Figure 5

Tlr3 is consistently activated in transgenic HBV-s-mut mice and thereby controls HBV replication.
Transgenic HBV (HBV-s-mut) mice were crossbred with Toll-like receptor 3-deficient (Tlr3−/−) mice. Two-month-old HBV-negative littermates (WT), Tlr3−/− mice, HBV-s-mut mice and HBV-s-mut/Tlr3−/− mice were put to death. RNA was extracted from liver tissue and changes in gene expression of Ifnb1 (A), Isg15 (B), Ifit1 (C), Tlr3 (G) and HBV mRNA expression (D) were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Copy numbers were normalized to 100,000 copies of Gapdh (mean ± SEM). DNA was extracted from liver tissue and changes in HBV DNA were quantified by PCR (E). Proteins were extracted from liver tissue, HBcAg was detected by western blot analysis and densitometric analysis was performed (F). Group size n = 8 (A–D), n = 4 (E,G) and n = 3 (F) animals; *p < 0.05, **p < 0.01, ***p < 0.001; HBV-s-mut, Tg1.4HBV-S-Mut3; WT, wild type.