rologie i - European Congress of Virology

Recommendations

Info

Virologie 2013, 17 (supplément 2) : 117-284Poster presentations summaryp. S118 CATEGORY 01: Oncogenic mechanisms of virusesReferences from 001 to 008p. S121 CATEGORY 02: Oncolytic viruses and gene therapyReferences from 009 to 015p. S123 CATEGORY 03: Innate immunity against virusesReferences from 016 to 036p. S129 CATEGORY 04: Adaptive immunity and VaccinesReferences from 037 to 061p. S136 CATEGORY 05: Viral (immuno) pathogenesisReferences from 062 to 076p. S141 CATEGORY 06: Restriction factors of viral infection, interferingRNA & immune responseReferences from 077 to 088p. S144 CATEGORY 07: Cellular factors controling viral infectionand role of host geneticsReferences from 089 to 104p. S148 CATEGORY 08: Antiviral therapy and Resistance to acuteviral infectionReferences from 105 to 126p. S155 CATEGORY 09: Antiviral therapy and Resistance to chronicviral infectionReferences from 130 to 146p. S160 CATEGORY 10: Virus entry: envelope glycoproteins, receptors,endocytosisReferences from147 to 168p. S166 CATEGORY 11: Virus exit: assembly, maturation and releaseReferences from 169 to 180p. S170 CATEGORY 12: Viral gene expression – transcription, translationReferences from 181 to 197p. S175 CATEGORY 13: Viral replication strategiesReferences from 198 to 215p. S180 CATEGORY 14: Virus structure, dynamic imaging and traffickingReferences from 216 to 229p. S184 CATEGORY 15: Highly pathogenic virusesReferences from 230 to 251p. S190 CATEGORY 16: Zoonotic viruses (Antigone, Predemics)References from 252 to 271p. S196 CATEGORY 17: Vector borne viral infections (EUROWN,VECTORIE, WINGS)References from 272 to 293p. S203 CATEGORY 18: Emerging diseases in veterinary virology(ESVV)References from 294 to 344p. S216 CATEGORY 19: Viral evolution and quasispeciesReferences from 346 to 359p. S220 CATEGORY 20: Virus EpidemiologyReferences from 360 to 396p. S231 CATEGORY 21: Virus discovery and metagenomics(EMPERIE)References from 397 to 416p. S236 CATEGORY 22: Innovative methods in viral diagnosisReferences from 417 to 460p. S248 CATEGORY 23: Viral diagnosis in chronic infection andduring pregnancyReferences from 461 to 491p. S257 CATEGORY 24: Typing of viruses (molecular epidemiology,taxonomy)References from 492 to 507p. S262 CATEGORY 25: Respiratory virus infectionsReferences from 508 to 538p. S270 CATEGORY 26: Viral infections in transplant and immunocompromisedpatientsReferences from 539 to 562p. S277 CATEGORY 27: Neurotropic virusesReferences from 563 to 577p. S281 CATEGORY 28: Gastrointestinal viral infectionsReferences from 578 to 589doi:10.1684/vir.2013.0527Virologie, Vol 17, supplément 2, septembre 2013S117
5 th European Congress of VirologyPOSTERS01. ONCOGENIC MECHANISMS OFVIRUSESPosters: REF 001 to REF 008deleted at the expected sites. The EBER 1 deletion mutants have beencloned into EBER expression plasmids carrying the EBV oriP and hygromycin/ampicillinresistance genes. These plasmids have now been stablytransfected into 293T cells and a Burkitt’s lymphoma cell line (BL30) andtheir effect on cell proliferation and apoptosis will be presented.Understanding the function of EBERs may shed light on the molecularmechanism(s) by which EBV induces tumorigenesis.REF 001Selective activation of non canonical NF kappaB through a uniqueTRAF 3 binding motif in the viral oncoprotein TioBrigitte BIESINGER 1 , Sarah Jill DE JONG 1,4 , Jens ChristianALBRECHT 1 , Fabian GIEHLER 2 , Arnd KIESER 2 , Heinrich STICHT 31 Virologisches Institut, Friedrich Alexander Universitaet, Erlangen,GERMANY; 2 Abteilung Genvektoren, Helmholtz Zentrum Muenchen,Muenchen, GERMANY; 3 Institut fuer Biochemie, Friedrich AlexanderUniversiaet, Erlangen, GERMANY; 4 St. Giles Laboratory of Human Geneticsof Infectious Diseases, The Rockefeller University, New York, USAHerpesvirus ateles is capable to transform human T cells to long termgrowth in culture. Its oncoprotein Tio (Two in one) transfers this phenotypeto a transformation deficient recombinant herpesvirus saimiri. Oligomeric,membrane anchored Tio constitutes a signaling platform that recruitsSrc family kinases to activate STAT factors and TRAF6 to activate canonicalNF kappaB. Independent of these interaction partners, Tio inducesNIK stabilization and p100 processing, the hallmarks of non canonicalNF kappaB activation, through an as yet unidentified mechanism. We nowidentified a distinct sequence motif in Tio that specifically recruits TRAF3,a negative regulator of non canonical NF kappaB signaling. Through thisunique motif, Tio triggers a ubiquitin independent depletion of TRAF3from the cytosol and thereby releases the intrinsic activity of the non canonicalNF kappaB signaling cascade leading to p100 processing. Notably,mutation of the TRAF3 binding site does not affect canonical signalingintermediates and target gene regulation. Thus, Tio targets TRAF3 toinduce non canonical NF kappaB independent of cross talk into the canonicalcascade. In summary, we have identified a new and unique type ofTRAF3 binding motif that selectively mediates non canonical NF kappaBactivation and discloses studies into the specific functions of this pathwayand its role in T cell growth regulation.REF 002Creation of Epstein Barr virus encoded small RNA (EBER) mutantsand analysis of their functionGulfaraz KHAN, Pretty PHILIP, Waqar AHMEDUAE University, College of Medicine, Al Ain, UAEEpstein Barr virus (EBV), an oncogenic lymphotropic herpesvirus is implicatedin the pathogenesis of a number of human malignancies. Althoughthe mechanism by which EBV leads to cell transformation is not clear, anumber of viral latent gene products, including non protein coding smallRNAs have been implicated in the transformation/proliferation process.EBER 1 and EBER 2 are two such RNA molecules which are abundantlyexpressed in all EBV infected cells, but their function is poorly understood.Both of these RNA molecules have a secondary structure and are boundto cellular proteins. We set out to investigate the functions of EBER 1 bycreating EBER 1 mutants. We used spliced overlap extension PCR (SOEPCR) approach to create EBER 1 mutants with deletions in regions normallybound to cellular proteins. Using this approach, we have successfullydeleted stem loops (SL) 1, 3 and 4 of EBER 1. The subsequent mutantswere cloned and sequenced to verify that the intended target regions wereREF 003Human cytomegalovirus activates pro oncogenic pathways in primaryhuman hepatocytes and HepG2 cellsAmit KUMAR, Wasim ABBAS, Quentin LEPILLER, GeorgesHERBEINUniversity of Franche Comté, Besançon, FRANCEBackground: In the recent past, there has been increased concern in thepotential involvement of human cytomegalovirus (HCMV) in carcinogenesis.HCMV seroprevalence was enhanced in patients with hepatocellularcarcinoma (HCC) however, a possible link between HCC and HCMVinfection remains to be assessed. The aim of this work was to investigatethe protumor influence of HCMV on primary human hepatocytes (PHH)and HepG2 cells. Methods: Following infection of PHH and HepG2 cellsby two different strains of HCMV, we measured the production of IL 6 inculture supernatants by ELISA and the protein levels of STAT3, pSTAT3,JAK, cyclin D1, survivin, p53, p21, and Mdm2 by western blotting ininfected and uninfected cells. Ki67Ag expression was measured as a proliferationmarker whereas transformation was probed using soft agar colonyformation and tumorsphere assay. Results: PHH and HepG2 cells infectedwith HCMV resulted in the production of IL 6 and the subsequent activationof the IL 6R JAK STAT3 pathway. Expression of Cyclin D1, Survivinand Ki67Ag was upregulated by HCMV despite a paradoxical overexpressionof p53 and p21. Notably, we observed the formation of coloniesin soft agar seeded with PHH infected with HCMV and 2.5 fold moretumorspheres in HCMV infected HepG2 cultures than in uninfected ones.Conclusion: HCMV activated the IL 6 JAK STAT3 pathway in PHH andHepG2 cells, favored cellular proliferation, induced PHH transformationand enhanced HepG2 tumorsphere formation. Our observations raise thepossibility that HCMV infection might be involved in the onset of HCC.REF 004MicroRNA profiling in E6/E7 HPV transformed human keratinocytesGiorgio MANGINO 1 , Maria Vincenza CHIANTORE 2 , MarcoIULIANO 1 , Maria Simona ZANGRILLO 1 , Gabriele VACCARI 3 , RositaACCARDI 4 , Massimo TOMMASINO 4 , Gianna FIORUCCI 2,5 ,Giovanna ROMEO 1,51 Sapienza University of Rome/Dept. of Medico Surgical Sciences andBiotechnologies, Latina, ITALY; 2 Istituto Superiore di Sanità/Dept. ofInfectious, Parasitic and Immune mediated Diseases, Rome, ITALY;3 Istituto Superiore di Sanità/Dept. of Veterinary Public Health andFood Safety, Rome, ITALY; 4 International Agency for Research onCancer WHO/Infections and Cancer Biology Group, Lyon, FRANCE;5 CNR/Institute of Molecular Biology and Pathology, Rome, ITALYMicroRNAs (miRNAs) are naturally occurring noncoding RNAs that playa key role in gene regulation. They are highly conserved single strandedRNAs (∼22 nucleotides) that are cleaved from larger precursor transcripts.miRNAs exert their regulatory effects by cleaving the mRNAtargets or repressing their translation and are predicted to regulate at leastone third of all human genes. This posttranscriptional gene regulationhas been demonstrated to be active in fundamental cellular processes ascell proliferation, differentiation, and death. miRNAs are also involvedin the development and progression of human diseases, such as cancer.S118 Virologie, Vol 17, supplément 2, septembre 2013
Page 3 and 4:
Contents5 th European Congress of V
Page 5 and 6:
i r o l o g i eList of Keynote Spea
Page 7 and 8:
i r o l o g i eList of Chairpersons
Page 9 and 10:
i r o l o g i eWelcomeWelcome to th
Page 11 and 12:
5 th European Congress of VirologyY
Page 13 and 14:
i r o l o g i eExhibitorsThe indust
Page 15:
i r o l o g i eFacilities for the 5
Page 18 and 19:
i r o l o g i eGeneral Information
Page 20 and 21:
PROGRAMME AT A GLANCEWednesday 11th
Page 22 and 23:
5 th European Congress of VirologyW
Page 24 and 25:
Page 26 and 27:
Page 28 and 29:
Page 30 and 31:
Page 32 and 33:
Scientific Programme -Saturday 14 t
Page 34 and 35:
5 th European Congress of Virology1
Page 36 and 37:
Page 38 and 39:
Page 40 and 41:
Page 42 and 43:
Page 44 and 45:
Page 46 and 47:
Page 48 and 49:
5 th European Congress of VirologyT
Page 50 and 51:
Page 52 and 53:
Page 54 and 55:
5 th European Congress of VirologyR
Page 56 and 57:
Page 58 and 59:
5 th European Congress of Virologyw
Page 60 and 61:
Page 62 and 63:
Page 64 and 65:
5 th European Congress of Virologyt
Page 66 and 67:
Page 68 and 69: 5 th European Congress of VirologyT
Page 70 and 71: 5 th European Congress of VirologyA
Page 72 and 73: 5 th European Congress of Virologyp
Page 74 and 75: 5 th European Congress of VirologyR
Page 76 and 77: 5 th European Congress of VirologyF
Page 80 and 81: 5 th European Congress of Virologyc
Page 86 and 87: 5 th European Congress of Virologyt
Page 88 and 89: 5 th European Congress of VirologyH
Page 96 and 97: 5 th European Congress of VirologyS
Page 106 and 107: 5 th European Congress of Virology1
Page 126 and 127: 5 th European Congress of VirologyH
Page 128 and 129: 5 th European Congress of Virologys
Page 132 and 133: 5 th European Congress of Virologyf
Page 134 and 135: 5 th European Congress of VirologyE
Page 144 and 145: 5 th European Congress of Virologyi
Page 146 and 147: 5 th European Congress of Virologyr
Page 160 and 161: 5 th European Congress of VirologyB
Page 162 and 163: 5 th European Congress of Virologyr
Page 168 and 169:
5 th European Congress of VirologyI
Page 170 and 171:
5 th European Congress of Virologyf
Page 172 and 173:
5 th European Congress of Virologya
Page 174 and 175:
5 th European Congress of VirologyS
Page 176 and 177:
Page 178 and 179:
Page 180 and 181:
5 th European Congress of VirologyV
Page 182 and 183:
5 th European Congress of Virologyc
Page 184 and 185:
Page 186 and 187:
Page 188 and 189:
Page 190 and 191:
5 th European Congress of VirologyA
Page 192 and 193:
5 th European Congress of Virologyn
Page 194 and 195:
5 th European Congress of Virologyi
Page 196 and 197:
Page 198 and 199:
Page 200 and 201:
5 th European Congress of Virology(
Page 202 and 203:
Page 204 and 205:
Page 206 and 207:
5 th European Congress of Virologyo
Page 208 and 209:
Page 210 and 211:
Page 212 and 213:
Page 214 and 215:
Page 216 and 217:
Page 218 and 219:
5 th European Congress of Virologyp
Page 220 and 221:
Page 222 and 223:
5 th European Congress of Virology(
Page 224 and 225:
Page 226 and 227:
5 th European Congress of Virologyn
Page 228 and 229:
Page 230 and 231:
5 th European Congress of Virologyo
Page 232 and 233:
Page 234 and 235:
Page 236 and 237:
Page 238 and 239:
Page 240 and 241:
Page 242 and 243:
Page 244 and 245:
5 th European Congress of Virologyc
Page 246 and 247:
Page 248 and 249:
5 th European Congress of Virologyh
Page 250 and 251:
Page 252 and 253:
5 th European Congress of VirologyC
Page 254 and 255:
5 th European Congress of VirologyM
Page 256 and 257:
Page 258 and 259:
Page 260 and 261:
Page 262 and 263:
Page 264 and 265:
Page 266 and 267:
5 th European Congress of VirologyM
Page 268 and 269:
Page 270 and 271:
5 th European Congress of Virologyp
Page 272 and 273:
5 th European Congress of Virologyu
Page 274 and 275:
5 th European Congress of VirologyO
Page 276 and 277:
5 th European Congress of Virologys
Page 278 and 279:
Page 280 and 281:
Page 282 and 283:
Page 284 and 285:
5 th European Congress of VirologyA
Page 286 and 287:
Page 288 and 289:
5 th European Congress of VirologyB
Page 290 and 291:
5 th European Congress of VirologyD
Page 292 and 293:
5 th European Congress of VirologyG
Page 294 and 295:
5 th European Congress of VirologyJ
Page 296 and 297:
5 th European Congress of VirologyL
Page 298 and 299:
5 th European Congress of VirologyN
Page 300 and 301:
Page 302 and 303:
5 th European Congress of VirologyS
Page 304 and 305:
show all

rologie i - European Congress of Virology

Create successful ePaper yourself

Delete template?

Save as template?