![]() ![]() ![]() This use of an innate immune response to enhance its replication and persistence may represent a novel strategy that HBV uses to enhance its growth and spread in the early stage of viral infection when the viral level is low. Further studies revealed an important role of IFN-α/β in stimulating viral growth and prolonging viremia when viral load is low. In contrast, IFN-α/β enhanced viral replication by inducing the transcription factor HNF3γ and activating STAT3, which together stimulated HBV gene expression and replication. ![]() IFN-α/β apparently suppressed HBV replication via transcriptional and post-transcriptional regulations. Interestingly, our results indicated that IFN-α/β could have opposite effects on HBV: they suppressed HBV replication when viral load was high and enhanced HBV replication when viral load was low. By using HBV transgenic mice as a model and by using hydrodynamic injection to introduce HBV DNA into the mouse liver, we studied the effect of IFN-α/β on HBV in vivo. However, the use of IFN-α to treat hepatitis B virus (HBV) patients generated sustained response to only a minority of patients. Interferons α and β (IFN-α/β) are type I interferons produced by the host to control microbial infections. Tian, Yongjun Chen, Wen-ling Ou, Jing-hsiung James Effects of Interferon-α/β on HBV Replication Determined by Viral Load ![]()
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January 2023
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