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[PMID]: 27519553 [Au] Autor: Enose-Akahata Y; Caruso B; Haner B; Charlip E; Nair G; Massoud R; Billioux BJ; Ohayon J; Switzer WM; Jacobson S [Ad] Endereço: Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 9000 Rockville Pike, Building 10 Room 5C-103, Bethesda, MD, 20892, USA. [Ti] Título: Development of neurologic diseases in a patient with primate T lymphotropic virus type 1 (PTLV-1). [So] Source: Retrovirology;13(1):56, 2016 Aug 12. [Is] ISSN: 1742-4690 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: BACKGROUND: Virus transmission from various wild and domestic animals contributes to an increased risk of emerging infectious diseases in human populations. HTLV-1 is a human retrovirus associated with acute T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 originated from ancient zoonotic transmission from nonhuman primates, although cases of zoonotic infections continue to occur. Similar to HTLV-1, the simian counterpart, STLV-1, causes chronic infection and leukemia and lymphoma in naturally infected monkeys, and combined are called primate T-lymphotropic viruses (PTLV-1). However, other clinical syndromes typically seen in humans such as a chronic progressive myelopathy have not been observed in nonhuman primates. Little is known about the development of neurologic and inflammatory diseases in human populations infected with STLV-1-like viruses following nonhuman primate exposure. RESULTS: We performed detailed laboratory analyses on an HTLV-1 seropositive patient with typical HAM/TSP who was born in Liberia and now resides in the United States. Using a novel droplet digital PCR for the detection of the HTLV-1 tax gene, the proviral load in PBMC and cerebrospinal fluid cells was 12.98 and 51.68 %, respectively; however, we observed a distinct difference in fluorescence amplitude of the positive droplet population suggesting possible mutations in proviral DNA. A complete PTLV-1 proviral genome was amplified from the patient's PBMC DNA using an overlapping PCR strategy. Phylogenetic analysis of the envelope and LTR sequences showed the virus was highly related to PTLV-1 from sooty mangabey monkeys (smm) and humans exposed via nonhuman primates in West Africa. CONCLUSIONS: These results demonstrate the patient is infected with a simian variant of PTLV-1, suggesting for the first time that PTLV-1smm infection in humans may be associated with a chronic progressive neurologic disease. [Mh] Termos MeSH primário: Infecções por Deltaretrovirus/complicações Infecções por Deltaretrovirus/virologia Paraparesia Espástica Tropical/virologia Vírus 1 Linfotrópico T de Primatas/isolamento & purificação [Mh] Termos MeSH secundário: África Ocidental Idoso Animais Infecções por Deltaretrovirus/transmissão Genes pX Haplorrinos/virologia Seres Humanos Leucócitos Mononucleares/virologia Masculino Filogenia Reação em Cadeia da Polimerase Vírus 1 Linfotrópico T de Primatas/genética Vírus 1 Linfotrópico T de Primatas/patogenicidade Provírus/genética [Pt] Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE [Em] Mês de entrada: 1705 [Cu] Atualização por classe: 170512 [Lr] Data última revisão: 170512 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160814 [St] Status: MEDLINE [do] DOI: 10.1186/s12977-016-0290-9

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[PMID]: 27317318 [Au] Autor: De Oliveira CH; Resende CF; Oliveira CM; Barbosa JD; Fonseca AA; Leite RC; Reis JK [Ad] Endereço: Laboratório de Retroviroses, Escola de Veterinária, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil; Setor de Medicina Veterinária Preventiva, Escola de Veterinária e Zootecnia, Universidade Federal de Goiás, Goiânia, Goiás, Brazil. Electronic address: cairo@ufg.br. [Ti] Título: Absence of Bovine leukemia virus (BLV) infection in buffaloes from Amazon and southeast region in Brazil. [So] Source: Prev Vet Med;129:9-12, 2016 Jul 01. [Is] ISSN: 1873-1716 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: Enzootic bovine leucosis is an infectious disease caused by Bovine leukemia virus (BLV) and is well described in bovines. The majority of infected animals are asymptomatic, one to five percent develop lymphoma and from 30 to 50% present a persistent lymphocytosis. The virus occurs naturally in cattle and experimentally in buffaloes, capybaras and rabbits. The occurrence of lymphoma in buffaloes has been attributed to BLV infection by some authors in India and Venezuela, but not confirmed by other studies and little information on natural BLV infection in buffaloes is available. The aim of this study was to evaluate the occurrence of BLV in a sub-sample of buffalo from Amazon and southeast regions in Brazil. Three hundred and fifteen serum samples were negative using commercial AGID and ELISA (ELISA-gp51) which detect anti-BLV glycoprotein gp51 antibodies. The same samples were also evaluated for antibodies to whole virus through a commercial ELISA (ELISA-BLV) in which 77 (24.44%) were found seropositive and two (0.63%) inconclusive. On the other hand, all animals were negative by PCR to BLV targeted to the env and tax genes. These results suggest that ELISA-BLV produces false positive results in buffalo serum (p<0.001). In addition, one buffalo lymphoma sample was negative in both PCR assays used in this study. BLV was not detected in buffaloes from the Amazon basin and the southeast region of Brazil. Serological tests, like ELISA-BLV, usually used for cattle may produce false-positive results for BLV in buffaloes and direct detection tests such as PCR should be chosen in these surveys. The occurrence of lymphoma in buffalo was not associated with BLV infection in the one case analyzed in this work and the etiology and pathogenesis of this disease should be clarified. [Mh] Termos MeSH primário: Búfalos Leucose Enzoótica Bovina/diagnóstico Vírus da Leucemia Bovina/imunologia Vírus da Leucemia Bovina/isolamento & purificação [Mh] Termos MeSH secundário: Animais Anticorpos Antivirais/sangue Brasil Bovinos DNA Viral/sangue Leucose Enzoótica Bovina/sangue Ensaio de Imunoadsorção Enzimática/veterinária Reações Falso-Negativas Genes env Genes pX Imunodifusão/métodos Linfoma/etiologia Linfoma/veterinária Reação em Cadeia da Polimerase/veterinária [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antibodies, Viral); 0 (DNA, Viral) [Em] Mês de entrada: 1704 [Cu] Atualização por classe: 170424 [Lr] Data última revisão: 170424 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160619 [St] Status: MEDLINE

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[PMID]: 26435148 [Au] Autor: Tarasevich A; Filatov A; Pichugin A; Mazurov D [Ti] Título: Monoclonal antibody profiling of cell surface proteins associated with the viral biofilms on HTLV-1 transformed cells. [So] Source: Acta Virol;59(3):247-56, 2015 Sep. [Is] ISSN: 0001-723X [Cp] País de publicação: Slovakia [La] Idioma: eng [Ab] Resumo: Human T lymphotropic virus 1 (HTLV-1) is a pathogenic retrovirus that spreads predominantly via cell-to-cell contact. Two models of cell-to-cell virus transmission are proposed: virological synapse (VS) and viral biofilms (VB). Both infectious structures can be involved in transmission and synergistically enhance HTLV-1 spread between cells. Although transmission of virus via VB has been reported, the molecular composition of VB remains poorly understood. In this study we generated new anti-VB monoclonal antibodies (MAbs) and screenedthem along with a panel of anti-human cluster of differentiation (CD) MAbs to select antigens associated with VB. Among four MAbs generated against VB, two MAbs were identified as anti-CD25 (IL-2RA). We found that antigens CD4, CD150, CD25, CD70, and CD80 were enriched in VB. We also determined that expression of viral protein Tax, a central molecule in HTLV-1 transmission, upregulates intercellular adhesion molecule 1 (ICAM-1), CD95, CD25, CD70, and CD80. Whether these antigens are essential for VB formation and HTLV-1 infection remains unknown and will be determined in further experiments. [Mh] Termos MeSH primário: Anticorpos Monoclonais/biossíntese Biofilmes Infecções por HTLV-I/transmissão Vírus 1 Linfotrópico T Humano/imunologia [Mh] Termos MeSH secundário: Transformação Celular Viral Genes pX/fisiologia Células HEK293 Seres Humanos [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antibodies, Monoclonal) [Em] Mês de entrada: 1512 [Cu] Atualização por classe: 151005 [Lr] Data última revisão: 151005 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 151006 [St] Status: MEDLINE

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[PMID]: 26265053 [Au] Autor: Baydoun HH; Cherian MA; Green P; Ratner L [Ad] Endereço: Division of Molecular Oncology, Department of Medicine Campus, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO, 63110, USA. hbaydoun@dom.wustl.edu. [Ti] Título: Inducible nitric oxide synthase mediates DNA double strand breaks in Human T-Cell Leukemia Virus Type 1-induced leukemia/lymphoma. [So] Source: Retrovirology;12:71, 2015 Aug 12. [Is] ISSN: 1742-4690 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is an aggressive and fatal malignancy of CD4(+) T-lymphocytes infected by the Human T-Cell Virus Type 1 (HTLV-1). The molecular mechanisms of transformation in ATLL have not been fully elucidated. However, genomic instability and cumulative DNA damage during the long period of latency is believed to be essential for HTLV-1 induced leukemogenesis. In addition, constitutive activation of the NF-κB pathway was found to be a critical determinant for transformation. Whether a connection exists between NF-κB activation and accumulation of DNA damage is not clear. We recently found that the HTLV-1 viral oncoprotein, Tax, the activator of the NF-κB pathway, induces DNA double strand breaks (DSBs). RESULTS: Here, we investigated whether any of the NF-κB target genes are critical in inducing DSBs. Of note, we found that inducible nitric oxide synthase (iNOS) that catalyzes the production of nitric oxide (NO) in macrophages, neutrophils and T-cells is over expressed in HTLV-1 infected and Tax-expressing cells. Interestingly, we show that in HTLV-1 infected cells, iNOS expression is Tax-dependent and specifically requires the activation of the classical NF-κB and JAK/STAT pathways. A dramatic reduction of DSBs was observed when NO production was inhibited, indicating that Tax induces DSBs through the activation of NO synthesis. CONCLUSIONS: Determination of the impact of NO on HTLV-1-induced leukemogenesis opens a new area for treatment or prevention of ATLL and perhaps other cancers in which NO is produced. [Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla Produtos do Gene tax/metabolismo Vírus 1 Linfotrópico T Humano Leucemia-Linfoma de Células T do Adulto/genética Leucemia-Linfoma de Células T do Adulto/virologia Óxido Nítrico Sintase Tipo II/genética Óxido Nítrico Sintase Tipo II/metabolismo [Mh] Termos MeSH secundário: Adulto Amidinas/farmacologia Cumarínicos/farmacologia Regulação da Expressão Gênica Genes pX Infecções por HTLV-I/genética Infecções por HTLV-I/virologia Vírus 1 Linfotrópico T Humano/patogenicidade Seres Humanos Janus Quinases/metabolismo Células Jurkat NF-kappa B/metabolismo Óxido Nítrico/metabolismo Fatores de Transcrição STAT/metabolismo Transdução de Sinais Ativação Transcricional Células Tumorais Cultivadas [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Amidines); 0 (Coumarins); 0 (Gene Products, tax); 0 (N-(6-bromo-7-hydroxycoumarin-4-yl)methoxycarbonyl-N-(3-(aminomethyl)benzyl)acetamide); 0 (NF-kappa B); 0 (STAT Transcription Factors); 0 (tax protein, Human T-lymphotrophic virus 1); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 2.7.10.2 (Janus Kinases) [Em] Mês de entrada: 1604 [Cu] Atualização por classe: 170220 [Lr] Data última revisão: 170220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150813 [St] Status: MEDLINE [do] DOI: 10.1186/s12977-015-0196-y

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[PMID]: 26251144 [Au] Autor: Tanaka Y; Kanda Y [Ad] Endereço: Division of Hematology, Saitama Medical Center, Jichi Medical University. [Ti] Título: [Development of Tax-redirected T-cell immunotherapy using TCR gene transduction in patients with ATL]. [So] Source: Rinsho Ketsueki;56(7):815-24, 2015 Jul. [Is] ISSN: 0485-1439 [Cp] País de publicação: Japan [La] Idioma: jpn [Ab] Resumo: ATL is an aggressive T-cell malignancy caused by HTLV-1 virus infection. Tax, which is the most important regulatory protein of HTLV-1, is associated with aggressive proliferation of host cells and is also a major target antigen for CD8â�º cytotoxic T-cells (CTLs). Recently, allogeneic hematopoietic stem cell transplantation (allo-HSCT) has proven effective for ATL, and donor-derived Tax-specific CTL might contribute to graft-versus-ATL effects in some recipients who maintained complete remission after allo-HSCT. We, for the first time, analyzed the Tax-specific T-cell receptor (TCR) repertoire, phenotypes and functions of Tax-specific CTLs at single-cell levels in HLA-A24â�º ATL patients who underwent allo-HSCT. We found that 1) a particular amino acid sequence motif (PDR) in the CDR3 region of TCR-ß was conserved in different patients and also within the same patient before and after allo-HSCT, and 2) the PDRâ�º Tax-specific CTL clone selectively expanded in ATL long-term survivors as less-differentiated effector memory CTLs. Actually, the PDRâ�º CTL showed not only strong binding activity for the Tax-tetramer but also strong killing activity against patients' HTLV-1-infected T-cells without any reaction against normal cells. We are presently evaluating the killing activities of PDRâ�º TCR-transduced T-cells against Tax in immunodeficient mice, with the aim of developing a new immunotherapy for ATL. [Mh] Termos MeSH primário: Genes pX Imunoterapia Leucemia-Linfoma de Células T do Adulto/terapia Receptores de Antígenos de Linfócitos T/genética Linfócitos T/imunologia [Mh] Termos MeSH secundário: Aloenxertos Animais Infecções por HTLV-I Transplante de Células-Tronco Hematopoéticas Vírus 1 Linfotrópico T Humano/genética Seres Humanos Leucemia-Linfoma de Células T do Adulto/genética Leucemia-Linfoma de Células T do Adulto/imunologia Receptores de Antígenos de Linfócitos T/imunologia [Pt] Tipo de publicação: ENGLISH ABSTRACT; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Receptors, Antigen, T-Cell) [Em] Mês de entrada: 1511 [Cu] Atualização por classe: 150807 [Lr] Data última revisão: 150807 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150808 [St] Status: MEDLINE [do] DOI: 10.11406/rinketsu.56.815

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[PMID]: 25774694 [Au] Autor: Pujari R; Hunte R; Thomas R; van der Weyden L; Rauch D; Ratner L; Nyborg JK; Ramos JC; Takai Y; Shembade N [Ad] Endereço: Department of Microbiology and Immunology, Viral Oncology Program, Sylvester Comprehensive Cancer Center, Miller School of Medicine, The University of Miami, Miami, Florida, United States of America. [Ti] Título: Human T-cell leukemia virus type 1 (HTLV-1) tax requires CADM1/TSLC1 for inactivation of the NF-κB inhibitor A20 and constitutive NF-κB signaling. [So] Source: PLoS Pathog;11(3):e1004721, 2015 Mar. [Is] ISSN: 1553-7374 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Persistent activation of NF-κB by the Human T-cell leukemia virus type 1 (HTLV-1) oncoprotein, Tax, is vital for the development and pathogenesis of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). K63-linked polyubiquitinated Tax activates the IKK complex in the plasma membrane-associated lipid raft microdomain. Tax also interacts with TAX1BP1 to inactivate the NF-κB negative regulatory ubiquitin-editing A20 enzyme complex. However, the molecular mechanisms of Tax-mediated IKK activation and A20 protein complex inactivation are poorly understood. Here, we demonstrated that membrane associated CADM1 (Cell adhesion molecule1) recruits Ubc13 to Tax, causing K63-linked polyubiquitination of Tax, and IKK complex activation in the membrane lipid raft. The c-terminal cytoplasmic tail containing PDZ binding motif of CADM1 is critical for Tax to maintain persistent NF-κB activation. Finally, Tax failed to inactivate the NF-κB negative regulator ubiquitin-editing enzyme A20 complex, and activate the IKK complex in the lipid raft in absence of CADM1. Our results thus indicate that CADM1 functions as a critical scaffold molecule for Tax and Ubc13 to form a cellular complex with NEMO, TAX1BP1 and NRP, to activate the IKK complex in the plasma membrane-associated lipid rafts, to inactivate NF-κB negative regulators, and maintain persistent NF-κB activation in HTLV-1 infected cells. [Mh] Termos MeSH primário: Moléculas de Adesão Celular/metabolismo Infecções por Deltaretrovirus/metabolismo Genes pX/fisiologia Imunoglobulinas/metabolismo NF-kappa B/metabolismo Transdução de Sinais/fisiologia [Mh] Termos MeSH secundário: Animais Molécula 1 de Adesão Celular Cisteína Endopeptidases/metabolismo Proteínas de Ligação a DNA/metabolismo Ensaio de Desvio de Mobilidade Eletroforética Vírus 1 Linfotrópico T Humano Seres Humanos Immunoblotting Imunoprecipitação Peptídeos e Proteínas de Sinalização Intracelular/metabolismo Células Jurkat Camundongos Camundongos Knockout Microscopia Confocal Proteínas Nucleares/metabolismo Reação em Cadeia da Polimerase Via Transcriptase Reversa Transfecção Proteína 3 Induzida por Fator de Necrose Tumoral alfa Enzimas de Conjugação de Ubiquitina/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (CADM1 protein, human); 0 (Cadm1 protein, mouse); 0 (Cell Adhesion Molecule-1); 0 (Cell Adhesion Molecules); 0 (DNA-Binding Proteins); 0 (Immunoglobulins); 0 (Intracellular Signaling Peptides and Proteins); 0 (NF-kappa B); 0 (Nuclear Proteins); EC 2.3.2.23 (UBE2N protein, human); EC 2.3.2.23 (Ube2n protein, mouse); EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes); EC 3.4.19.12 (TNFAIP3 protein, human); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.22.- (Tnfaip3 protein, mouse) [Em] Mês de entrada: 1601 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150317 [St] Status: MEDLINE [do] DOI: 10.1371/journal.ppat.1004721

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[PMID]: 25234742 [Au] Autor: Hotz A; Bourrat E; Hausser I; Haftek M; da Silva MV; Fischer J [Ad] Endereço: Institute of Human Genetics, University Medical Center Freiburg, Freiburg, Germany. [Ti] Título: Two novel mutations in the LOR gene in three families with loricrin keratoderma. [So] Source: Br J Dermatol;172(4):1158-62, 2015 Apr. [Is] ISSN: 1365-2133 [Cp] País de publicação: England [La] Idioma: eng [Mh] Termos MeSH primário: Genes pX/genética Proteínas de Membrana/genética Dermatopatias Genéticas/genética [Mh] Termos MeSH secundário: Adulto Idoso Feminino Heterozigoto Seres Humanos Ceratodermia Palmar e Plantar Masculino Meia-Idade Adulto Jovem [Pt] Tipo de publicação: CASE REPORTS; LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Membrane Proteins); 0 (loricrin) [Em] Mês de entrada: 1601 [Cu] Atualização por classe: 160318 [Lr] Data última revisão: 160318 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140920 [St] Status: MEDLINE [do] DOI: 10.1111/bjd.13414

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[PMID]: 25205102 [Au] Autor: Vernin C; Thenoz M; Pinatel C; Gessain A; Gout O; Delfau-Larue MH; Nazaret N; Legras-Lachuer C; Wattel E; Mortreux F [Ad] Endereço: Université de Lyon 1, CNRS UMR5239, Oncovirologie et Biothérapies, Laboratoire de Biologie Moléculaire de la Cellule, Faculté de Médecine Lyon Sud, Pierre Bénite, France. [Ti] Título: HTLV-1 bZIP factor HBZ promotes cell proliferation and genetic instability by activating OncomiRs. [So] Source: Cancer Res;74(21):6082-93, 2014 Nov 01. [Is] ISSN: 1538-7445 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Viruses disrupt the host cell microRNA (miRNA) network to facilitate their replication. Human T-cell leukemia virus type I (HTLV-1) replication relies on the clonal expansion of its host CD4(+) and CD8(+) T cells, yet this virus causes adult T-cell leukemia/lymphoma (ATLL) that typically has a CD4(+) phenotype. The viral oncoprotein Tax, which is rarely expressed in ATLL cells, has long been recognized for its involvement in tumor initiation by promoting cell proliferation, genetic instability, and miRNA dysregulation. Meanwhile, HBZ is expressed in both untransformed infected cells and ATLL cells and is involved in sustaining cell proliferation and silencing virus expression. Here, we show that an HBZ-miRNA axis promotes cell proliferation and genetic instability, as indicated by comet assays that showed increased numbers of DNA-strand breaks. Expression profiling of miRNA revealed that infected CD4(+) cells, but not CD8(+) T cells, overexpressed oncogenic miRNAs, including miR17 and miR21. HBZ activated these miRNAs via a posttranscriptional mechanism. These effects were alleviated by knocking down miR21 or miR17 and by ectopic expression of OBFC2A, a DNA-damage factor that is downregulated by miR17 and miR21 in HTLV-1-infected CD4(+) T cells. These findings extend the oncogenic potential of HBZ and suggest that viral expression might be involved in the remarkable genetic instability of ATLL cells. [Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/genética Proliferação Celular/genética Instabilidade Genômica Leucemia-Linfoma de Células T do Adulto/genética Proteínas Virais/genética [Mh] Termos MeSH secundário: Adulto Fatores de Transcrição de Zíper de Leucina Básica/metabolismo Linfócitos T CD4-Positivos/imunologia Linfócitos T CD8-Positivos/imunologia Regulação Viral da Expressão Gênica Genes pX/genética Vírus 1 Linfotrópico T Humano/genética Seres Humanos Leucemia-Linfoma de Células T do Adulto/imunologia Leucemia-Linfoma de Células T do Adulto/patologia Proteínas dos Retroviridae Proteínas Virais/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Basic-Leucine Zipper Transcription Factors); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (Retroviridae Proteins); 0 (Viral Proteins) [Em] Mês de entrada: 1501 [Cu] Atualização por classe: 161125 [Lr] Data última revisão: 161125 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140911 [St] Status: MEDLINE [do] DOI: 10.1158/0008-5472.CAN-13-3564

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[PMID]: 24962725 [Au] Autor: Zhou F; Fu H; Liu L; Cui Y; Zhang Z; Chang R; Yue Z; Yang S; Zhang X [Ad] Endereço: Institute of Dermatology and Department of Dermatology at No. 1 Hospital, Anhui Medical University, Hefei, Anhui, China; Department of Dermatology and Venereology, Anhui Medical University, Hefei, Anhui, China; State Key Laboratory of Dermatology Incubation, Ministry of Science and Technology, Hefei, Anhui, China. [Ti] Título: No exonic mutations at GJB2, GJB3, GJB4, GJB6, ARS (Component B), and LOR genes responsible for a Chinese patient affected by progressive symmetric erythrokeratodermia with pseudoainhum. [So] Source: Int J Dermatol;53(9):1111-3, 2014 Sep. [Is] ISSN: 1365-4632 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: OBJECTIVE: Progressive symmetric erythrokeratodermia (PSEK) is characterized by symmetric and growing erythematous hyperkeratotic patches over the body shortly after birth, particularly trunk and limbs, the buttocks, and the face, sometimes together with palmoplantar keratoderma (PPK). The GJB2, GJB3, GJB4, GJB6, ARS (Component B), and LOR gene mutation might contribute to PSEK manifestation. This study aimed to identify sequence alteration of these genes in a Chinese PSEK patient with pseudoainhum. METHODS: Genomic DNA was purified from the patient's peripheral blood. Mutation analysis of target genes was performed by direct sequencing using ABI 3730 sequencer RESULTS: No exonic mutations was identified in the aforementioned genes. CONCLUSIONS: The result underlines the genetic heterogeneity of PSEK and other related erythrokeratodermas. [Mh] Termos MeSH primário: Ainhum/genética Constrição Patológica/genética Eritroceratodermia Variável/genética [Mh] Termos MeSH secundário: Adolescente Antígenos Ly/genética Grupo com Ancestrais do Continente Asiático/genética China Conexina 26 Conexina 30 Conexinas/genética Genes pX/genética Seres Humanos Masculino Mutação Análise de Sequência de DNA Ativador de Plasminogênio Tipo Uroquinase/genética [Pt] Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antigens, Ly); 0 (Connexin 30); 0 (Connexins); 0 (DFNA3 protein, human); 0 (GJB6 protein, human); 0 (SLURP1 protein, human); 127120-53-0 (Connexin 26); 136362-16-8 (GJB3 protein, human); 147652-21-9 (connexin 30.3); EC 3.4.21.73 (Urokinase-Type Plasminogen Activator) [Em] Mês de entrada: 1507 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140626 [St] Status: MEDLINE [do] DOI: 10.1111/ijd.12494

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[PMID]: 24791004 [Au] Autor: Ohashi T; Nakamura T; Kidokoro M; Zhang X; Shida H [Ad] Endereço: Division of Molecular Virology, Institute for Genetic Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-ku, Sapporo, Hokkaido 060-0815, Japan. [Ti] Título: Combined cytolytic effects of a vaccinia virus encoding a single chain trimer of MHC-I with a Tax-epitope and Tax-specific CTLs on HTLV-I-infected cells in a rat model. [So] Source: Biomed Res Int;2014:902478, 2014. [Is] ISSN: 2314-6141 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Adult T cell leukemia (ATL) is a malignant lymphoproliferative disease caused by human T cell leukemia virus type I (HTLV-I). To develop an effective therapy against the disease, we have examined the oncolytic ability of an attenuated vaccinia virus (VV), LC16m8Δ (m8Δ), and an HTLV-I Tax-specific cytotoxic T lymphocyte (CTL) line, 4O1/C8, against an HTLV-I-infected rat T cell line, FPM1. Our results demonstrated that m8Δ was able to replicate in and lyse tumorigenic FPM1 cells but was incompetent to injure 4O1/C8 cells, suggesting the preferential cytolytic activity toward tumor cells. To further enhance the cytolysis of HTLV-I-infected cells, we modified m8Δ and obtained m8Δ/RT1AlSCTax180L, which can express a single chain trimer (SCT) of rat major histocompatibility complex class I with a Tax-epitope. Combined treatment with m8Δ/RT1AlSCTax180L and 4O1/C8 increased the cytolysis of FPM1V.EFGFP/8R cells, a CTL-resistant subclone of FPM1, compared with that using 4O1/C8 and m8Δ presenting an unrelated peptide, suggesting that the activation of 4O1/C8 by m8Δ/RT1AlSCTax180L further enhanced the killing of the tumorigenic HTLV-I-infected cells. Our results indicate that combined therapy of oncolytic VVs with SCTs and HTLV-I-specific CTLs may be effective for eradication of HTLV-I-infected cells, which evade from CTL lysis and potentially develop ATL. [Mh] Termos MeSH primário: Genes pX/genética Infecções por HTLV-I/imunologia Linfócitos T Citotóxicos/imunologia Vacinas Sintéticas/imunologia Vírus Vaccinia/genética Vacinas Virais/imunologia [Mh] Termos MeSH secundário: Animais Linhagem Celular Sobrevivência Celular/efeitos dos fármacos Infecções por HTLV-I/prevenção & controle Infecções por HTLV-I/virologia Vírus 1 Linfotrópico T Humano/genética Interferon gama/análise Interferon gama/imunologia Interferon gama/metabolismo Ratos Vacinas Sintéticas/genética Vacinas Sintéticas/metabolismo Vacinas Sintéticas/farmacologia Vírus Vaccinia/imunologia Vacinas Virais/genética Vacinas Virais/metabolismo Vacinas Virais/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Vaccines, Synthetic); 0 (Viral Vaccines); 82115-62-6 (Interferon-gamma) [Em] Mês de entrada: 1412 [Cu] Atualização por classe: 170220 [Lr] Data última revisão: 170220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140503 [St] Status: MEDLINE [do] DOI: 10.1155/2014/902478

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