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Background  The concentrations of hepatitis B virus (HBV) DNA and surface antigen (HBsAg) are two critical virological variables to be monitored in chronic hepatitis B. HBsAg is derived from the HBV genome. Thus, higher HBV-DNA concentrations should implicate higher HBsAg levels. Nevertheless, the two variables do not manifest a simple linear relationship due to elusive host factor involvements. The aim of this study was to address the discrepancy of HBV DNA and HBsAg levels by a quantitative modeling of HBsAg concentrations.    Methods  Pretreatment hematological, histological and virus serological records of 327 chronic hepatitis B patients were reviewed. Two independent patient cohorts were used for validation.    Results  Univariate/multivariate analysis showed that ISHAK fibrosis stages, HBV-DNA levels and hepatitis e-antigen status were independently associated with HBsAg concentrations. In agreement with the natural history of chronic hepatitis B, HBsAg concentrations were negatively correlated with ISHAK fibrosis stages (adjusted  P  = 0.002). Subgroup analysis showed that significant HBsAg-DNA correlation existed in high-viral-titer patients with HBV-DNA > 6 log 10  IU/mL ( P  < 0.001), but not in low-viral-titer patients with HBV-DNA ≤ 6 log10 IU/mL ( P  = 0.076). A backward stepwise linear regression analysis in the low-viral-titer subgroup revealed a significant correlation between HBsAg levels and a linear combination of HBV-DNA levels and platelet counts. A biphasic model was thus established to accommodate patients with high and low HBV-DNA titers:   \documentclass[12pt]{minimal} 				\usepackage{amsmath} 				\usepackage{wasysym}  				\usepackage{amsfonts}  				\usepackage{amssymb}  				\usepackage{amsbsy} 				\usepackage{mathrsfs} 				\usepackage{upgreek} 				\setlength{\oddsidemargin}{-69pt} 				\begin{document}$$ \mathrm{HB}\mathrm{sAg}=0.538\ast \mathrm{H}\mathrm{B}\mathrm{V}{\textstyle \hbox{-}}\mathrm{D}\mathrm{N}\mathrm{A}+0.001\ast \mathrm{platelet}\ast \left(\left|6{\textstyle \hbox{-}}\mathrm{H}\mathrm{B}\mathrm{V}{\textstyle \hbox{-}}\mathrm{D}\mathrm{N}\mathrm{A}\right|+6{\textstyle \hbox{-}}\mathrm{HB}\mathrm{V}\mathrm{D}\mathrm{N}\mathrm{A}\right){\textstyle \hbox{-} }0.321 $$\end{document}    H  B  s  A  g   =  0.538  ∗   H    B    V    -    D    N    A   +  0.001  ∗   p  l  a  t  e  l  e  t   ∗   (   |  6   -    H    B    V    -    D    N    A   |   +  6   -    H    B    V    D    N    A   )    -   0.321The estimated HBsAg concentrations correlated well with the measured HBsAg levels not only in the model construction cohort ( N  =327,  P  < 0.001), but also in two validation cohorts comprising respectively the patients who had received pretreatment liver biopsy assessments ( N  = 45,  P  = 0.001), and the treatment-naïve patients who had not received liver biopsy ( N  = 80,  P  < 0.001).    Conclusion  HBsAg concentrations can be quantitatively estimated by viral DNA concentrations and human platelet counts.

bmc infectious diseases

Platelet counts modulate the quantitative relationship between hepatitis B viral DNA and surface antigen concentrations: a cross-sectional study of hematological, histological and viral factors