Our assay method does not require HBV infection or radioactive <sup>3</sup>H-TCA and provides a facile way to identify viral entry inhibitors via measuring bile acid transport activity of NTCP.
Human NTCP transgenic mouse still could not support productive HBV infection, and humanized mouse liver with human hepatocytes which supported whole HBV life cycle still dominates HBV infection in vivo, a value but expensive model until now.
CXCR5<sup>+</sup>CD8<sup>+</sup>T cells are partially exhausted while possess a more potent antiviral activity through producing high levels of HBV-specific IFN-γ and IL-21 in chronic HBV infection.
Sodium taurocholate cotransporting polypeptide (NTCP) is expressed at the surface of human hepatocytes and functions as an entry receptor of hepatitis B virus (HBV).
The in vitro HBV infection assay system was established in primary human hepatocytes infected with HBV derived from the plasmid containing 1.3-mer HBV genome, and treated with IFN-γ.
In this study, we provide evidence linking the coexistence of hepatitis B virus X protein (HBx) and transforming growth factor beta 1 (TGF-β1) with miR-199a-3p in the malignant transformation of HPCs.
Controversies exist regarding the classification of the different clinical phases of chronic hepatitis B (CHB) because hepatitis B virus (HBV) DNA and alanine aminotransferase levels fluctuate over time.<sup>1,2</sup> To improve the distinction of clinical phases and the associated spectrum of clinical outcome,<sup>3,4</sup> hepatitis B surface antigen (HBsAg) levels may be of help.<sup>5-7</sup> We hypothesize that HBV genotype specific HBsAg levels are needed for the identification of different clinical HBV disease phases.<sup>7</sup>.
CXCR5<sup>+</sup>CD8<sup>+</sup>T cells are partially exhausted while possess a more potent antiviral activity through producing high levels of HBV-specific IFN-γ and IL-21 in chronic HBV infection.
In part 2, participants were required to have HBeAg-positive or HBeAg-negative chronic HBV infection, with serum HBV DNA concentrations of at least 2 × 10<sup>4</sup> IU/mL (HBeAg-positive) or 2 × 10<sup>3</sup> IU/mL (HBeAg-negative) and serum alanine aminotransferase concentrations less than seven times the upper limit of normal.
The methylation level of Pdcd1 was significantly lower in CHB patients (p<0.001), and the methylation level of Pdcd1 was negatively correlated with PD-1 expression level in CD8<sup>+</sup> T cells (p<0.001) and hepatitis-B surface antigen (HBsAg) (p<0.001).
CXCR5<sup>+</sup>CD8<sup>+</sup>T cells are partially exhausted while possess a more potent antiviral activity through producing high levels of HBV-specific IFN-γ and IL-21 in chronic HBV infection.
Peripheral blood mononuclear cells (PBMCs) were isolated by Ficoll-Hypaque density-based centrifugation from 10 patients with HBeAg-negative chronic hepatitis B [HBeAg(-) CHB;HBV-DNA>2000IU/mL], eight patients with HBeAg-negative chronic HBV infection [HBeAg(-) CI;undetectable HBV-DNA] and 8 healthy controls (HCs). p38MAPK phosphorylation was assessed by phospho-specific flow cytometry in PBMCs and cell subsets (CD3+,CD3-,CD56+,CD56-) after stimulation with cytokines (IL-12+IL-2 and IL-12+IL-18) or nonspecific stimuli [arsenite, phorbol 12-myristate 13-acetate (PMA) and ionomycin] at 0,30,60,120 and 240 minutes using p38 phospho-specific conjugated antibodies.
Using well-characterized cohort of treatment-naïve patients with chronic HBV infection in The Gambia, we evaluated the accuracy of serum HBcrAg to diagnose HBV DNA levels, and to indicate treatment eligibility determined by the American Association for the Study of Liver Diseases, based on the reference tests (HBV DNA, HBV e antigen (HBeAg), alanine transaminase (ALT), liver histopathology and/or FibroScan).
The primary efficacy outcome was a virological response (VR), and the secondary efficacy outcomes were hepatitis B e antigen (HBeAg) seroconversion and alanine aminotransferase (ALT) normalization.
Peripheral blood mononuclear cells (PBMCs) were isolated by Ficoll-Hypaque density-based centrifugation from 10 patients with HBeAg-negative chronic hepatitis B [HBeAg(-) CHB;HBV-DNA>2000IU/mL], eight patients with HBeAg-negative chronic HBV infection [HBeAg(-) CI;undetectable HBV-DNA] and 8 healthy controls (HCs). p38MAPK phosphorylation was assessed by phospho-specific flow cytometry in PBMCs and cell subsets (CD3+,CD3-,CD56+,CD56-) after stimulation with cytokines (IL-12+IL-2 and IL-12+IL-18) or nonspecific stimuli [arsenite, phorbol 12-myristate 13-acetate (PMA) and ionomycin] at 0,30,60,120 and 240 minutes using p38 phospho-specific conjugated antibodies.
In HCC cells, hepatitis B virus X protein (HBx) and palmitic acid (PA) increased the level of acetylated AFP by disrupting SIRT1-mediated deacetylation.
Through intracellular IFN-γ and TNF-α staining, HBV-specific CD4 T cells were analyzed in 68 patients with chronic HBV infection and alanine aminotransferase (ALT) <2x the upper limit of normal (ULN), and 28 patients with a hepatitis B flare.
At the end of follow-up, 8.8% of patients progressed to cirrhosis, the average estimate values of hepatitis B virus DNA and alanine aminotransferase demonstrated a downward trend, the aspartate aminotransferase/alanine aminotransferase ratio showed a flat trend overall.