Clinical and histological impact of previous hepatitis B virus infection in patients with chronic hepatitis C

Background: Recent reports suggest that hepatitis C virus (HCV) carriers with serological markers of prior hepatitis B virus (HBV) infection have more advanced liver fibrosis, irrespective of HBV‐DNA detection. Aims: We sought to assess the prevalence and impact of previous HBV infection in patients with HCV chronic infection. Methods: This cross‐sectional study included hepatitis B surface antigen‐ and human immunodeficiency virus‐negative subjects with positive HCV‐RNA. All patients had prior parenteral exposure as the probable source of HCV infection. Serum samples were tested for HBV‐DNA using a commercial assay. The METAVIR system was used for histological analysis. Results: One‐hundred and eleven patients were evaluated. Thirty‐one out of 111 patients (28%) tested positive for antihepatitis B core antigen (anti‐HBc). HBV‐DNA was not detected in any sample. Anti‐HBc‐positive patients showed higher histological grading, staging and a higher fibrosis progression rate. By multivariate analysis, anti‐HBc‐positivity was predictive of moderate to severe activity [odds ratio (OR)=3.532; P=0.032] and significant hepatic fibrosis (OR=3.364; P=0.017). After approximately 20 years of infection, advanced liver fibrosis (F3/F4) can be expected in 13% of anti‐HBc‐negative subjects who acquired HCV before the age of 30 and in 57% of those anti‐HBc‐positive patients who were infected by HCV after 30 years of age (P<0.001). Conclusion: Previous HBV infection is common among HCV carriers and may exert a negative impact on the natural history of HCV infection, independently of the presence of significant HBV replication.     

Hepatitis delta virus propagation enabled by hepatitis C virus—Scientifically intriguing,but is it relevant to clinical practice?

In vitro cell culture experiments and animal models have demonstrated that hepatitis delta virus (HDV) can theoretically propagate being enveloped by human pathogenic viruses other than hepatitis B virus (HBV), namely hepatitis C virus (HCV) and dengue virus. However, the clinical relevance of these findings and whether HDV replication occurs in real‐world hepatitis B surface antigen (HBsAg)–negative HCV patient cohorts remain unknown. To this aim, we analysed 323 HCV‐RNA–positive and HBsAg‐negative sera for the presence of HDV‐RNA and anti‐HDV antibodies (anti‐HDV). All 323 (100%) samples were negative for HDV‐RNA. Interestingly, 8/316 samples tested positive for anti‐HDV. The HBV serology of these eight patients showed a positive result for HBV core antibodies (anti‐HBc) indicating a seroconversion of an acute HBV infection in the past. None of the anti‐HBc–negative patients were positive for anti‐HDV. Our results indicate a distinctly low probability of replicative HDV infection in HCV mono‐infected patients in Germany. Current German clinical guidelines rightly recommend performing HDV screening only in HBsAg‐positive patients. However, larger studies on this subject should be performed in regions that are endemic for chronic HBV/HDV as well as HCV infections.     

Factors associated with isolated anti‐hepatitis B core antibody in HIV‐positive patients: impact of compromised immunity

Summary. In regions that are hyperendemic for chronic hepatitis B virus (HBV) infection, prevalence of and risk factors associated with isolated anti‐hepatitis B core antibody (anti‐HBc) in HIV‐positive patients are less well described. HIV‐positive patients who were tested for hepatitis B surface antigen (HBsAg), anti‐hepatitis B surface antibody (anti‐HBs) and anti‐HBc at designated hospitals for HIV care in Taiwan were included for analysis. HBV DNA was detected by real‐time polymerase chain reaction in patients with and without isolated anti‐HBc. Of 2351 HIV‐positive patients, 450 (19.1%) were HBsAg positive, 411 (17.5%) were anti‐HBc positive alone and 963 (41.0%) for both anti‐HBs and anti‐HBc. Compared with patients who were positive for both anti‐HBs and anti‐HBc, patients with isolated anti‐HBc were older, less likely to have anti‐hepatitis C virus antibody (anti‐HCV), had lower CD4 lymphocyte counts and higher plasma HIV RNA loads. Older age (adjusted odds ratio, 1.029; 95% confidence interval, 1.015–1.043) and CD4 <100 cells/μL (adjusted odds ratio, 1.524; 95% confidence interval, 1.025–2.265) were independently associated with isolated anti‐HBc by logistic regression, while presence of anti‐HCV and injecting drug use were not. HBV DNA was detectable in 8.3% of 277 patients with isolated anti‐HBc and 14.3% of 56 patients with both anti‐HBs and anti‐HBc (P = 0.160). In a country hyperendemic for HBV infection, HIV‐positive patients at older age and with CD4 <100 cells/μL were more likely to have isolated anti‐HBc, suggesting that compromised immunity plays a role in the presence of this marker.     

Influence of anti‐HBc seropositivity on the risk of hepatocellular carcinoma in HCV‐infected patients after adjusting for confounding factors

Summary. It is controversial whether past hepatitis B virus infection constitutes an additional risk of hepatocellular carcinoma (HCC) among patients with hepatitis C virus (HCV). The incidence of HCC between 1994 and 2004 was analysed among 1262 patients who were only positive for HCV. The cumulative incidence of HCC was assessed by Kaplan–Meier analysis and the difference between two groups was assessed by the log‐rank test. The effect of anti‐HBc positivity on the risk of HCC was assessed with multivariate Cox proportional analysis. Anti‐HBc was positive in 522 (41.4%) patients. The proportion of male patients (56.7 vs 46.8%, P < 0.001) and mean age (60.8 vs 56.9 years, P < 0.001) were significantly higher in the anti‐HBc positive group. HCC developed in 339 patients (mean follow‐up 7.0 years), with cumulative incidence rates at 3, 5 and 10 years of 12.7, 24.5 and 41.9% in the anti‐HBc positive group and 10.6, 17.7 and 33.4% in the negative group, respectively (P = 0.005). However, anti‐HBc seropositivity did not reach statistical significance in multivariate analysis including age and gender (hazard ratio, 1.06; 95% CI, 0.85–1.31; P = 0.63). Anti‐HBc positivity and HCC incidence were confounded by male gender and older age.     

HBV reactivation in patients with HCV/HBV cirrhosis on treatment with direct‐acting antivirals

Anecdotal reports suggest that patients with chronic hepatitis C virus (HCV) hepatitis and overt or occult hepatitis B virus (HBV) coinfection may reactivate HBV when HCV is suppressed or cleared by direct‐acting antivirals (DAAs). We assessed the prevalence of overt or previous HBV coinfection and the risk of HBV reactivation in patients with HCV cirrhosis treated with DAAs. This was a retrospective cohort of 104 consecutive patients with HCV cirrhosis treated with DAAs. Serum HCV‐RNA and HBV‐DNA were tested at weeks 4, 8 and 12 of DAAs therapy and at week 12 of follow‐up. At the start of DAAs, eight patients (7.7%) were HBsAg positive/HBeAg negative with undetectable HBV‐DNA and low levels of quantitative HBsAg (four on nucleos(t)ide analogues [NUCs] and four inactive carriers), 37 patients (35.6%) had markers of previous HBV infection (25 anti‐HBc positive, 12 anti‐HBc/anti‐HBs positive) and 59 (56.7%) had no evidence of HBV infection. Sixty‐seven patients (64.4%) were HCV‐RNA negative at week 4 and 98 (94.2%) achieved sustained virological response. All four HBsAg‐positive patients treated with NUCs remained HBV‐DNA negative, but three of four untreated patients showed an increase in HBV‐DNA of 2‐3 log without a biochemical flare and achieved HBV‐DNA suppression when given NUCs. During or after DAAs, by conventional assay, HBV‐DNA remained not detectable in all 37 anti‐HBc‐positive patients but in three of them (8.1%) HBV‐DNA became detectable with a highly sensitive PCR. HBV reactivation is likely to occur in untreated HBV/HCV‐coinfected cirrhotic patients when they undergo HCV treatment with DAAs. Pre‐emptive therapy with NUCs should be considered in this setting. Anti‐HBc‐positive patients rarely reactivate HBV without clinical or virological outcomes.     

Baseline hepatitis B core antibody predicts treatment response in chronic hepatitis B patients receiving long‐term entecavir

Studies regarding the clinical significance of quantitative hepatitis B core antibody (anti‐HBc) in patients with chronic hepatitis B receiving first‐line nucleos(t)ide analogues is limited. The aim of this study was to determine the performance of anti‐HBc as a predictor for hepatitis B e antigen (HBeAg) seroconversion in HBeAg‐positive CHB patients treated with entecavir. This was a retrospective cohort study consisting of 139 Chinese patients enrolled in a multicenter clinical trial treated with entecavir or entecavir maleate for up to 240 weeks. Anti‐HBc evaluation was conducted for all the available samples using a newly developed double‐sandwich anti‐HBc immunoassay. At week 240, 35 (25.2%) patients achieved a serological response (HBeAg seroconversion) and these patients at week 240 had significantly higher levels of anti‐HBc (P<.01). We defined 4.65 log₁₀ IU·mL^?1, with a maximum sum of sensitivity and specificity, as the optimal cut‐off value of baseline anti‐HBc level to predict seroconversion. Patients with baseline anti‐HBc ≥4.65 log₁₀ IU·mL^?1 had 28.0% (26/93) and 35.5% (33/93) chance of seroconversion at weeks 144 and 240, respectively. The baseline anti‐HBc level was the strongest predictor for seroconversion at week 144 (OR: 5.78, 95% confidence interval [CI]: 2.05‐16.34, P=.001). The baseline anti‐HBc level was a strong predictor for seroconversion at week 240 (OR: 5.36, 95% CI: 2.17‐13.25, P<.001). Hence, baseline anti‐HBc titre is a useful predictor of long‐term entecavir therapy efficacy in HBeAg‐positive CHB patients, which could be used to optimize antiviral therapy.     

De novo hepatitis B virus infection in hepatocellular carcinoma following eradication of hepatitis C virus by interferon therapy

Epidemiological studies have revealed that hepatocellular carcinoma (HCC) is still observed in hepatitis C virus (HCV)‐positive patients with a sustained response to interferon (IFN) treatment, although a substantial decrease in the incidence of hepatocellular carcinoma (HCC) has been achieved in those patients. Why HCC develops in patients who have a complete clearance of HCV remains unclear. Here, we provided evidence of latent hepatitis B virus (HBV) infection in an initially HCV‐positive chronic hepatitis patient who developed HCC after the complete eradication of HCV by IFN therapy. Although he was initially negative for anti‐hepatitis B surface antigen (HBsAg) or circulating HBV DNA but positive for anti‐hepatitis B core antigen (anti‐HBc) in his sera, he developed HBsAg and HBV DNA during the course of the management of a series of cancers. HBV DNA was detectable in the liver tissues before HBV reactivation and the viral sequences derived from his anti‐HBc‐positive liver showed 100% homology to that from the serum after HBsAg appearance. These findings indicates that HCV‐positive individuals who are positive for anti‐HBc in the absence of HBsAg could have latent HBV infection in their liver tissues and intrahepatic HBV infection may play a pivotal role in the development of HCC after the IFN‐mediated eradication of HCV.     

Meta‐analysis of the association between anti‐HBc seropositivity and a poor prognosis of chronic HCV infection

Aim: The impact of serological HBsAg? and anti‐HBc+ on the prognosis of chronic hepatitis C virus (HCV) infection is unknown. We conducted a systematic review to analyze whether anti‐HBc positivity imposes any effect on the course of HCV‐related chronic liver disease. Methods: We retrieved references from online databases that included PubMed and EMBASE. Data were gathered with regard to demographic information, disease progression and prognosis, and the results of serological tests. The development of hepatocellular carcinoma (HCC) was the endpoint of follow‐up of all cohort studies. Results: Eighteen references were included in this study, of which four were cohort studies. Twelve studies were retrospective, observational and non‐interventional studies. According to our meta‐analysis, the rate of serological HBsAg? and anti‐HBc+ was higher among HCC patients compared with non‐HCC patients (odds ratio [OR], 1.55; 95% CI, 1.22–1.98). HCV patients that were anti‐HBc+ had a greater chance of developing HCC than their anti‐HBc? counterparts (OR, 2.15; 95% CI, 1.34–3.47). Conclusions: The serological status of HBsAg? and anti‐HBc+ appears to be correlated with a poor prognosis for chronic HCV infection. Though the general quality of these references was low, and multiple confounding factors existed, the likelihood of a poorer outcome of HCV patients that are positive for anti‐HBc should be considered by their physicians.     

Seronegative hepatitis C virus infection in patients with lymphoproliferative disorders

It has been reported that hepatitis C virus (HCV) RNA may be present in serum and/or lymphoid cells in the absence of specific circulating antibodies. The current study analysed seronegative HCV infection in patients with lymphoproliferative disorders. We studied 77 anti‐HCV‐negative patients (45 male and 32 female, mean age 54.8 ± 14.2 years) with various lymphoproliferative disorders. HCV‐RNA was detected by RT‐PCR in plasma, peripheral blood mononuclear cells (PBMC) and bone marrow. Furthermore, the presence of viral nonstructural protein 3 (NS3) was determined in PBMC and bone marrow by immunostaining. HCV‐RNA was detectable in at least one compartment in 27 (35.1%) patients. Viral RNA was found in bone marrow in 22 patients (28.6%), in PBMC in 13 (16.9%) and in plasma in 10 (13%) patients. In nine patients, evidence of infection was confined to the bone marrow compartment. Viral load in HCV‐RNA‐positive plasma ranged from 15 to 1.17 × 10³ IU/mL. NS3 was detected in all but two HCV‐RNA‐positive bone marrow samples and in all but one HCV‐RNA‐positive PBMC samples. All 27 HCV‐RNA‐positive patients remained anti‐HCV‐negative when tested again after 6–12 months, but only four remained HCV‐RNA positive. In conclusion, among patients with lymphoproliferative disorders, HCV can be present in plasma, PBMC and bone marrow despite the lack of circulating specific antibodies. Further studies are required to analyse the phenomenon of seronegative infection and to determine whether such patients are infectious.     

Occult Hepatitis B Virus Infection in Japanese Chronic Hemodialysis Patients

We investigated the prevalence of occult hepatitis B virus (HBV) infection in Japanese chronic hemodialysis patients. Hemodialysis patients (n = 1041) were screened for occult HBV. The presence of hepatitis B surface antigen (HBsAg), hepatitis B surface antibody, and hepatitis B core antibody (anti‐HBc) was determined by various chemiluminescent immunoassays. HBV‐DNA was quantified in patients positive for anti‐HBc using quantitative real‐time polymerase chain reaction. Among the 1041 patients, six (0.6%) were HBsAg‐positive and 218 (20.9%) were anti‐HBc‐positive. All HBsAg‐positive patients also tested positive for the presence of HBV DNA. Of 212 HBsAg‐negative and anti‐HBc‐positive patients, three were positive for HBV DNA. Our study showed that the prevalence of occult HBV infection in chronic hemodialysis patients from eastern Japan was 0.3%.     

Effect of immunosuppressive therapy on patients with inflammatory bowel diseases and hepatitis B or C virus infection

Viral hepatitis reactivation has been widely reported in patients undergoing immunosuppressive therapy; however, few data are available about the risk of HBV and HCV reactivation in patients with inflammatory bowel disease, receiving immunosuppressive drugs. The aim of our study was to assess the prevalence of HBV and HCV infection in a consecutive series of patients with inflammatory bowel disease and to value the effects of immunosuppressive therapy during the course of the infection. Retrospective observational multicenter study included all consecutive patients with inflammatory bowel disease who have attended seven Italian tertiary referral hospitals in the last decade. A total of 5096 patients were consecutively included: 2485 Crohn's disease and 2611 Ulcerative Colitis. 30.5% and 29.7% of the patients were investigated for HBV and HCV infection. A total of 30 HBsAg positive, 17 isolated anti‐HBc and 60 anti‐HCV‐positive patients were identified. In all, 20 patients with HBV or HCV infection received immunosuppressive therapy (six HBsAg+; four isolated anti‐HBc+ and 10 anti‐HCV+). One of six patients showed HBsAg+ and one of four isolated anti‐HBc+ experienced reactivation of hepatitis. Two of six HBsAg patients received prophylactic therapy with lamivudine. Only one of 10 anti‐HCV+ patients showed mild increase in viral load and ALT elevation. Screening procedures for HBV and HCV infection at diagnosis have been underused in patients with inflammatory bowel disease. We confirm the role of immunosuppressive therapy in HBV reactivation, but the impact on clinical course seems to be less relevant than previous reported.     

High rates of active hepatitis B and C co-infections in HIV-1 infected Cameroonian adults initiating antiretroviral therapy

Objectives

To investigate the presence of hepatitis B virus (HBV) DNA and hepatitis C virus (HCV) RNA in HIV‐infected patients initiating antiretroviral therapy in Cameroon.

Methods

Baseline blood samples from 169 patients were tested retrospectively for hepatitis B surface antigens (HBsAg), anti‐hepatitis B core (anti‐HBc), anti‐HCV and – if HBsAg or anti‐HCV result was positive or indeterminate – for HBV DNA or HCV RNA, respectively, using the Cobas Ampliprep/Cobas TaqMan quantitative assay (Roche Diagnostics GmbH, Mannheim, Germany).

Results

HBV DNA was detected in 14 of the 18 patients with positive or indeterminate HBsAg results [8.3% of the total study population, 95% confidence interval (CI) 4.6–13.5]. The median HBV viral load was 2.47 × 10⁷ IU/mL [interquartile range (IQR) 3680–1.59 × 10⁸; range 270 to >2.2 × 10⁸]. Twenty‐one patients (12.4%, 95% CI 7.9–18.4) were found with HCV RNA (all with positive HCV serology). The median HCV viral load was 928 000 IU/mL (IQR 178 400–2.06 × 10⁶; range 640–5.5 × 10⁶). No patient was co‐infected with HBV and HCV. In multivariate analysis, HCV co‐infection was associated with greater age [≥45 years vs. <45 years, odds ratio (OR) 11.89, 95% CI 3.49–40.55, P<0.001] and abnormal serum alanine aminotransferase level [≥1.25 × upper limit of normal (ULN) vs. <1.25 × ULN, OR 7.81, 95% CI 1.54–39.66, P=0.01]; HBV co‐infection was associated with abnormal serum aspartate aminotransferase level (OR 4.33, 95% CI 1.32–14.17, P=0.02).

Conclusions

These high rates of active HBV and HCV co‐infections in HIV‐positive Cameroonian patients requiring antiretroviral therapy underline the need to promote: (i) screening for HBV and HCV before treatment initiation; (ii) accessibility to tenofovir (especially in HBV‐endemic African countries); and (iii) accessibility to treatment for HBV and HCV infections.     

Prevalence of seromarkers of HBV and HCV among blood donors in eastern Saudi Arabia, 1998–2001

The prevalence of serological markers of HBV and HCV were determined for blood donors in eastern Saudi Arabia. Between 1998 and 2001, 13 443 donors (10 778 Saudi and 2665 non‐Saudi), were screened for HBsAg, anti‐HBc Ab, and anti‐HCV Ab using commercial kits. There was a steady decrease in the HBsAg (2.58 and 1.67%), anti‐HBc rates (15.32 and 9.15%), and anti‐HCV (1.04 and 0.59%) rates between 1998 and 2001, respectively. However, there was a marked difference between Saudi and non‐Saudi donors with regard to anti‐HBc (P < 0.001) and anti‐HCV (P < 0.01), but not HBsAg prevalence rates in the same time period.     

T‐ and B‐cell responses and previous exposure to hepatitis B virus in ‘anti‐HBc alone’ patients

A serologic response to hepatitis B virus (HBV) defined as ‘anti‐HBc alone’ is commonly observed, but its significance remains unclear. This study aimed to define the relationship between ‘anti‐HBc alone’ serostatus and HBV infection, including HBV‐specific T‐ and B‐cell memory responses. We enrolled 31 ‘anti‐HBc alone’ patients. Total HBV DNA and cccDNA were tested by nested polymerase chain reaction (PCR) analysis in liver samples from 22 ‘anti‐HBc alone’ patients vs controls (chronic or resolved HBV infection), followed by HBsAg/HBcAg immunohistochemical (IHC) staining. IFN‐γ secretion by HBV‐specific T cells was compared in individuals who were ‘anti‐HBc alone’ (n = 27), resolved HBV (n = 21), chronic HBV (n = 24) and 12 healthy controls using enzyme‐linked immunospot (ELISpot) assays. An HBsAg‐IgG B‐cell ELISpot assay was performed in ‘anti‐HBc alone’ patients before and after one dose of recombinant HBsAg vaccine. The majority (23/31, 74.2%) of the ‘anti‐HBc alone’ individuals were co‐infected with HCV. Infrequent intrahepatic total HBV DNA (2/22, 9.1%) and cccDNA (1/22, 4.5%) were detected in biopsies; HBsAg and HBcAg IHC staining was negative. HBV‐specific T‐cell responses were similar between ‘anti‐HBc alone’ individuals and HBV resolvers. Circulating HBV‐memory B‐cell responses were detected in all ‘anti‐HBc alone’ individuals, consistent with an HBsAg‐specific memory pool. After one HBV vaccine dose, increased anti‐HBs antibody levels were observed, accompanied by an expansion of HBsAg‐specific memory B cells (P = 0.0226). ‘Anti‐HBc alone’ individuals showed HBV‐specific T‐cell and memory B‐cell responses typical of previous viral exposure and protective memory, suggesting a resolved infection.     

Fatal outcome of a hepatitis B virus transfusion‐transmitted infection

Background and Objectives In 2008, hepatitis B virus (HBV) DNA testing was not yet mandatory for the screening of blood donations in Switzerland. At that time, HBsAg was the only specific mandatory marker for HBV. The importance of high sensitivity for HBV NAT screening is shown. Materials and Methods Donor and recipient of a transfusion‐transmitted HBV infection were followed up. Multiple samples were tested for HBV serological and molecular markers. Results At donation, the donor appeared healthy, HBsAg was negative and had a normal ALAT level. Ten weeks later, clinical symptoms suggested acute HBV infection as was confirmed with positive HBsAg, HBeAg, anti‐HBc IgG, anti‐HBc IgM and anti‐HBe. The archived sample from the original donation was negative for anti‐HBc, but positive for HBV DNA (17 IU/ml). A recipient transfused with the red cell concentrate was HBV DNA positive (3100 IU/ml) 3 months post‐transfusion. After five months, HBsAg, HBeAg, anti‐HBc and HBV DNA (1·1 × 10¹¹ IU/ml) were positive. Two weeks later, the patient died from complications associated with HBV infection and his underlying bone marrow disease. Conclusions The present case illustrates the importance of introducing highly sensitive HBV NAT screening strategy to prevent possible HBV transfusion‐transmitted infections from donors with low viral load.     

Reduction of the risk of transfusion‐transmitted viral infection by nucleic acid amplification testing in the Western Cape of South Africa: a 5‐year review

Background and Objectives In October 2005, individual donation nucleic acid amplification testing (ID‐NAT) for HIV, HBV and HCV was introduced in the Western Cape Province of South Africa. After 5 years, the impact on HIV, HBV and HCV transmission risk was assessed. Materials and Methods A total of 649 745 donations were tested by ID‐NAT using the Ultrio assay on the Tigris instrument (Novartis Diagnostics) and for anti‐HIV, HBsAg and anti‐HCV (Abbott Prism). Initial reactive samples were repeated in duplicate. Discrepant repeat reactive samples were subjected to confirmatory assays. ID‐NAT nonrepeat reactive donations were further screened for occult HBV infection (OBI) by anti‐HBc assay. Results ID‐NAT yielded 6 HIV‐RNA‐positive donations in the anti‐HIV‐negative window period (WP) but only 2 were p24 Ag nonreactive (1:325 000). Mathematical modelling estimated a similar HIV transmission risk for lapsed and repeat donations, in the order of 3 per million. The WP risk for HBV was 13 per million. Eight acute (1:81 000) and 13 chronic OBI yield cases (1:50 000) were interdicted. There were significantly more anti‐HBc‐positive donors in the Ultrio initial reactive/nonrepeat reactive group (12%) than in an Ultrio nonreactive control group (6%). Conclusion ID‐NAT in the Western Cape Province of South Africa has contributed significantly to enhancing blood safety, particularly for HBV transmission risk and to a lesser extent for HIV. Anti‐HBc testing of NAT nonrepeat reactive donations seems useful in identifying a subgroup of donors with OBI who may be at risk of transmitting HBV.     

Acquirement and disappearance of HBsAg and anti‐HCV in an aged population: a follow‐up study in an endemic township

Background: HBsAg and anti‐hepatitis C virus (anti‐HCV) are stable markers and widely used. The seroconversion and seroclearance of HBsAg and anti‐HCV are important for disease control and prognosis of diseases. Aims: To investigate acquirement and disappearance of HBsAg and anti‐HCV in an endemic area. Methods: Seven years after a community screening, 1002 of 2909 residents of Tzukuan Township were recruited. HBsAg, anti‐HCV and alanine transaminase (ALT) were checked in all who participated and hepatitis B virus (HBV) DNA, anti‐HBs, anti‐HBc, HCV RNA, anti‐HDV and upper abdominal ultrasonography were studied in different groups. Results: There were 461 male and 541 female residents with a mean age of 66.7±8.6 years. No new HBsAg carrier was noted and the HBsAg clearance rate was 1.58% per year. One of the 17 cases with HBsAg clearance had positive HBV DNA, three had ALT elevation, two had cirrhosis and seven had anti‐HBs seroconversion. Quantitative of HBsAg and HBV DNA were concordant and 78.1% subjects had low levels of titration. Anti‐HBc alone contributed to 32.1% and was prominent in old age and the anti‐HCV‐positive group. The anti‐HCV seroconversion rate was only 0.74% per year and household transmission was the only risk factor. Only 37.5% of cases with anti‐HCV seroconversion had HCV viraemia and the anti‐HCV seroreversion rate was 0.63% per year. The anti‐HDV seroconversion rate was 0.72% per year and no subject showed anti‐HDV clearance. Conclusions: Much higher rates of HBsAg seroclearance, anti‐HCV seroreversion and anti‐HBc alone were noted in this endemic area and no subject showed anti‐HDV clearance.     

Significant background rates of HBV and HCV infections in patients and risks of blood transfusion from donors with low anti-HBc titres or high anti-HBc titres with high anti-HBs titres in Japan: a prospective, individual NAT study of transfusion-transmitted HBV, HCV and HIV infections

Background The Japanese Red Cross (JRC) conducted a prospective study to evaluate the frequency of transfusion‐transmitted HBV, HCV and HIV infections to assess the risk of transfusion of blood components routinely supplied to hospitals. Study Design and Methods Post‐transfusion specimens from patients at eight medical institutes were examined for evidence of infection with HBV (2139 cases), HCV (2091) and HIV (2040) using individual nucleic acid amplification testing (NAT). If these specimens were reactive, pre‐transfusion specimens were also examined for the virus concerned by individual NAT. In the event that the pre‐transfusion specimen was non‐reactive, then all repository specimens from implicated donors were tested for the viruses by individual donation NAT. In addition, a further study was carried out to evaluate the risk of transfusion of components from donors with low anti‐HBc titres or high anti‐HBc with high anti‐HBs titres. Results Transfusion‐transmitted HCV and HIV infections were not observed. One case of post‐transfusion HBV infection was identified (rate, 0·0004675; 95% CI for the risk of transmission, 1 in 451–41 841). The background rates of HBV, HCV and HIV infections in patients prior to transfusion were 3·4% (72/2139), 7·2% (150/2091) and 0% (0/2040), respectively. Sixty‐four anti‐HBc‐ and/or anti‐HBs‐reactive blood components were transfused to 52 patients non‐reactive for anti‐HBc or anti‐HBs before and after transfusion (rate, 0; 95% CI for the risk of transmission, <1 in 22). Conclusion This study demonstrated that the current criteria employed by JRC have a low risk, but the background rates of HBV and HCV infections in Japanese patients are significant.     

Prevalence of occult hepatitis B & C in HIV patients infected through sexual transmission.

BACKGROUND: Prevalence of Hepatitis B virus (HBV) and Hepatitis C virus (HCV) markers including active and occult infection has not been described in diverse cohorts among HIV-infected patients in India. Earlier studies have explained the role of HBV/HCV co-infection in cohorts of injection drug users (IDUs) but the sexual co-transmission of HBV/ HCV is not completely understood. OBJECTIVE: The objective of this study was to assess the prevalence of occult HBV & HCV infection in HIV positive sexually acquired transmission risk group. MATERIALS AND METHODS: 58 sexually acquired HIV positive patients were taken up for the study of occult HBV/HCV co-infection. Data on demographics, sexual behaviour, sexually transmitted diseases (STD), medical history, laboratory tests viz., serum ALT and CD4 count were recorded. HBV serology included HBsAg, anti HBs, IgG anti HBc and HBV DNA (PCR). HCV serology included anti HCV & HCV RNA (RT-PCR). RESULTS: Occult HBV infection (HBV DNA) was observed in 12.2% (7/58 with HBsAg -ve and IgG anti HBc +ve subjects) while an overall prevalence of HBV DNA was 13.7% (12% occult & 1.7% in HBsAg+ve patients). Out of 58 HIV positive patients 29.3% demonstrated reactivity for any marker of past or current HBV infection. (HBsAg 1.7%, anti HBs 10.3% anti HBc IgG 17.2%). 4/58 (6.8%) revealed anti HCV positivity along with HCV RNA positivity by RT-PCR while 6/58 (10.3%) individuals revealed an occult HCV infection (anti HCV negative). The overall HCV RNA prevalence was 17.2%. 2 out of 58 (3.4%) individuals were positive for occult infection of both HBV DNA & HCV RNA (Triple infection HIV/HBV/ HCV). The HBV/HCV co-infected group (n = 18) showed a significantly high ALT (114.3 + 12.3 U/I) & low CD4 count (202.5 + 33.7 cells/mm3). The percent prevalence of HBV/ HCV co-infection was higher in the illiterate group, in men less than 30 years of age, and in those who were married and exhibited polygamous activity. CONCLUSIONS: The study demonstrated that in HIV infected patients testing only serological viral markers like HBsAg, antiHBcIgG & anti HCV, fails to identify the true prevalence of co-infection with HBV & HCV. Qualitative PCR for HBV DNA & HCV RNA detects co-infection in patients who are negative for serological markers. Also, in subjects who had only a sexual risk factor for parenterally transmitted infections, HIV may enhance the sexual transmission of HBV and HCV.