Serum and liver WHV measurements in the wIFN-α and placebo groups.

<p>N/A: not applicable.</p><p>^aTreatment response groups were defined as follows: R, responder ≥1 log₁₀ reduction in WHsAg at week 15 (end-of-treatment) and week 23 (end-of study); PR, partial responder ≥1 log₁₀ reduction in WHsAg at week 15 but not week 23; NR, non-responder <1 log₁₀ reduction in WHsAg at week 15 and week 23.</p><p>^bSerum WHV DNA and WHsAg levels at week -3 (pre-treatment baseline).</p><p>^cThe serum and intrahepatic viral endpoint differentials at weeks 0–23/25 (end-of-study) were calculated relative to the week -3 (pre-treatment) timepoint.</p><p>^dWHsAg levels for animals M1002, M1004 and F1022 were ≤ lower limit of detection (LLOD; 20 ng/mL) at one or more timepoints; the LLOD was used to calculate the maximum WHsAg decline for these animals.</p><p>^eM1004 had substantially lower week-3 baseline WHsAg and WHV DNA relative to the other study animals; WHsAg levels in this animal dropped by 1.5 log₁₀ between week -3 and the start of treatment (week 0), and then fell to ≤ LLOD after only 2 weeks of low dose wIFN-α. This animal subsequently developed very high titer anti-WHs (<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005103#ppat.1005103.s012" target="_blank">S1 Table</a>).</p><p>†Animal died during the study: M1006 (wIFN-α group); euthanized week 3 due to deteriorating health conditions which were likely related to underlying metabolism abnormalities, M1007 (wIFN-α group); died week 11, likely due to biopsy-related hemorrhage, F1020 (wIFN-α group); died week 16, cause of death unknown, F1023 (wIFN-α group); died week 2, likely related to severe pneumonia, M1010 (placebo group); euthanized week 17 due to symptoms associated with terminal HCC, F1017: (placebo group); euthanized week 17 due to symptoms associated with terminal HCC, F1024 (placebo group); died week 11, likely due to biopsy-related hemorrhage.</p><p>Serum and liver WHV measurements in the wIFN-α and placebo groups.