Hepatitis B Core Antigens ; immunology ; Hepatitis B virus ; genetics ; immunology ; Hepatitis B, Chronic ; virology ; Humans ; T-Lymphocytes, Cytotoxic ; immunology

<b>OBJECTIVEb>To observe the effect of hepatitis virus B on the detection rate of core antigen of hepatitis virus C in sera of chronic hepatitis C patients.

<b>METHODb>HCVcAg and HCV RNA in sera were detected in 88 patients with chronic hepatitis C and 62 patients co-infected with HCV and HBV. At the same time, HBV DNA and HBeAg in sera were detected in 62 patients infected with HCV and HBV. Then we analyzed the correlation between HCVcAg and HBeAg/HBV DNA. The detection rates of HCVcAg in 88 patients with chronic hepatitis C and 62 patients co-infected with HCV and HBV were 72.7% (64/88) and 38.7% (24/62), respectively (x2 = 17.358, P less than 0.01).

<b>RESULTSb>The detection rates of HCV RNA in 88 patients with chronic hepatitis C and 62 patients co-infected with HCV and HBV was 81.8% (72/88) and 53.2% (33/62)respectively (x2=20.110, P less than 0.01). In 62 patients infected with HCV and HBV, the detection rate of HCVcAg in HBeAg positive patients and HBeAg negative patients were 28.6% (12/42) and 60% (12/20), respectively (x2 = 7.547, P = 0.011). Moreover, the positive rates of HBV DNA in HBeAg positive patients and HBeAg negative patients were 42.9% (18/42) and 80% (16/20), respectively (P more than 0.05). The detection rates of HCVcAg in HBV DNA positive patients and HBV DNA negative patients were 39.1% (18/46) and 37.5% (6/16), respectively (x2 = 0.013, P = 0.908). Compared with the detection rates of HCVcAg in patients only infected with HCV, the detection rate of HCVcAg in HBeAg or HBV DNA negative patients infected with HCV and HBV were 60% (12/20) (x2 = 1.266, P = 0.261) and 37.5% (6/16) (x2 =7.635, P less than 0.01), respectively.

<b>CONCLUSIONb>The detection rate of HCVcAg in patients infected with HCV and HBV is relatively low. The reason is possibly that HBeAg inhibits duplication of HCV and decreases the expression of HCVcAg.

Coinfection ; immunology ; virology ; DNA, Viral ; Hepacivirus ; immunology ; Hepatitis B ; immunology ; virology ; Hepatitis B virus ; Hepatitis C Antigens ; blood ; Hepatitis C, Chronic ; immunology ; virology ; Humans

Hepatitis B virus ; Hepatitis B, Chronic ; immunology ; virology ; Humans ; T-Lymphocytes ; immunology

<b>OBJECTIVEb>This study aimed to assess the clinical significance of intrahepatic hepatitis B core antigen (HBcAg) (+) in patients with chronic hepatitis B (CHB).

<b>METHODSb>200 CHB patients were prospectively studied using fluorescence quantitative PCR (FQ-PCR), combined PCR with fluorescence probe hybridization technique, to determine serum HBV DNA. Serum HBeAg was measured quantitatively. Liver biopsies were performed and immunohistochemistry stained liver slides were examined in all the cases. Correlation analyses were performed.

<b>RESULTSb>Based on the HBV DNA levels, the patients were divided into 5 groups: group A (<3 log10 copies/ml) n=20, group B (>or=3 log10 copies/ml-<5 log10 copies/ml) n=13, group C (>or=5 log10 copies/ml-<6 log10 copies/ml) n=24, group D (>or=6 log10 copies/ml-<8 log10 copies/ml) n=116, and group E (>or=8 log10 copies/ml) n=27, and 87.5% of the CHB patients were intrahepatic HBcAg (+). The rate of HBcAg (+) was 55.0% (11/20) in group A, 53.8% (7/13) in group B, 75.0% (19/24) in group C, 96.6% (112/116) in group D, and 100% (27/27) in group E. A strong correlation was found between the rate of HBcAg (+) and the level of serum HBV DNA (r=0.80). This type of association also appeared between serum HBV DNA levels and HBeAg (+) (r=0.47). Of 20 CHB patients who were serum HBV DNA negative, 25% (5) were HBeAg (+), and 55% (11) were HBcAg (+), whereas 15 patients were both HBV DNA (-) and HBeAg (-), and 46.7% (7) were HBcAg (+).

<b>CONCLUSIONSb>Intrahepatic HBcAg (+) in CHB patients might be more reliable in reflecting HBV replication. Determination of HBcAg (+) may have clinical significance for evaluating the efficacy of antiviral therapy and for predicting the therapeutic responses to different antiviral agents.

Adult ; DNA, Viral ; blood ; Female ; Hepatitis B Core Antigens ; analysis ; Hepatitis B virus ; immunology ; physiology ; Hepatitis B, Chronic ; immunology ; virology ; Humans ; Liver ; virology ; Male ; Virus Replication ; Young Adult

BACKGROUND/AIMS: The long-term virologic and biochemical changes in patients with HBeAg negative HBV infection, especially in Asia, remain unclear. To address this issue, we conducted a 3 year- retrospective, cohort study. METHODS: A total of 157 patients with HBeAg negative HBV infection who were monitored without treatment were reviewed between January 1999 and March 2004. Those patients were followed up every 3 months with liver function tests and serologic tests. All patients were stratified into 3 groups; inactive carrier (IC), viremic carrier (VC) and chronic hepatitis (CH). Serum HBV DNA was measured by a hybridization assay (sensitivity: 1.4 x 10(5) genomes/mL, Digene Diagnostics, Silver Spring, USA). RESULTS: The median age of enrolled patients was 42.7 years (M:F=2.3:1). By single time-point observations, the 3 year-cohort prevalence of HBeAg negative CH varied from 12.7 to 35.8% (median 20.7%) HBeAg negative CH was accumulated over time (P=0.002) and transition rates among three groups after 3 years of follow-up are as follows: IC to CH, 6.0%; IC to VC, 4.1%; VC to CH, 23.2%. VC seems to be a disease state in the middle of transition from IC to CH. CONCLUSIONS: We demonstrated the dynamic changing patterns of HBeAg negative CH with time, of which the change from IC or VC to CH was dominant.
Middle Aged ; Male ; Humans ; Hepatitis B, Chronic/*immunology/virology ; Hepatitis B e Antigens/*blood ; Female ; Carrier State/immunology ; Adult

<b>OBJECTIVEb>This review discusses progress in the studies of hepatitis B virus (HBV)/human immunodeficiency virus (HIV) coinfection and focuses on the interaction among HIV infection, chronic HBV infection, and host immunity.

<b>DATA SOURCESb>Data and studies published mainly from 2008 to 2011 were selected using PubMed.

<b>STUDY SELECTIONb>Original articles and critical reviews concerning HBV/HIV coinfection and HBV and HIV pathogenesis were selected.

<b>RESULTSb>HIV may accelerate HBV progression by lowering CD4 count, weakening HBV-specific immunity, "enriching" HBV mutants, causing immune activation, etc. On the other hand, HBV may enhance HIV replication by activating HIV long terminal repeat (LTR) with X protein (HBX) and cause immune activation in synergy with HIV. Paradoxically, HBV may also inhibit HIV dissemination via dendritic cells.

<b>CONCLUSIONSb>The interaction among HIV, HBV, and host immunity remains poorly understood. Further research is warranted to elucidate the detailed molecular mechanisms and to translate these mechanisms into clinical practice.

HIV ; pathogenicity ; HIV Infections ; immunology ; Hepatitis B virus ; pathogenicity ; Hepatitis B, Chronic ; virology ; Humans ; Immunity, Innate ; immunology

Animals ; Hepatitis B Surface Antigens ; blood ; genetics ; immunology ; Hepatitis B Vaccines ; immunology ; Hepatitis B, Chronic ; virology ; Humans ; Protein Precursors ; blood ; genetics ; immunology

<b>OBJECTIVEb>To study the relationship between liver pathological changes and serum HBeAg and HBV DNA in 1057 patients with chronic hepatitis B.

<b>METHODSb>Liver puncture biopsy for histopathological examinations were performed in 1057 patients with chronic hepatitis B. The quantitative analysis of serum HBV DNA by fluorogenic quantitative PCR and HBeAg by chemoluminescence were also conducted.

<b>RESULTSb>The inflammatory grade and fibrosis stage were higher in HBeAg-negative patients (G4 and S4 were 7.83% and 12.17% respectively) than in HBeAg-positive patients (G4 and S4 were 3.39% and 5.44% respectively). The inflammatory grade and fibrosis stage were higher in HBeAg-positive patients with low-level HBV DNA (G3G4 was 45.64% and S3S4 was 30.20% for HBV DNA104-105), whereas they were higher in HBeAg-negative patients with high-level HBV DNA (G3G4 was 54.55% for HBV DNA106-107 and S3S4 was 42.85% for HBV DNA108-109).

<b>CONCLUSIONb>There were some correlation between the liver pathological changes and serum HBeAg and HBV DNA levels in patients with chronic hepatitis B. It is important to perform the liver pathological examination and antiviral therapy as early as possible in patients with HBeAg-negative chronic hepatitis B.

DNA, Viral ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B virus ; genetics ; immunology ; Hepatitis B, Chronic ; blood ; pathology ; virology ; Humans ; Liver ; pathology ; virology

Antiviral Agents ; therapeutic use ; DNA, Viral ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B virus ; drug effects ; immunology ; Hepatitis B, Chronic ; drug therapy ; immunology ; virology ; Humans

<b>OBJECTIVEb>To explore the association between HBV genotyping and clinical characteristics and expression of TH1/TH2 cytokines.

<b>METHODSb>The expression of IL-4 and IFN-gamma was detected with flow cytometry for 102 HBV infections and 48 healthy controls. 50 CHB patients were randomly selected for HBV genotyping with real-time fluorescence PCR assay.

<b>RESULTSb>Higher expression of IL-4 in peripheral blood was detected in patients with HBV infection than healthy controls (P < 0.001); No significant differences on expression of Th1/Th2 cytokines were observed in CHB patients with different HBV DNA levels or HBeAg status (P > 0.05). There were 34 (68%) patients with genotype B infection and 16 (32%) with genotype C infection. Compared to patients with genotype B infection, the patients with genotype C infection showed higher levels of IL-4 (P = 0.018), and Th1/Th2 ratio decreased,but the difference was not statistically significant (P = 0.2262).

<b>CONCLUSIONb>The different expression of TH1/TH2 cytokines may elucidate cellular immune response and clinical outcome difference between patients with genotype B infection and genotype C infection.

Adult ; Female ; Genotype ; Hepatitis B virus ; genetics ; immunology ; Hepatitis B, Chronic ; immunology ; virology ; Humans ; Interferon-gamma ; biosynthesis ; Interleukin-4 ; biosynthesis ; Male ; Th1 Cells ; immunology ; Th2 Cells ; immunology