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  • Furthermore we also found that both

    2022-01-27

    Furthermore, we also found that both activation of oncogenes and inactivation of tumor suppressor genes occurred in HBV oval cells, which showed opposite pattern in HBV hepatocytes. These genes might take part in neoplastic transformation of oval cells induced by HBV regarding the multipotent role of oval cells. Given the regulatory elements of evolutionarily related species are conserved, the gene expression signatures reflecting similar phenotypes in different species may also be conserved [38]. This hypothesis is supported by numerous studies showing that comparison of gene expression data from human HCC and rodent HCC models can identify conserved molecular pathways responsible for aberrant phenotypes [[39], [40], [41]]. Indeed, staining results from human samples were consistent with microarray data from HBV mice, suggesting molecules and signaling pathways identified in this model help us understand the biology and carcinogenesis of HBV related diseases.
    Study approval
    Funding This work was supported by grant from the Key Project of National Natural Science Foundation of China [Grant number 30430670], grants from National Natural Science Foundation of China [Grant number 81201554 and 81300523] and China National Key Projects for Infectious Diseases [Grant number 2008ZX10002-025].
    Conflicts of interest statement
    Acknowledgments
    Background Hepatitis B virus (HBV) may cause chronic hepatitis B virus infection (CHB). The occurrence of CHB is dependent on the age of the individual acquiring infection [1]. The majority of infected adults achieves immune control of the infection and does not possess markers of active virus infection. In contrast, infection acquired perinatally or in early childhood often establishes CHB. CHB is associated with significant risk for development of liver failure and hepatocellular carcinoma and the risk for these complications is strongly associated with the levels of HBV DNA present in serum or plasma [2], [3]. Antiviral treatment with nucleotide or nucleoside analogues is capable of suppressing viral replication and improve prognosis of chronic HBV infection [4], [5], [6]. The measurement of HBV DNA by sensitive and dynamic nucleic adipor1 amplification technologies (NAAT) is therefore in addition to their use as diagnostic tools recommended as clinical support for the initiation and efficacy monitoring of antiviral therapy [7]. HBV is a reverse transcribing DNA virus, and because of the lack of proofreading activity of the reverse transcriptase nucleotide substitutions are continuously introduced into the virus genome [8]. HBV strains may on the basis of genome sequence analysis be classified into 10 genotypes (A–J) that are up to 8% divergent based on nucleotide alignment [9]. Sequence diversity constitutes a challenge for NAATs that for their analytical performance rely on the identification of oligonucleotide sequences uniformly conserved among clinical strains. The Hologic Aptima HBV Quant Assay is a relatively new test for the determination of HBV DNA in serum and plasma samples. It differs from other commercially available test by using target enrichment for nucleic acid purification and using real time transcription mediated amplification (TMA) instead of PCR for nucleic acid amplification and quantification. Furthermore, it incorporates dual targets to improve homogenous quantification of diverse clinical HBV strains. In the present study, we compared the analytical performance of the new Aptima assay with the COBAS Ampliprep/COBAS TaqMan HBV version2.0 Test frequently used in many clinical laboratories.
    Objectives
    Study design
    Results
    Discussion In this study, we compared the analytical performance of the Aptima and CAPCTMv2 HBV tests and found the two tests tightly correlated with a minimal average bias of −0.19 Log IU/mL (SD: 0.33 Log IU/mL). The same bias was observed over several Logs of HCV RNA concentrations when linearity was evaluated on clinical samples, and seemed decisive for discrepant categorization at clinical decision levels. Our results are in agreement with a recent study from France, in which average bias between the two tests was −0.15 Log IU/mL (SD: 0.37 Log IU/mL) [11]. The correlation between the tests appears to be at least as high as between the CAPCTMv2 and other commercial tests. Average bias between the Abbott RealTime HBV and CAPCTMv2 tests were estimated to be −0.25 Log IU/mL (SD: 0.35 Log IU/mL) in a French study [11] and +0.31 Log IU/mL (SD: 0.46 Log IU/mL) in a study from Taiwan [12]. The differences observed between the two studies emphasize that performance of tests will vary because of the geographic distribution of HBV genotypes and lineages [9]. In a comparison of the artus HBV QS-RCQ HBV test and the CAPCTMv2 from Korea [13] an average bias of −0.63 Log IU/mL (SD: 0.43 Log IU/mL) was observed. Although the studies generally showed a good correlation between tests, they all identified samples that appeared underquantified by one of the tests. This was also the case in the present study. Such underquantification may indicate that genetic variation of HBV challenges inclusivity of most current tests.