rologie i - European Congress of Virology

Recommendations

Info

5 th European Congress of VirologyThursday 12 th September 2013,15h00 – 17h15WORKSHOP 23: “VIRAL DIAGNOSIS IN CHRONICINFECTION AND DURING PREGNANCY”Chairpersons: Peter COYLE (UNITED KINGDOM)& Hubert NIESTERS (Groningen, THE NETHERLANDS)AmphitheaterKEYNOTE:Diagnosis and prognosis of human cytomegalovirus (HCMV) infectionin pregnancyMaria GRAZIA REVELLOSC Ostetricia e Ginecologia, Fondazione IRCCS Policlinico San Matteo,Pavia and Fondazione Carlo Denegri, Torino, ITALYHuman cytomegalovirus (HCMV) is still the leading infectious agent causingmental retardation and sensorineural deafness in neonates. In theabsence of a vaccine, accurate diagnosis of primary infection in the mother,and of congenital infection in the fetus remain key points in the managementof pregnancies complicated by HCMV infection. The combinationof standard and new serological assays together with virological and clinicalfindings allow diagnosis and dating of primary HCMV infection in themother in the majority of cases. Maternal correlates of vertical transmissionremain elusive. As for diagnosis of HCMV infection in the fetus, thetechnique employed for HCMV detection, time interval between maternalinfection and the procedure as well as delayed transmission in utero aremajor variables affecting sensitivity of prenatal diagnosis. A high viral loadin amniotic fluid is a poor predictor of clinical outcome. Some promisingprognostic markers of congenital disease are currently being investigatedin fetal blood. In conclusion, reliable diagnosis of primary maternalinfection is the first issue to be addressed. Then, prenatal diagnosis can beoffered, and the woman, properly counselled, can decide how to proceedwith her pregnancy.ORAL COMMUNICATIONSREF O70Human Cytomegalovirus specific hyperimmune globulin for preventionof congenital infection following primary infection in pregnancyMilena FURIONEFondazione Carlo Denegri, Torino, ITALYBackground: Primary HCMV infection in pregnancy carries the highestrisk of vertical transmission and congenital disease. A non randomizedstudy (Nigro et al, NEJM 2005) reported that HCMV specific hyperimmuneglobulin (HIG) significantly reduced the risk of congenital infectionfrom 40% to 16% in pregnant women with primary infection.Objective: To verify HIG efficacy under controlled conditions.Patients and Methods: An independent, phase IIB, double blind, drug vsplacebo multicenter trial was conducted. Primary objective was to assessdrug efficacy by comparing the number of infected fetuses/newborns in thetwo arms of treatment. Pregnant women with primary HCMV infection at5 26 weeks’ gestation were randomized to receive, within 6 weeks after thepresumed onset of infection, HIg or placebo every 4 weeks until 36 weeks’gestation or HCMV positive amniocentesis. Sixty women/arm were neededin order to show a reduction from 40% to 16% vertical transmission(80% power, 5% type I error, 10% attrition).Results: Transmission rate was 44% (27/62) in the placebo arm and 30%(18/61) in the drug arm (95% CI 31.7 – 2.2; p=0.13). No significant differencewas noted between the two study groups for virus specific antibodyand T cell response. Similarly, no significant difference was noted betweentransmitter and nontransmitter mothers in each arm for the same parameters.An higher number of serious adverse events was reported in the HIGarm compared to the placebo arm.Conclusions: Safety and efficacy of HIG need to be assessed in largerphase III studies.REF O71Phylogenetic analysis of human parvovirus B19 in pregnant womenin Lyon (FRANCE)Yahia MEKKI 1 , Clément LABOIS 1 , Jean Sébastien CASALEGNO 1 ,Daniel EIBACH 1 , Genevieve BILLAUD 1 , Annabelle SERVANTDELMAS 2 , Jerome MASSARDIER 2 , Mona MASSOUD 2 , CyrilHUISSOUD 2 , Axel FICHEZ 2 , Pascal GAUCHERAND 3 , Rene CharlesRUDIGUOZ 4 , Frederique LEBRETON 5 , Veronique TARDY 6 , BrunoLINA 71 Centre hospitalo universsitaire Lyon/Virologie/HFME, Lyon, FRANCE;2 Laboratoire de virologie/INTS/Hôpital Armand Trousseau, PARIS,France; 3 Centre hospitalo universsitaire Lyon/Gynecologie obstétrique/HFME, Lyon, FRANCE; 4 Centre hospitalo universsitaire Lyon/Gynecologie obstétrique/Croix Rousse, Lyon, FRANCE; 5 Centre hospitalouniverssitaire Lyon/Anatomie pathologie/HFME, Lyon, FRANCE;6 Centre hospitalo universsitaire Lyon/Biochimie, Lyon, FRANCE; 7 Centrehospitalo universsitaire Lyon/Virologie, Lyon, FRANCEParvovirus infection during pregnancy is an important cause of hydropsfetalis. It is attributed to anemia caused by viral induced destruction ofred blood cells. Other organs have been reported to be affected includingthe heart, liver and lungs. Parvovirus B19 is a human virus consisting ofthree distinct genotypes (1, 2 and 3). In our hospital laboratory we detectedseveral epidemics of Parvovirus touching pregnant women. Most of themare deadly for the embryos.We retrospectively performed sequencing and phylogenic classificationof ninety six laboratory samples currently detected by the diagnosticvirology laboratory (RT PCR Abbott ® ) were analyzed. The ninety sixsamples were composed of 4 placenta, 12 necropsies, 15 amniotic fluidand 65 blood samples. Sixty four samples were identified as genotype 1by genotype specific PCR (analysis NS1 VP1U region), and thirty onesamples were negative. Seventy laboratory samples undetected by RTPCR Abbott ® resulted in 4 samples identified as genotype 1 and 66 asnegative.In conclusion during a 6 years period (2005 to 2011), only Parvovirus B19genotype 1 has been detected in pregnant women and fetal infections inour hospital.REF O72Determination of Rubella Virus Specific Humoral and Cell MediatedImmunity in pregnant women with negative of equivocal rubellaspecific IgGChristelle VAULOUP FELLOUS 2 , Olivier PICONE 1 , Yousra BEJAOUIOLHMANN 2 , Anne Gaël CORDIER 3 , Sophie NEDELLEC 3 ,PDEVILLIER 4 , Nicolas GAIDOT 2 , Liliane GRANGEOT KEROS 21 Department of Gynecology and Obstetrics, Foch Hospital, Suresnes,FRANCE; 2 AP HP, Laboratory of Virology, Rubella Materno foetalinfection National Reference Center, Paul Brousse Hospital, Villejuif,FRANCE; 3 AP HP, Department of Gynecology and Obstetrics, AntoineBéclère Hospital, Clamart, FRANCE; 4 Department of Clinical Research,Foch Hospital, Suresnes, FRANCEVirologie, Vol 17, supplément 2, septembre 2013S67
5 th European Congress of VirologyObjectives: Immunity to Rubella virus is commonly determined by measuringspecific IgG (RV IgG). However, RV IgG results may be verydifferent and even discordant, depending on the assay used. Cell mediatedimmunity plays also a role in resistance to infection but is not routinelyinvestigated for diagnostic purposes. Our aim was to investigateboth humoral and cellular immunity of pregnant women with negativeor equivocal RV IgG titers before and after the recommended post partumvaccination.Methods: 86 patients were included in the study. In the pre vaccinationperiod, humoral immunity was investigated with 4 RV IgG ELISA assays, awestern blot and a cell mediated immunity test (based on the − interferonresponse after stimulation by rubella antigens). In the post vaccinal period,measuring rubella specific IgM and RV IgG avidity allowed us to determinewhether a primary or a secondary immune response occurred.Results: Patients, who initially had negative RV IgG but above half thecut off of the assay, had positive RV IgG E1 antibodies, positive cellmediated immunity and experienced a secondary immune response aftervaccination (44/86). Patients with RV IgG below half the cut off of theassay had negative RV IgG E1 antibodies, negative cell mediated immunityand experienced a primary immune response after vaccination (42/86).Conclusion: These results indicate that several individuals may beimmune despite negative RV IgG. This could lead us to reduce the sensitivitythreshold of the rubella serologic assays, with respect to theirdiagnostic accuracy.REF O73A delay in the maternal antibody response to human cytomegalovirus(HCMV) gH/gL/pUL128 130 131 complex is associated with virustransmission to the fetusDaniele LILLERI 1,2 , Anna KABANOVA 2 , Maria Grazia REVELLO 1 ,Elena PERCIVALLE 1 , Antonella SARASINI 1 , Emilia GENINI 1 ,Federica SALLUSTO 2 , Antonio LANZAVECCHIA 2 , Davide CORTI 2 ,Giuseppe GERNA 11 Fondazione IRCCS Policlinico San Matteo, Pavia, ITALY; 2 Institute forResearch in Biomedicine, Bellinzona, SWITZERLANDPrimary HCMV infection during pregnancy is associated with a high riskof virus transmission to the fetus. Serial serum samples from 43 HCMVtransmitter (T) and non transmitter (NT) pregnant women with primaryHCMV infection were analyzed for neutralizing antibodies against HCMVglycoprotein complexes to identify correlates of HCMV transmission. Inthis study, we report that early detection of HCMV neutralizing antibodiesdirected against the pentameric complex gH/gL/pUL128 131 and, in particular,to the UL128 131 gene products appears to be associated with alower rate of HCMV transmission from the mother to the fetus. This wasshown by the finding that NT mothers exhibit an earlier antibody responseto different antigenic sites of the pentamer as compared to T mothers. Thisassociation was found to be consistent with the lower number of neutralizationsites recognized by T as compared to NT women at the 1st andthe 2nd month post infection onset. Furthermore, anti pentamer antibodiesdisplay an in vitro inhibition of cell to cell spreading and virus transferto leukocytes. The biological relevance of anti pentamer antibodies hasbeen in parallel highlighted by the finding that antibodies to HCMV gBare produced by NT and T mothers with the same kinetics and in comparableamounts. Taken together, these findings indicate that: i) the pentamercomplex is a major target of the antibody mediated maternal immunity;ii) T women elicit a lower neutralizing antibody response in the first 2months after onset of infection as compared to NT women.REF 074Development of a multiplex PCR approach for detection of dual infectionsand recombinants involving HIV variantsPierre CAPPY, Fabienne DE OLIVEIRA, Marie GUEUDIN, JeanChristophe PLANTIERRouen University Hospital, Rouen, FRANCEBackground: The high genetic diversity of HIV necessitates consistentattention to diagnostic tools and patient follow up. Due to the co circulationof different HIV types and groups, dual infections (DIs) and recombinants(Rec) have been described, which may hinder diagnosis and therapeuticmanagement.Methods: We designed 2 multiplex PCRs (mPCRs) coupled to capillaryelectrophoresis: MMO2, targeting 2 genes for the screening of HIV M+Oand M+2 DIs, and MMO, targeting 5 genes for the detection of HIV M+ODIs and HIV MO Rec. mPCRs were assessed on DNA and RNA extractsfrom HIV M, O and 2 virus cultures, then on DNA and RNA mixtures,simulating DIs. They were finally assessed on material from clinical monoinfection and from patients presenting with an HIV M+O or an HIV MOinfection.Results: In vitro samples. For MMO2, the overall sensitivity was 88% onDNA and 100% on RNA, along with a specificity of 100%. For MMO,the sensitivity was 100%, along with a specificity of 94% on DNA and100% on RNA. On simulated DIs, both mPCRs correctly detected 90%and 100% of DNA and RNA samples respectively. Clinical samples. ThemPCRs specificity was 100%, with a global sensitivity of 87% and 91%for MMO2, and 60% and 81% for MMO, on DNA and RNA respectively.Finally, both mPCRs were able to detect 4 out of 6 DIs on RNA,2 out of 2 DIs on DNA for MMO2, and 2 out of 2 MO Rec on RNAfor MMO.Conclusions: Altogether, on in vitro and clinical samples, MMO2 turnsout to be an excellent screening tool to detect M+2 and M+O DIs, andMMO to detect both MO DIs and MO mosaic patterns.REF O75Clinical Evaluation of BioPlex 2200 HIV Ag Ab: An AutomatedScreening Method Providing Discreet Detection of HIV 1 p24, HIV1 Antibody, and HIV 2 AntibodyFrançois SIMON 1 , Maud SALMONA 1 , Sarah MAYLIN 1 , LucGUERRIER 2 , Bill LINK 31 AP HP Hôpital Saint Louis, Laboratoire de virologie, Paris, FRANCE;2 Bio Rad Laboratories, Inc., Marnes La Coquette, FRANCE; 3 Bio RadLaboratories, Inc., Hercules, USABackground/Purpose: To assess the clinical sensitivity/specificity of theBioPlex 2200 HIV Ag Ab assay. The study was performed at the laboratoryof Virology of St. Louis Hospital, Paris.Methods: The BioPlex 2200 HIV Ag Ab assay uses multiplex flow IA todetect p24 Ag, HIV 1 Ab (Groups M/O) and HIV 2 Ab in a single reactionvessel using a mixture of 4 dyed bead populations. Each populationis coated with a different HIV Ag or p24 Ab, and results can be reportedindividually. Ab reactive specimens can be typed as HIV 1 or HIV 2. Specimenswith similar levels of HIV 1/2 Ab reactivity are reported as reactiveundifferentiated. The study included 1505 prospective fresh samples fromhospitalized patients, 420 stored samples from infected patients with HIV1 (different B or non B/CRF subtypes incl. 8 HIV 1 Grp O), a panel of 15samples collected during Primary HIV infection (PHI)/86 HIV 2 samples.S68 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 32 and 33: Scientific Programme -Saturday 14 t
Page 34 and 35: 5 th European Congress of Virology1
Page 48 and 49: 5 th European Congress of VirologyT
Page 54 and 55: 5 th European Congress of VirologyR
Page 58 and 59: 5 th European Congress of Virologyw
Page 64 and 65: 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 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 104 and 105: 5 th European Congress of VirologyA
Page 118 and 119:
Virologie 2013, 17 (supplément 2)
Page 120 and 121:
5 th European Congress of VirologyA
Page 122 and 123:
5 th European Congress of Virology0
Page 124 and 125:
Page 126 and 127:
5 th European Congress of VirologyH
Page 128 and 129:
5 th European Congress of Virologys
Page 130 and 131:
Page 132 and 133:
5 th European Congress of Virologyf
Page 134 and 135:
5 th European Congress of VirologyE
Page 136 and 137:
5 th European Congress of Virologyt
Page 138 and 139:
Page 140 and 141:
5 th European Congress of Virologyp
Page 142 and 143:
Page 144 and 145:
5 th European Congress of Virologyi
Page 146 and 147:
5 th European Congress of Virologyr
Page 148 and 149:
Page 150 and 151:
Page 152 and 153:
Page 154 and 155:
5 th European Congress of VirologyR
Page 156 and 157:
Page 158 and 159:
Page 160 and 161:
5 th European Congress of VirologyB
Page 162 and 163:
5 th European Congress of Virologyr
Page 164 and 165:
Page 166 and 167:
Page 168 and 169:
5 th European Congress of VirologyI
Page 170 and 171:
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:
5 th European Congress of Virologyw
Page 186 and 187:
Page 188 and 189:
Page 190 and 191:
Page 192 and 193:
5 th European Congress of Virologyn
Page 194 and 195:
Page 196 and 197:
Page 198 and 199:
5 th European Congress of VirologyT
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:
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:
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:
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:
5 th European Congress of VirologyW
show all

rologie i - European Congress of Virology

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?