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A Role Of Toll-Like Receptor 3 In Infectious Bursal Disease Virus Infection

Posted on:2008-11-05Degree:MasterType:Thesis
Country:ChinaCandidate:L ShiFull Text:PDF
GTID:2143360212988031Subject:Cell biology
Abstract/Summary:PDF Full Text Request
Infectious bursal disease virus (IBDV) is the etiological agent of infectious bursal disease (IBD) which is a highly contagious disease in 3-12 weeks old chickens. Infection by this virus leads to a severe immunosuppression characterized by the destruction of B cells present in the bursa of Fabricius, inducing immunodepression increases susceptibility to other pathogens, and thus causing severe damage to the poultry industry. However, whether innate immune system plays a role in the course of IBDV infection is still not clear. In this study, we designed six pairs of specific primers for Toll-like receptor (TLR) genes in chicken according to relevant published sequences. Analyses of conventional and real-time reverse transcription (RT)-PCR showed that TLR3 gene expression was significantly increased in IBDV-infected chicken embryo fibroblast (CEF) cells at transcriptional level after infection, as compared to that of other TLR genes. Specific small interfering RNA (siRNA) fragment against TLR3 gene was used to transfect CEF cells followed by infection with IBDV, the results indicated that whereby inhibition of TLR3 expression by the siRNA fragment decreased dramatically IBDV replication by indirect immunofluorescence assay as well as Western-blotting analysis to determine expression of VP2 protein, and release of IBDV virion by TCID50 assay to detect viral titers in the supernatant after infection. In conclusion, the study suggests that TLR3 might play an important role in the course of IBDV infection. This might facilitate further to studying mechanism on TLR3 signaling transduction in IBDV infection and offer a new scientific clue to controlling IBDV infection by novel therapeutics.
Keywords/Search Tags:Chicken infectious bursal disease virus (IBDV), Toll-like receptor (TLR), Gene transcription, Viral replication, Release of virion, RNA interference
PDF Full Text Request
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