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  1. Article ; Online: Infectious causes of cancer and their detection.

    Dalton-Griffin, Lucy / Kellam, Paul

    Journal of biology

    2009  Volume 8, Issue 7, Page(s) 67

    Abstract: Molecular techniques for identifying pathogens associated with cancer continue to be developed, including one reported recently in BMC Medical Genomics. Identifying a causal infectious agent helps in understanding the biology of these cancers and can ... ...

    Abstract Molecular techniques for identifying pathogens associated with cancer continue to be developed, including one reported recently in BMC Medical Genomics. Identifying a causal infectious agent helps in understanding the biology of these cancers and can lead ultimately to the development of antimicrobial drugs and vaccines for their treatment and prevention.
    MeSH term(s) Genetic Techniques ; Helicobacter Infections/complications ; Helicobacter Infections/diagnosis ; Helicobacter Infections/microbiology ; Humans ; Molecular Diagnostic Techniques ; Neoplasms/etiology ; Schistosomiasis haematobia/complications ; Schistosomiasis haematobia/diagnosis ; Schistosomiasis haematobia/parasitology ; Tumor Virus Infections/complications ; Tumor Virus Infections/diagnosis ; Tumor Virus Infections/virology
    Language English
    Publishing date 2009-08-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2082214-5
    ISSN 1475-4924 ; 1475-4924
    ISSN (online) 1475-4924
    ISSN 1475-4924
    DOI 10.1186/jbiol168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: X-box binding protein 1 contributes to induction of the Kaposi's sarcoma-associated herpesvirus lytic cycle under hypoxic conditions.

    Dalton-Griffin, Lucy / Wilson, Sam J / Kellam, Paul

    Journal of virology

    2009  Volume 83, Issue 14, Page(s) 7202–7209

    Abstract: Kaposi's sarcoma-associated herpesvirus (KSHV), like other herpesviruses, has two stages to its life cycle: latency and lytic replication. KSHV is required for development of Kaposi's sarcoma, a tumor of endothelial origin, and is associated with the B- ... ...

    Abstract Kaposi's sarcoma-associated herpesvirus (KSHV), like other herpesviruses, has two stages to its life cycle: latency and lytic replication. KSHV is required for development of Kaposi's sarcoma, a tumor of endothelial origin, and is associated with the B-cell tumor primary effusion lymphoma (PEL) and the plasmablastic variant of multicentric Castleman's disease, all of which are characterized by predominantly latent KSHV infection. Recently, we and others have shown that the activated form of transcription factor X-box binding protein 1 (XBP-1) is a physiological trigger of KSHV lytic reactivation in PEL. Here, we show that XBP-1s transactivates the ORF50/RTA promoter though an ACGT core containing the XBP-1 response element, an element previously identified as a weakly active hypoxia response element (HRE). Hypoxia induces the KSHV lytic cycle, and active HREs that respond to hypoxia-inducible factor 1alpha are present in the ORF50/RTA promoter. Hypoxia also induces active XBP-1s, and here, we show that both transcription factors contribute to the induction of RTA expression, leading to the production of infectious KSHV under hypoxic conditions.
    MeSH term(s) Binding Sites ; Cell Hypoxia ; Cell Line ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Herpesvirus 8, Human/genetics ; Herpesvirus 8, Human/physiology ; Humans ; Hypoxia ; Immediate-Early Proteins/chemistry ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Promoter Regions, Genetic ; Regulatory Factor X Transcription Factors ; Response Elements ; Sarcoma, Kaposi/metabolism ; Sarcoma, Kaposi/virology ; Trans-Activators/chemistry ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptional Activation ; Virus Activation ; X-Box Binding Protein 1
    Chemical Substances DNA-Binding Proteins ; Immediate-Early Proteins ; Regulatory Factor X Transcription Factors ; Rta protein, Human herpesvirus 8 ; Trans-Activators ; Transcription Factors ; X-Box Binding Protein 1 ; XBP1 protein, human
    Language English
    Publishing date 2009-04-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00076-09
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: X box binding protein XBP-1s transactivates the Kaposi's sarcoma-associated herpesvirus (KSHV) ORF50 promoter, linking plasma cell differentiation to KSHV reactivation from latency.

    Wilson, Sam J / Tsao, Edward H / Webb, Benjamin L J / Ye, Hongtao / Dalton-Griffin, Lucy / Tsantoulas, Christoforos / Gale, Catherine V / Du, Ming-Qing / Whitehouse, Adrian / Kellam, Paul

    Journal of virology

    2007  Volume 81, Issue 24, Page(s) 13578–13586

    Abstract: Reactivation of lytic replication from viral latency is a defining property of all herpesviruses. Despite this, the authentic physiological cues for the latent-lytic switch are unclear. Such cues should ensure that viral lytic replication occurs under ... ...

    Abstract Reactivation of lytic replication from viral latency is a defining property of all herpesviruses. Despite this, the authentic physiological cues for the latent-lytic switch are unclear. Such cues should ensure that viral lytic replication occurs under physiological conditions, predominantly in sites which facilitate transmission to permissive uninfected cells and new susceptible hosts. Kaposi's sarcoma-associated herpesvirus (KSHV) is associated with the B-cell neoplasm primary effusion lymphoma (PEL), in which the virus remains latent. We have previously shown that PEL cells have the gene expression profile and immunophenotype of cycling preplasma cells (plasmablasts). Here, we show that the highly active spliced isoform of plasma cell transcription factor X box binding protein 1 (XBP-1s) is a lytic switch for KSHV. XBP-1s is normally absent in PEL, but the induction of endoplasmic reticulum stress leads to XBP-1s generation, plasma cell-like differentiation, and lytic reactivation of KSHV. XBP-1s binds to and activates the KSHV immediate-early gene ORF50 and synergizes with the ORF50 gene product RTA to induce a full lytic cycle. These data suggest that KSHV remains latent until B-cell terminal differentiation into plasma cells, the transcriptional environment of which provides the physiological "lytic switch" through XBP-1s. This links B-cell terminal differentiation to KSHV lytic reactivation.
    MeSH term(s) Animals ; Cell Differentiation ; Cell Line ; Chlorocebus aethiops ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Endoplasmic Reticulum/ultrastructure ; Gene Expression Regulation, Viral ; Herpesvirus 8, Human/genetics ; Herpesvirus 8, Human/metabolism ; Herpesvirus 8, Human/physiology ; Humans ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Microscopy, Confocal ; Molecular Sequence Data ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Plasma Cells/cytology ; Promoter Regions, Genetic ; Regulatory Factor X Transcription Factors ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors ; Transcriptional Activation ; Vero Cells ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Virus Activation ; Virus Latency ; Virus Replication ; X-Box Binding Protein 1
    Chemical Substances DNA-Binding Proteins ; Immediate-Early Proteins ; Nuclear Proteins ; Regulatory Factor X Transcription Factors ; Rta protein, Human herpesvirus 8 ; Trans-Activators ; Transcription Factors ; Viral Proteins ; X-Box Binding Protein 1 ; XBP1 protein, human
    Language English
    Publishing date 2007-10-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.01663-07
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: SARS-CoV-2 Omicron-B.1.1.529 leads to widespread escape from neutralizing antibody responses

    Dejnirattisai, Wanwisa / Huo, Jiandong / Zhou, Daming / Zahradník, Jiří / Supasa, Piyada / Liu, Chang / Duyvesteyn, Helen M.E. / Ginn, Helen M. / Mentzer, Alexander J. / Tuekprakhon, Aekkachai / Nutalai, Rungtiwa / Wang, Beibei / Dijokaite, Aiste / Khan, Suman / Avinoam, Ori / Bahar, Mohammad / Skelly, Donal / Adele, Sandra / Johnson, Sile Ann /
    Amini, Ali / Ritter, Thomas G. / Mason, Chris / Dold, Christina / Pan, Daniel / Assadi, Sara / Bellass, Adam / Omo-Dare, Nicola / Koeckerling, David / Flaxman, Amy / Jenkin, Daniel / Aley, Parvinder K. / Voysey, Merryn / Clemens, Sue Ann Costa / Naveca, Felipe Gomes / Nascimento, Valdinete / Nascimento, Fernanda / Fernandes da Costa, Cristiano / Resende, Paola Cristina / Pauvolid-Correa, Alex / Siqueira, Marilda M. / Baillie, Vicky / Serafin, Natali / Kwatra, Gaurav / Da Silva, Kelly / Madhi, Shabir A. / Nunes, Marta C. / Malik, Tariq / Openshaw, Peter J.M. / Baillie, J. Kenneth / Semple, Malcolm G. / Townsend, Alain R. / Huang, Kuan-Ying A. / Tan, Tiong Kit / Carroll, Miles W. / Klenerman, Paul / Barnes, Eleanor / Dunachie, Susanna J. / Constantinides, Bede / Webster, Hermione / Crook, Derrick / Pollard, Andrew J. / Lambe, Teresa / Paterson, Neil G. / Williams, Mark A. / Hall, David R. / Fry, Elizabeth E. / Mongkolsapaya, Juthathip / Ren, Jingshan / Schreiber, Gideon / Stuart, David I. / Screaton, Gavin R. / Conlon, Christopher / Deeks, Alexandra S. / Frater, John / Frending, Lisa / Gardiner, Siobhan / Jämsén, Anni / Jeffery, Katie / Malone, Tom / Phillips, Eloise / Rothwell, Lucy / Stafford, Lizzie / Baillie, J Kenneth / Openshaw, Peter JM. / Carson, Gail / Alex, Beatrice / Andrikopoulos, Petros / Bach, Benjamin / Barclay, Wendy S. / Bogaert, Debby / Chand, Meera / Chechi, Kanta / Cooke, Graham S. / da Silva Filipe, Ana / de Silva, Thushan / Docherty, Annemarie B. / dos Santos Correia, Gonçalo / Dumas, Marc-Emmanuel / Dunning, Jake / Fletcher, Tom / Green, Christoper A. / Greenhalf, William / Griffin, Julian L. / Gupta, Rishi K. / Harrison, Ewen M. / Hiscox, Julian A. / Wai Ho, Antonia Ying / Horby, Peter W. / Ijaz, Samreen / Khoo, Saye / Law, Andrew / Lewis, Matthew R. / Liggi, Sonia / Lim, Wei Shen / Maslen, Lynn / Merson, Laura / Meynert, Alison M. / Moore, Shona C. / Noursadeghi, Mahdad / Olanipekun, Michael / Osagie, Anthonia / Palmarini, Massimo / Palmieri, Carlo / Paxton, William A. / Pollakis, Georgios / Price, Nicholas / Rambaut, Andrew / Robertson, Dave / Russell, Clark D. / Sancho-Shimizu, Vanessa / Sands, Caroline J. / Scott, Janet T. / Sigfrid, Louise / Solomon, Tom / Sriskandan, Shiranee / Stuart, David / Summers, Charlotte / Swann, Olivia V. / Takats, Zoltan / Takis, Panteleimon / Tedder, Richard S. / Thompson, AA Roger / Thomson, Emma C. / Thwaites, Ryan S. / Turtle, Lance CW. / Zambon, Maria / Hardwick, Hayley / Donohue, Chloe / Griffiths, Fiona / Oosthuyzen, Wilna / Donegan, Cara / Spencer, Rebecca G. / Norman, Lisa / Pius, Riinu / Drake, Thomas M. / Fairfield, Cameron J. / Knight, Stephen R. / Mclean, Kenneth A. / Murphy, Derek / Shaw, Catherine A. / Dalton, Jo / Girvan, Michelle / Saviciute, Egle / Roberts, Stephanie / Harrison, Janet / Marsh, Laura / Connor, Marie / Halpin, Sophie / Jackson, Clare / Gamble, C. / Plotkin, Daniel / Lee, James / Leeming, Gary / Wham, Murray / Clohisey, Sara / Hendry, Ross / Scott-Brown, Jas / Shaw, Victoria / McDonald, Sarah E. / Keating, Seán / Ahmed, Katie A. / Armstrong, Jane A. / Ashworth, Milton / Asiimwe, Innocent G. / Bakshi, Siddharth / Barlow, Samantha L. / Booth, Laura / Brennan, Benjamin / Bullock, Katie / Catterall, Benjamin WA. / Clark, Jordan J. / Clarke, Emily A. / Cole, Sarah / Cooper, Louise / Cox, Helen / Davis, Christopher / Dincarslan, Oslem / Dunn, Chris / Dyer, Philip / Elliott, Angela / Evans, Anthony / Finch, Lorna / Fisher, Lewis WS. / Foster, Terry / Garcia-Dorival, Isabel / Gunning, Philip / Hartley, Catherine / Jensen, Rebecca L. / Jones, Christopher B. / Jones, Trevor R. / Khandaker, Shadia / King So, Katharine / Kiy, Robyn T. / Koukorava, Chrysa / Lake, Annette / Lant, Suzannah / Latawiec, Diane / Lavelle-Langham, Lara / Lefteri, Daniella / Lett, Lauren / Livoti, Lucia A. / Mancini, Maria / McDonald, Sarah / McEvoy, Laurence / McLauchlan, John / Metelmann, Soeren / Miah, Nahida S. / Middleton, Joanna / Mitchell, Joyce / Murphy, Ellen G. / Penrice-Randal, Rebekah / Pilgrim, Jack / Prince, Tessa / Reynolds, Will / Ridley, P. Matthew / Sales, Debby / Shaw, Victoria E. / Shears, Rebecca K. / Small, Benjamin / Subramaniam, Krishanthi S. / Szemiel, Agnieska / Taggart, Aislynn / Tanianis-Hughes, Jolanta / Thomas, Jordan / Trochu, Erwan / van Tonder, Libby / Wilcock, Eve / Zhang, J. Eunice / Flaherty, Lisa / Maziere, Nicole / Cass, Emily / Carracedo, Alejandra Doce / Carlucci, Nicola / Holmes, Anthony / Massey, Hannah / Murphy, Lee / McCafferty, Sarah / Clark, Richard / Fawkes, Angie / Morrice, Kirstie / Maclean, Alan / Wrobel, Nicola / Donnelly, Lorna / Coutts, Audrey / Hafezi, Katarzyna / MacGillivray, Louise / Gilchrist, Tammy / Adeniji, Kayode / Agranoff, Daniel / Agwuh, Ken / Ail, Dhiraj / Aldera, Erin L. / Alegria, Ana / Allen, Sam / Angus, Brian / Ashish, Abdul / Atkinson, Dougal / Bari, Shahedal / Barlow, Gavin / Barnass, Stella / Barrett, Nicholas / Bassford, Christopher / Basude, Sneha / Baxter, David / Beadsworth, Michael / Bernatoniene, Jolanta / Berridge, John / Berry, Colin / Best, Nicola / Bothma, Pieter / Chadwick, David / Brittain-Long, Robin / Bulteel, Naomi / Burden, Tom / Burtenshaw, Andrew / Caruth, Vikki / Chambler, Duncan / Chee, Nigel / Child, Jenny / Chukkambotla, Srikanth / Clark, Tom / Collini, Paul / Cosgrove, Catherine / Cupitt, Jason / Cutino-Moguel, Maria-Teresa / Dark, Paul / Dawson, Chris / Dervisevic, Samir / Donnison, Phil / Douthwaite, Sam / Drummond, Andrew / DuRand, Ingrid / Dushianthan, Ahilanadan / Dyer, Tristan / Evans, Cariad / Eziefula, Chi / Fegan, Chrisopher / Finn, Adam / Fullerton, Duncan / Garg, Sanjeev / Garg, Atul / Gkrania-Klotsas, Effrossyni / Godden, Jo / Goldsmith, Arthur / Graham, Clive / Hardy, Elaine / Hartshorn, Stuart / Harvey, Daniel / Havalda, Peter / Hawcutt, Daniel B. / Hobrok, Maria / Hodgson, Luke / Hormis, Anil / Jacobs, Michael / Jain, Susan / Jennings, Paul / Kaliappan, Agilan / Kasipandian, Vidya / Kegg, Stephen / Kelsey, Michael / Kendall, Jason / Kerrison, Caroline / Kerslake, Ian / Koch, Oliver / Koduri, Gouri / Kōśi, Jōrjj / Laha, Shondipon / Laird, Steven / Larkin, Susan / Leiner, Tamas / Lillie, Patrick / Limb, James / Linnett, Vanessa / Little, Jeff / Lyttle, Mark / MacMahon, Michael / MacNaughton, Emily / Mankregod, Ravish / Masson, Huw / Matovu, Elijah / McCullough, Katherine / McEwen, Ruth / Meda, Manjula / Mills, Gary / Minton, Jane / Mirfenderesky, Mariyam / Mohandas, Kavya / Mok, Quen / Moon, James / Moore, Elinoor / Morgan, Patrick / Morris, Craig / Mortimore, Katherine / Moses, S. / Mpenge, Mbiye / Mulla, Rohinton / Murphy, Michael / Nagel, Megan / Nagarajan, Thapas / Nelson, Mark / Norris, Lillian / O’Shea, Matthew K. / Otahal, Igor / Ostermann, Marlies / Pais, Mark / Panchatsharam, Selva / Papakonstantinou, Danai / Paraiso, Hassan / Patel, Brij / Pattison, Natalie / Pepperell, Justin / Peters, Mark / Phull, Mandeep / Pintus, Stefania / Pooni, Jagtur Singh / Planche, Tim / Post, Frank / Price, David / Prout, Rachel / Rae, Nikolas / Reschreiter, Henrik / Reynolds, Tim / Richardson, Neil / Roberts, Mark / Roberts, Devender / Rose, Alistair / Rousseau, Guy / Ruge, Bobby / Ryan, Brendan / Saluja, Taranprit / Schmid, Matthias L. / Shah, Aarti / Shanmuga, Prad / Sharma, Anil / Shawcross, Anna / Sizer, Jeremy / Shankar-Hari, Manu / Smith, Richard / Snelson, Catherine / Spittle, Nick / Staines, Nikki / Stambach, Tom / Stewart, Richard / Subudhi, Pradeep / Szakmany, Tamas / Tatham, Kate / Thomas, Jo / Thompson, Chris / Thompson, Robert / Tridente, Ascanio / Tupper-Carey, Darell / Twagira, Mary / Vallotton, Nick / Vancheeswaran, Rama / Vincent-Smith, Lisa / Visuvanathan, Shico / Vuylsteke, Alan / Waddy, Sam / Wake, Rachel / Walden, Andrew / Welters, Ingeborg / Whitehouse, Tony / Whittaker, Paul / Whittington, Ashley / Papineni, Padmasayee / Wijesinghe, Meme / Williams, Martin / Wilson, Lawrence / Winchester, Stephen / Wiselka, Martin / Wolverson, Adam / Wootton, Daniel G. / Workman, Andrew / Yates, Bryan / Young, Peter

    Cell. 2022 Feb. 03, v. 185, no. 3 p.467-484.e15

    2022  

    Abstract: On 24ᵗʰ November 2021, the sequence of a new SARS-CoV-2 viral isolate Omicron-B.1.1.529 was announced, containing far more mutations in Spike (S) than previously reported variants. Neutralization titers of Omicron by sera from vaccinees and convalescent ... ...

    Institution OPTIC Consortium
    ISARIC4C Consortium
    Abstract On 24ᵗʰ November 2021, the sequence of a new SARS-CoV-2 viral isolate Omicron-B.1.1.529 was announced, containing far more mutations in Spike (S) than previously reported variants. Neutralization titers of Omicron by sera from vaccinees and convalescent subjects infected with early pandemic Alpha, Beta, Gamma, or Delta are substantially reduced, or the sera failed to neutralize. Titers against Omicron are boosted by third vaccine doses and are high in both vaccinated individuals and those infected by Delta. Mutations in Omicron knock out or substantially reduce neutralization by most of the large panel of potent monoclonal antibodies and antibodies under commercial development. Omicron S has structural changes from earlier viruses and uses mutations that confer tight binding to ACE2 to unleash evolution driven by immune escape. This leads to a large number of mutations in the ACE2 binding site and rebalances receptor affinity to that of earlier pandemic viruses.
    Keywords Severe acute respiratory syndrome coronavirus 2 ; evolution ; neutralization ; pandemic ; vaccines ; SARS-CoV-2 ; Omicron ; variants ; immune evasion ; receptor interaction ; Spike ; RBD
    Language English
    Dates of publication 2022-0203
    Size p. 467-484.e15.
    Publishing place Elsevier Inc.
    Document type Article ; Online
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2021.12.046
    Database NAL-Catalogue (AGRICOLA)

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