14th ICID - Poster Abstracts - International Society for Infectious ...

More documents

Recommendations

Info

When citing these abstracts please use the following reference: Author(s) of abstract. Title of abstract [abstract]. Int J Infect Dis 2010;14S1: Abstract number. Please note that the official publication of the International Journal of Infectious Diseases 2010, Volume 14, Supplement 1 is available electronically on http://www.sciencedirect.com Final Abstract Number: 84.021 Session: Virology and Viral Infections (Non-HIV) Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation Study on the prevalence of human bocavirus among children with acute respiratory tract infection in Guangdong, China X. Lu Affiliated Shenzhen Futian People’S Hospital of Guangdong Medical College, ShenZhen, China Background: To investigate the prevalence of human bocavirus (HBoV) among children with acute respiratory tract infection (ARTI) in Guangdong,China. Methods: 447 nasopharyngeal aspirates or swabs from children with acute respiratory tract infection in Guangdong were collected from Jun.2007 to May.2008. HBoV capsid protein VP gene fragments were detected by using PCR. Positive PCR products were sequenced. The DNA and the translated amino acid sequences were aligned with known HBoV sequences in GenBank and were done phylogenetic analysis. Results: 23 (5.1%) specimens were positive for HBoV, among which 43.5% 10/23 were codetected with other respiratory virus. The mainly diagnosis for HBoV positive children were wheezing pneumonia, bronchiolitis and bronchial pneumonia. HBoV positive children ranged from 43days to 6 years old, mainly aged 1year, among which 43.5% 10/23 were aged 1~6 months and 39.1% 9/23 were aged 7~12 months. HBoV were mainly detected in summer, early autumn and late spring. Through sequence alignment and phylogenetic analysis, The DNA and translated amino acid sequences of VP gene fragments of HBoV positive strains showed 97.8~98.8% and 98.5%~99.2% identity with ST1, respectively. Conclusion: HBoV was the important pathogen of ARTI children in Guangdong and was more prevalent in infants 1year. Although VP gene fragments of HBoV were conservative, there were still some mutant strains leading to amino acid change.
When citing these abstracts please use the following reference: Author(s) of abstract. Title of abstract [abstract]. Int J Infect Dis 2010;14S1: Abstract number. Please note that the official publication of the International Journal of Infectious Diseases 2010, Volume 14, Supplement 1 is available electronically on http://www.sciencedirect.com Final Abstract Number: 84.022 Session: Virology and Viral Infections (Non-HIV) Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation Deciphering the infectious entry process of human entrovirus 71 K. Mohamed Hussain, K. L. J. Leong, M. L. Ng, J. J. H. Chu National University of Singapore, Singapore, Singapore Background: Enterovirus 71 (HEV71) is one of the most clinically significant enteroviruses known to cause severe morbidity and mortality and is most frequently presented as hand, foot and mouth disease (HFMD) in children, although infected individuals could also develop neurological complications. In the absence of anti-viral agents or vaccines, urgent emphasis is therefore being placed on developing anti-viral strategies against this viral pathogen. As yet, little is known of the initial interaction between HEV71 and host cells, which may represent potential anti-viral targeting sites. Methods: A targeted small-interfering RNA (siRNA) screening platform assay was established and validated to identify and profile key cellular genes involved in processes of endocytosis, cytoskeletal dynamics and endosomal trafficking essential for HEV71 infection. Screen evaluation was conducted via the expression of well-characterised dominant-negative mutants, bioimaging studies (double-labeled immunofluorescence assays, transmission electron microscopy analysis), secondary siRNA-based dosage dependency studies and drug inhibition assays. Results: The infectious entry of HEV71 into RD cells was shown to be significantly inhibited by siRNAs targeting genes associated with clathrin-mediated endocytosis (CME), such as AP2A1, ARRB1, CLTC, CLTCL1, SYNJ1, ARPC5, PAK1, ROCK1 and WASF1. The functional role of CME was verified by the observation of strong co-localisation between HEV71 particles and clathrin as well as dose-dependent inhibition of HEV71 infection upon siRNA knockdown of CMEassociated genes. HEV71 entry by CME was further confirmed via inhibition by dominantnegative EPS15 mutants and treatment of CME drug inhibitors, with more than 80% inhibition observed at 20μM chlorpromazine. The involvement of other entry pathways, such as caveolaemediated endocytosis and macropinocytosis, was also found to be minimal, based on the failure of associated drug inhibitors in hampering HEV71 infection. Furthermore, HEV71 infection was shown to be sensitive to the disruption of human genes in regulating early to late endosomal trafficking as well as endosomal acidic pH. The importance and involvement of actin dynamics in mediating the infectious entry of HEV71 was also investigated. Conclusion: The identification of clathrin-mediated endocytosis as the entry pathway for HEV71 infection of susceptible host cells contributes to a better understanding of HEV71 pathogenesis and enables future development of anti-viral strategies against HEV71 infection.
Page 1 and 2:
When citing these abstracts please
Page 3 and 4:
Page 5 and 6:
Page 7 and 8:
Page 9 and 10:
Page 11 and 12:
Page 13 and 14:
Page 15 and 16:
Page 17 and 18:
Page 19 and 20:
Page 21 and 22:
Page 23 and 24:
Page 25 and 26:
Page 27 and 28:
Page 29 and 30:
Page 31 and 32:
Page 33 and 34:
Page 35 and 36:
Page 37 and 38:
Page 39 and 40:
Page 41 and 42:
Page 43 and 44:
Page 45 and 46:
Page 47 and 48:
Page 49 and 50:
Page 51 and 52:
Page 53 and 54:
Page 55 and 56:
Page 57 and 58:
Page 59 and 60:
Page 61 and 62:
Page 63 and 64:
Page 65 and 66:
Page 67 and 68:
Page 69 and 70:
Page 71 and 72:
Page 73 and 74:
Page 75 and 76:
Page 77 and 78:
Page 79 and 80:
Page 81 and 82:
Page 83 and 84:
Page 85 and 86:
Page 87 and 88:
Page 89 and 90:
Page 91 and 92:
Page 93 and 94:
Page 95 and 96:
Page 97 and 98:
Page 99 and 100:
Page 101 and 102:
Page 103 and 104:
Page 105 and 106:
Page 107 and 108:
Page 109 and 110:
Page 111 and 112:
Page 113 and 114:
Page 115 and 116:
Page 117 and 118:
Page 119 and 120:
Page 121 and 122:
Page 123 and 124:
Page 125 and 126:
Page 127 and 128:
Page 129 and 130:
Page 131 and 132:
Page 133 and 134:
Page 135 and 136:
Page 137 and 138:
Page 139 and 140:
Page 141 and 142:
Page 143 and 144:
Page 145 and 146:
Page 147 and 148:
Page 149 and 150:
Page 151 and 152:
Page 153 and 154:
Page 155 and 156:
Page 157 and 158:
Page 159 and 160:
Page 161 and 162:
Page 163 and 164:
Page 165 and 166:
Page 167 and 168:
Page 169 and 170:
Page 171 and 172:
Page 173 and 174:
Page 175 and 176:
Page 177 and 178:
Page 179 and 180:
Page 181 and 182:
Page 183 and 184:
Page 185 and 186:
Page 187 and 188:
Page 189 and 190:
Page 191 and 192:
Page 193 and 194:
Page 195 and 196:
Page 197 and 198:
Page 199 and 200:
Page 201 and 202:
Page 203 and 204:
Page 205 and 206:
Page 207 and 208:
Page 209 and 210:
Page 211 and 212:
Page 213 and 214:
Page 215 and 216:
Page 217 and 218:
Page 219 and 220:
Page 221 and 222:
Page 223 and 224:
Page 225 and 226:
Page 227 and 228:
Page 229 and 230:
Page 231 and 232:
Page 233 and 234:
Page 235 and 236:
Page 237 and 238: When citing these abstracts please
Page 287: When citing these abstracts please
show all

14th ICID - Poster Abstracts - International Society for Infectious ...

Create successful ePaper yourself

Delete template?

Save as template?