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. 2017 Feb 24;13(2):e1006239. doi: 10.1371/journal.ppat.1006239

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© 2017 McFadden et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 8 — The percentage of CpG DNA methylation at each position within the HBV genome from male (A) and female (B) FoxA-expressing (HBVFoxA2^fl/flAlbCre(-), HBVFoxA1^fl/flFoxA2^fl/flAlbCre(-) and HBVFoxA1^fl/flFoxA2^fl/flFoxA3^+/-AlbCre(-)) and FoxA-deleted (HBVFoxA2^fl/flAlbCre(+), HBVFoxA1^fl/flFoxA2^fl/flAlbCre(+) and HBVFoxA1^fl/flFoxA2^fl/flFoxA3^+/-AlbCre(+)) HBV transgenic mice is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The average percent methylation of the CpG sites spanning nucleotide coordinate 1–706 is correlated with the level of serum HBeAg.