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

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

Hepatitis B ; immunology ; virology ; Hepatitis B Antibodies ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B virus ; immunology ; physiology ; Humans ; Immunologic Tests ; methods ; Virus Replication

Previously, we constructed a humanized antibody (HuS10) that binds to the common a antigenic determinant on the S protein of HBV. In this study, we evaluated its HBV-neutralizing activity in chimpanzees. A study chimpanzee was intravenously administered with a single dose of HuS10, followed by intravenous challenge with the adr subtype of HBV, while a control chimpanzee was only challenged with the virus. The result showed that the control chimpanzee was infected by the virus, and thus serum HBV surface antigen (HBsAg) became positive from the 14th to 20th week and actively acquired serum anti-HBc and anti-HBs antibodies appeared from the 19th and 23rd week, respectively. However, in the case of the study chimpanzee, serum HBsAg became positive from the 34th to 37th week, while actively acquired serum anti-HBc and anti-HBs antibodies appeared from the 37th and 40th week, respectively, indicating that HuS10 neutralized the virus in vivo and thus delayed the HBV infection. This novel humanized antibody will be useful in the immunoprophylaxis of HBV infection.
Animals ; CHO Cells ; Cricetinae ; Cricetulus ; Hepatitis B/blood/immunology/virology ; Hepatitis B Antibodies/blood/*immunology ; Hepatitis B Surface Antigens/*immunology ; Hepatitis B virus/*immunology ; Neutralization Tests ; Pan troglodytes/blood/*immunology/*virology

<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

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

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

<b>BACKGROUNDb>To serially observe the pathologic changes in livers of tree shrews and macaca assamensises infected with HHBV.

<b>METHODSb>10 adult tree shrews and 28 macaca assamensises were inoculated with HBV rich human sera. The liver of the animals were regularly biopsied. The liver samples were examined histopathologically by HE staining. Some samples were stained for HBsAg by immunohistochemistry (IH), and HBV DNA by in situ hybridization (ISH).

<b>RESULTSb>HBsAg in 80% of tree shrews infected with HHBV can be detected by IH, HBV DNA in 50% of those can be found by ISH.The positive rates of HBsAg in macaca assamensises' livers were 25% by IH, none HBV DNA was detected.

<b>CONCLUSIONb>The tree shrew model seems to be applicable for the research of human hepatitis B.

Animals ; Antibodies, Viral ; immunology ; Disease Models, Animal ; Female ; Hepatitis B ; immunology ; pathology ; virology ; Hepatitis B virus ; immunology ; physiology ; Humans ; Liver ; pathology ; virology ; Macaca ; Male ; Tupaiidae