摘要
Objective To investigate the dynamic change of coxsackievirus B3 (CVB3) in murine model ofchronic myocarditis and revel the molecular mechanism of the persistent infection of the tirus.Methods Strand - specific RT- PCR(ssRT- PCR), quantitative RT- PCR (qRT - PCR) and multiplexRT- PCR(mRT- PCR). Results The positive strand of CVB3 RNA existed in heart tissue up to 3 monthsalthough its amount decreased by 103～4 folds from acute to chronic phase. The negative strand RNA for virusreplication kept its amount on la moleculars per gram heart tissue. Some conserved areas of virus RNA 5’NTRand 3’NTR were lost in chronic phase. Conclusion The virus kept replication during the whole phase ofmyocarditis and speeded down on chronic period in the status of persistent infection. That may be due to theterminal lose of CVB RNA.
Objective To investigate the dynamic change of coxsackievirus B3 (CVB3) in murine model ofchronic myocarditis and revel the molecular mechanism of the persistent infection of the tirus.Methods Strand - specific RT- PCR(ssRT- PCR), quantitative RT- PCR (qRT - PCR) and multiplexRT- PCR(mRT- PCR). Results The positive strand of CVB3 RNA existed in heart tissue up to 3 monthsalthough its amount decreased by 103～4 folds from acute to chronic phase. The negative strand RNA for virusreplication kept its amount on la moleculars per gram heart tissue. Some conserved areas of virus RNA 5'NTRand 3'NTR were lost in chronic phase. Conclusion The virus kept replication during the whole phase ofmyocarditis and speeded down on chronic period in the status of persistent infection. That may be due to theterminal lose of CVB RNA.
