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HBV core protein allosteric modulators differentially alter cccDNA biosynthesis from de novo infection and intracellular amplification pathways

Fig 2

Inhibition of cccDNA formation by HBV capsid assembly modulators is time- and concentration-dependent.

(A) C3AhNTCP cells were infected with HBV at an MOI of 500 genome equivalents. The cells were mock-treated or treated with 100 nM of MyrB, 1 μM of ETV, 2.5 μM of Bay 41–4109, 1 μM of GLS-4, 5 μM of ENAN-34017 or 1,000 IU/ml of IFN-α., starting from 24 h before infection, at infection or 24 h post infection until harvesting at 3 days post infection. HBV cccDNA was quantified by a real-time PCR assay. (B) C3AhNTCP cells were infected with HBV at an MOI of 500 genome equivalents. The cells were mock-treated or treated with the indicated concentrations of Bay 41–4109, GLS4 or ENAN-34017, starting from 24 h before infection until harvesting at 3 days post infection. HBV cccDNA were quantified by a real-time PCR assay. Differences in viral cccDNA between mock-treated control and treated group cultures under each treatment schedule were statistically analyzed (t-test, * p <0.05, ** p <0.01, *** p <0.001).

Fig 2

doi: https://doi.org/10.1371/journal.ppat.1006658.g002