Curing hepatitis B virus (HBV) infection requires elimination of covalently closed circular DNA (cccDNA). Interferon (IFN)‐γ has noncytolytic antiviral potential; however, elimination of cccDNA could not be achieved. To enhance… Click to show full abstract
Curing hepatitis B virus (HBV) infection requires elimination of covalently closed circular DNA (cccDNA). Interferon (IFN)‐γ has noncytolytic antiviral potential; however, elimination of cccDNA could not be achieved. To enhance the regulatory effect, we comprehensively analyzed the host factors associated with cccDNA amplification and IFN‐γ and IFN‐α effects using an in vitro HBV infection system showing various transcription levels.
               
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