2714.2714.

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Abstract Abstract 2714 Poster Board II-690 Adult T cell leukemia (ATL) is one of the rare human cancers initiated by a transforming retrovirus, HTLV-I. After many years of controversy, it is now accepted that the viral transactivator protein Tax plays a critical role in initiating the leukemic process, because Tax transgenics develop a disease with striking ATL features. Long-term prognosis of ATL patients remains extremely poor, but we recently reported that the combination of As2O3, interferon-a (IFN), and zidovudine yielded unprecedented response rates. Indeed, in 10 chronic ATL patients, a
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Brady, H. J., C. G. Miles, D. J. Pennington, and E. A. Dzierzak. "Specific ablation of human immunodeficiency virus Tat-expressing cells by conditionally toxic retroviruses." Proceedings of the National Academy of Sciences 91, no. 1 (1994): 365–69. http://dx.doi.org/10.1073/pnas.91.1.365.

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36

Tajima, Shigeru, and Yoko Aida. "The Region between Amino Acids 245 and 265 of the Bovine Leukemia Virus (BLV) Tax Protein Restricts Transactivation Not Only via the BLV Enhancer but Also via Other Retrovirus Enhancers." Journal of Virology 74, no. 23 (2000): 10939–49. http://dx.doi.org/10.1128/jvi.74.23.10939-10949.2000.

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ABSTRACT Bovine leukemia virus (BLV) is associated with enzootic bovine leukosis and is closely related to human T-cell leukemia virus type 1 (HTLV-1). The Tax protein of BLV acts through the 5′ long terminal repeat (LTR) of BLV and activates the transcription of BLV. In this study, we amplified tax genes from BLV-infected cattle using PCR. We cloned the genes and monitored the transcriptional activities of the products. Seven independent mutant Tax proteins, with at least one amino acid substitution between residues 240 and 265, exhibited a markedly stronger ability to stimulate the viral LTR
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37

Ishikawa, Chie, Taeko Okudaira, Tetsuro Nakazato, Mariko Tomita, and Naoki Mori. "Human T-Cell Leukemia Virus Type I Tax Activates CD69 Gene Expression." Blood 108, no. 11 (2006): 2256. http://dx.doi.org/10.1182/blood.v108.11.2256.2256.

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Abstract The human T-cell leukemia virus type I (HTLV-I) is an oncogenic retrovirus that is etiologically linked to the genesis of adult T-cell leukemia (ATL). Emerging evidence suggests that the pathogenicity of ATL involves suppression of the overall immune response, although the underlying mechanism remains unclear. In this study, we demonstrated that HTLV-I transactivator Tax induces the aberrant expression of CD69, an early leukocyte activation molecule that plays an important role in downregulation of the immune response. In a panel of HTLV-I-infected T-cell lines, CD69 expression was hi
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Younis, Ihab, Brenda Yamamoto, Andrew Phipps, and Patrick 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 79, no. 23 (2005): 14473–81. http://dx.doi.org/10.1128/jvi.79.23.14473-14481.2005.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus associated primarily with adult T-cell leukemia and neurological disease. HTLV-1 encodes the positive trans-regulatory proteins Tax and Rex, both of which are essential for viral replication. Tax activates transcription initiation from the viral long terminal repeat and modulates the transcription or activity of a number of cellular genes. Rex regulates gene expression posttranscriptionally by facilitating the cytoplasmic expression of incompletely spliced viral mRNAs. Tax and Rex mutants have been identified that
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Ma, Guangyong, Jun-ichirou Yasunaga, Hirofumi Akari, and Masao Matsuoka. "TCF1 and LEF1 act as T-cell intrinsic HTLV-1 antagonists by targeting Tax." Proceedings of the National Academy of Sciences 112, no. 7 (2015): 2216–21. http://dx.doi.org/10.1073/pnas.1419198112.

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Human T-cell leukemia virus type 1 (HTLV-1) is a delta-type retrovirus that induces malignant and inflammatory diseases during its long persistence in vivo. HTLV-1 can infect various kinds of cells; however, HTLV-1 provirus is predominantly found in peripheral CD4 T cells in vivo. Here we find that TCF1 and LEF1, two Wnt transcription factors that are specifically expressed in T cells, inhibit viral replication through antagonizing Tax functions. TCF1 and LEF1 can each interact with Tax and inhibit Tax-dependent viral expression and activation of NF-κB and AP-1. As a result, HTLV-1 replication
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40

Schnell, Annika P., Stephan Kohrt, and Andrea K. Thoma-Kress. "Latency Reversing Agents: Kick and Kill of HTLV-1?" International Journal of Molecular Sciences 22, no. 11 (2021): 5545. http://dx.doi.org/10.3390/ijms22115545.

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Human T-cell leukemia virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), is a retrovirus, which integrates into the host genome and persistently infects CD4+ T-cells. Virus propagation is stimulated by (1) clonal expansion of infected cells and (2) de novo infection. Viral gene expression is induced by the transactivator protein Tax, which recruits host factors like positive transcription elongation factor b (P-TEFb) to the viral promoter. Since HTLV-1 gene expression is repressed in vivo by viral, cellular, and epigenetic mechanisms in late phases of infection, HTLV-1
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Fujita, M., K. Murata, and H. Shiku. "Selective inhibition of human T-lymphotropic virus type I-transformed human T-cell growth by a tax-targeted conditionally cytotoxic recombinant retrovirus." Blood 84, no. 8 (1994): 2591–96. http://dx.doi.org/10.1182/blood.v84.8.2591.2591.

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Abstract Adult T-cell leukemia (ATL), a disorder associated with high mortality rates, arises from human T-lymphotropic virus type I (HTLV-I)-infected CD4+ T cells. We designed a retroviral vector-based gene therapy approach to ATL. The long terminal repeat (LTR) of HTLV-I is transactivated by the viral tax protein. We constructed a hybrid gene consisting of herpes simplex virus thymidine kinase (HSV TK) under the control of the HTLV-I LTR and inserted it into a retroviral vector. When HTLV-I-transformed and tax-expressing human T-cell lines were infected with this recombinant retrovirus (LNLT
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42

Fujita, M., K. Murata, and H. Shiku. "Selective inhibition of human T-lymphotropic virus type I-transformed human T-cell growth by a tax-targeted conditionally cytotoxic recombinant retrovirus." Blood 84, no. 8 (1994): 2591–96. http://dx.doi.org/10.1182/blood.v84.8.2591.bloodjournal8482591.

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Adult T-cell leukemia (ATL), a disorder associated with high mortality rates, arises from human T-lymphotropic virus type I (HTLV-I)-infected CD4+ T cells. We designed a retroviral vector-based gene therapy approach to ATL. The long terminal repeat (LTR) of HTLV-I is transactivated by the viral tax protein. We constructed a hybrid gene consisting of herpes simplex virus thymidine kinase (HSV TK) under the control of the HTLV-I LTR and inserted it into a retroviral vector. When HTLV-I-transformed and tax-expressing human T-cell lines were infected with this recombinant retrovirus (LNLTK alpha v
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Béraud, C., S. C. Sun, P. Ganchi, D. W. Ballard, and W. C. Greene. "Human T-cell leukemia virus type I Tax associates with and is negatively regulated by the NF-kappa B2 p100 gene product: implications for viral latency." Molecular and Cellular Biology 14, no. 2 (1994): 1374–82. http://dx.doi.org/10.1128/mcb.14.2.1374.

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Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent of the adult T-cell leukemia, an aggressive and often fatal malignancy of activated human CD4 T cells. HTLV-I encodes an essential 40-kDa protein termed Tax that not only transactivates the long terminal repeat of this retrovirus but also induces an array of cellular genes. Tax-mediated transformation of T cells likely involves the deregulated expression of various cellular genes that normally regulate lymphocyte growth produced by altered activity of various endogenous host transcription factors. In particular, Tax is capable
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Béraud, C., S. C. Sun, P. Ganchi, D. W. Ballard, and W. C. Greene. "Human T-cell leukemia virus type I Tax associates with and is negatively regulated by the NF-kappa B2 p100 gene product: implications for viral latency." Molecular and Cellular Biology 14, no. 2 (1994): 1374–82. http://dx.doi.org/10.1128/mcb.14.2.1374-1382.1994.

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Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent of the adult T-cell leukemia, an aggressive and often fatal malignancy of activated human CD4 T cells. HTLV-I encodes an essential 40-kDa protein termed Tax that not only transactivates the long terminal repeat of this retrovirus but also induces an array of cellular genes. Tax-mediated transformation of T cells likely involves the deregulated expression of various cellular genes that normally regulate lymphocyte growth produced by altered activity of various endogenous host transcription factors. In particular, Tax is capable
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45

Nitta, Takayuki, Andrew Hofacre, Stacey Hull, and Hung Fan. "Identification and Mutational Analysis of a Rej Response Element in Jaagsiekte Sheep Retrovirus RNA." Journal of Virology 83, no. 23 (2009): 12499–511. http://dx.doi.org/10.1128/jvi.01754-08.

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ABSTRACT Jaagsiekte sheep retrovirus (JSRV) is a simple betaretrovirus causing a contagious lung cancer of sheep. JSRV encodes unspliced and spliced viral RNAs, among which unspliced RNA encodes Gag and Pol proteins and a singly spliced mRNA encodes Env protein. In another study we found that JSRV encodes a regulatory protein, Rej, that is responsible for synthesis of Gag polyprotein from unspliced viral RNA. Rej is encoded in the 5′ end of env, and it enhances nuclear export or accumulation of cytoplasmic unspliced viral RNA in 293T cells but not in most other cell lines (A. Hofacre, T. Nitta
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46

Geleziunas, Romas, Sharon Ferrell, Xin Lin та ін. "Human T-Cell Leukemia Virus Type 1 Tax Induction of NF-κB Involves Activation of the IκB Kinase α (IKKα) and IKKβ Cellular Kinases". Molecular and Cellular Biology 18, № 9 (1998): 5157–65. http://dx.doi.org/10.1128/mcb.18.9.5157.

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ABSTRACT Tax corresponds to a 40-kDa transforming protein from the pathogenic retrovirus human T-cell leukemia virus type 1 (HTLV-1) that activates nuclear expression of the NF-κB/Rel family of transcription factors by an unknown mechanism. Tax expression promotes N-terminal phosphorylation and degradation of IκBα, a principal cytoplasmic inhibitor of NF-κB. Our studies now demonstrate that HTLV-1 Tax activates the recently identified cellular kinases IκB kinase α (IKKα) and IKKβ, which normally phosphorylate IκBα on both of its N-terminal regulatory serines in response to tumor necrosis facto
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47

Hyun, Jinhee, Juan Carlos Ramos, Ngoc Toomey, et al. "Oncogenic Human T-Cell Lymphotropic Virus Type 1 Tax Suppression of Primary Innate Immune Signaling Pathways." Journal of Virology 89, no. 9 (2015): 4880–93. http://dx.doi.org/10.1128/jvi.02493-14.

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ABSTRACTHuman T-cell lymphotropic virus type I (HTLV-1) is an oncogenic retrovirus considered to be the etiological agent of adult T-cell leukemia (ATL). The viral transactivator Tax is regarded as the oncoprotein responsible for contributing toward the transformation process. Here, we demonstrate that Tax potently inhibits the activity of DEx(D/H) box helicases RIG-I and MDA5 as well as Toll-dependent TIR-domain-containing adapter-inducing interferon-β (TRIF), which function as cellular sensors or mediators of viral RNA and facilitate innate immune responses, including the production of type
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48

Zhang, Weiqing, John W. Nisbet, Joshua T. Bartoe, Wei Ding, and Michael D. Lairmore. "Human T-Lymphotropic Virus Type 1 p30IIFunctions as a Transcription Factor and Differentially Modulates CREB-Responsive Promoters." Journal of Virology 74, no. 23 (2000): 11270–77. http://dx.doi.org/10.1128/jvi.74.23.11270-11277.2000.

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ABSTRACT Human T-lymphotropic virus type 1 (HTLV-1), a complex retrovirus, causes adult T-cell lymphoma/leukemia and is linked to a variety of immune-mediated disorders. The roles of proteins encoded in the pX open reading frame (ORF) II gene region in HTLV-1 replication or in mediating virus-associated diseases remain to be defined. A nucleus-localizing 30-kDa protein, p30II, encoded within pX ORF II has limited homology with the POU family of transcription factors. Recently, we reported that selected mutations in pX ORF II diminish the ability of HTLV-1 to maintain high viral loads in infect
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49

Bodem, Jochen, Hans-Georg Kräusslich, and Axel Rethwilm. "Acetylation of the foamy virus transactivator Tas by PCAF augments promoter-binding affinity and virus transcription." Journal of General Virology 88, no. 1 (2007): 259–63. http://dx.doi.org/10.1099/vir.0.82169-0.

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It was shown recently that retrovirus transactivators interact with transcriptional coactivators, such as histone acetyltransferases (HATs). Foamy viruses (FVs) direct gene expression from the long terminal repeat and from an internal promoter. The activity of both promoters is strictly dependent on the DNA-binding transactivator Tas. Recently, it was shown that Tas interacts with the HATs p300 and PCAF. Based on these findings, it is demonstrated here that PCAF has the ability to acetylate Tas in vitro and in vivo. Tas acetylation resulted in enhanced DNA binding to the virus promoters. In vi
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Dolei, Antonina, Elena Uleri, Gabriele Ibba, Maurizio Caocci, Claudia Piu, and Caterina Serra. "The aliens inside human DNA: HERV-W/MSRV/syncytin-1 endogenous retroviruses and neurodegeneration." Journal of Infection in Developing Countries 9, no. 06 (2015): 577–87. http://dx.doi.org/10.3855/jidc.6916.

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The human genome contains remnants of ancestral retroviruses now endogenously transmitted, called human endogenous retroviruses (HERVs). HERVs can be variably expressed, and both beneficial and detrimental effects have described. This review focuses on the MSRV and syncytin-1 HERV-W elements in relationship to neurodegeneration in view of their neuro-pathogenic and immune-pathogenic properties. Multiple sclerosis (MS) and a neurodegenerative disease (neuroAIDS) are reported in this review. In vivo studies in patients and controls for molecular epidemiology and follow-up studies are reviewed, a
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