论文部分内容阅读
Aim:To study the efficacy of antiviral treatment with PNA for the duck model ofHBV (DHBV)-infected ducks.PNA is a 2-amine-9-(2,3-dideoxy-2,3-dihydro-β-D-arabinofuranosyl)-6-methoxy-9H-purine.Methods:The Sichuan Mallard duck-lings in the hepatitis B virus model were treated with PNA,a new antiviral agent.DHBV DNA from the blood serum and liver tissues were measured at 0,5,and 10d during the treatment and at 3 d withdrawal by real-time PCR.The duck hepatitisB surface antigen (DHBsAg) in the liver cells was observed by Immunohistochem-istry (IHC).Pathological changes in the liver tissues were also observed.Controlgroup Ⅰ was administered with distilled water and control group Ⅱ was adminis-tered with 3-thiacytidine.Treatment group Ⅰ was administered with PNA at a doseof 40 mg/kg and treatment group Ⅱ was administered perorally (po) with PNA at adose of 80 mg/kg.Treatment group Ⅲ was administered with PNA at a dose of 20mg/kg and treatment group Ⅳ was intravenously administered with PNA at a doseof 40 mg/kg.Each group contained 15 ducklings.Results:PNA can significantlylower the DHBV replication levels in serum and liver.Compared with controlgroup Ⅱ,there were no significant differences in inhibiting efficacy in treatmentgroups Ⅰ and Ⅲ (P>0.05) and there were significant differences in inhibiting effi-cacy in treatment groups Ⅱ and Ⅳ(P<0.05).Interestingly,significant differenceswere observed at 3 d withdrawal.The DHBV replication levels in each groupslightly increased at 3 d withdrawal,but rebounded slightly in the PNA treatmentgroups than in control group Ⅱ(P<0.05).The DHBV replication levels in thetreatment groups were lower than in control group Ⅰ.The DHBV replication levelsin sera had a positive relationship with that in the liver,but the DHBV replicationlevels in the liver was lower than that in sera.Pathological changes in the treat-ment groups were obviously improved and the changes were associated with liverviral DNA levels.Conclusion:The results demonstrate that PNA is a stronginhibitor of DHBV replication in the DHBV-infected duck model.
Aim: To study the efficacy of antiviral treatment with PNA for the duck model of HBV (DHBV) -infected ducks. PNA is a 2-amine-9- (2,3-dideoxy-2,3- dihydro-β-D-arabinofuranosyl ) -6-methoxy-9H-purine. Methods: The Sichuan Mallard duck-lings in the hepatitis B virus model were treated with PNA, a new antiviral agent. DHBV DNA from the blood serum and liver tissues were measured at 0,5, and 10d during the treatment and at 3 d withdrawal by real-time PCR. The duck hepatitis B surface antigen (DHBsAg) in the liver cells was observed by Immunohistochem-istry (IHC). Pathological changes in the liver tissues were also observed. Control group I was administered with distilled water and control group II was adminis-tered with 3-thiacytidine. Treatment group I was administered with PNA at a dose of 40 mg / kg and treatment group II was administered perorally (po) with PNA at adose of 80 mg / kg. Treatment group III was administered with PNA at a dose of 20 mg / kg and treatment group IV was intravenously administere d with PNA at a dose of 40 mg / kg. Each group contained 15 ducklings.Results: PNA can significantlylower the DHBV replication levels in serum and liver. Compared with controlgroup II, there were no significant differences in inhibiting efficacy in treatmentgroups I and III ( P> 0.05) and there were significant differences in inhibiting effi-cacy in treatment groups II and IV (P <0.05) .Interestingly, significant differences were observed at 3 d withdrawal. The DHBV replication levels in each groupslightly increased at 3 d withdrawal, but The rebound slightly in the PNA treatment groups than in control group II (P <0.05). The DHBV replication levels in the treatment groups were lower than in control group I. The DHBV replication levels in sera had a positive relationship with that in the liver, but the DHBV replicationlevels in the liver was lower than that in sera. Pathological changes in the treat-ment groups were significantly improved and the changes were associated with liverviral DNA levels. Confclusion: The results demonstrate that PNA is a strong inhibitor of DHBV replication in the DHBV-infected duck model.