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Hepatitis B virus (HBV) is global health problem. Family members of HBV infected people are considered as high-risk groups due to frequent household transmission of HBV among contacts of HBsAg carriers. The present study aimed to investigate the intrafamilial transmission of HBV among family members of HBV-infected persons and to identify the risk factors for viral transmission in these setting. 361 index cases and their 1083 family contacts were tested for markers of Hepatitis B, viz. HBsAg and HBcAb using commercial ELISA. The demographic details and risk factors for acquiring HBV infection among the family members were recorded using a structured questionnaire. The median (IQR) age of index cases and family members was 37 (27 − 48) and 26 (14 − 38) years, respectively. Among the screened family members, 9.23% (n = 100) members were positive for HBsAg and 32.75% (n = 355) were positive for HBcAb. At least one member of the family was affected in 229/361 (63.43%) index cases. Significantly lower percent of household contacts (9.23%, n = 100)were vaccinated against HBV.HBV transmission risk was significantly higher in families with more than four members(p < 0.0001). Multinomial logistics regression analysis for familial risk factors for transmission of HBV such asclose contact with carrier (aOR overt: 1.172, aOR occult: 1.173), sharing of bed/bedding (aOR overt: 1.258, aOR occult:1.264), personal hygiene items (aOR overt:1.260, aOR occult: 1.451), and eating in common utensils (aOR overt: 2.182, aOR occult: 1.307)were significantly associated with the transmission of HBV (p < 0.05). Close contact with carrier, sharing of bed/bedding or personal hygiene items and eating in common utensils were significantly associated with the transmission of HBV. Increasing awareness about Hepatitis B infection and vaccination of family members in close contact with carrier is essential to prevent Hepatitis B transmission. [ABSTRACT FROM AUTHOR]

Occult hepatitis B (OBI) and C (OCI) infections lead to hepatic crises including cases of liver cirrhosis and even hepatocellular carcinoma (HCC). OBI and OCI also pose a significant problem of their transmissibility. This study aimed to assess the overall prevalence of OBI and OCI in the African continent, a region highly endemic for classical hepatitis B and C viruses. For this systematic review and meta-analysis, we searched: PubMed, Web of Science, African Journal Online and African Index Medicus for published studies on the prevalence of OBI and OCI in Africa. Study selection and data extraction were performed by at least two independent investigators. Heterogeneity (I²) was assessed using the χ² test on the Cochran Q statistic and H parameters. Sources of heterogeneity were explored by subgroup analyses. This study was registered in PROSPERO, with reference number CRD42021252772. We obtained 157 prevalence data for this meta-analysis, from 134 studies for OBI prevalence; 23 studies on OCI prevalence, and a single study on the OBI case fatality rate. The overall estimate for the prevalence of OBI was 14.8% [95% CI = 12.2–17.7] among 18579 participants. The prevalence of seronegative OBI and seropositive OBI was 7.4% [95% CI = 3.8–11.8] and 20.0% [95% CI = 15.3–25.1] respectively. The overall estimate for the prevalence of OCI was 10.7% [95% CI = 6.6–15.4] among 2865 participants. The pooled prevalence of seronegative OCI was estimated at 10.7% [95%CI = 4.8–18.3] and that of seropositive OCI at 14.4% [95%CI = 5.2–22.1]. In Sub-group analysis, patients with malignancies, chronic hepatitis C, and hemodialysis had a higher OCI prevalence. While those with malignancies, liver disorders, and HIV positive registered highest OBI prevalence. This review shows a high prevalence of OBI and OCI in Africa, with variable prevalence between countries and population groups. [ABSTRACT FROM AUTHOR]

Occult hepatitis B infection (OBI) refers to a condition where replication-competent HBV DNA is present in the liver, with or without HBV DNA in the blood, in individuals with serum HBsAg negativity assessed by currently available assays. The episomal covalently closed circular DNA (cccDNA) in OBI is in a low replicative state. Viral gene expression is mediated by epigenetic control of HBV transcription, including the HBV CpG island methylation pathway and post-translational modification of cccDNA-bound histone, with a different pattern from patients with chronic HBV infection. The prevalence of OBI varies tremendously across patient populations owing to numerous factors, such as geographic location, assay characteristics, host immune response, coinfection with other viruses, and vaccination status. Apart from the risk of viral reactivation upon immunosuppression and the risk of transmission of HBV, OBI has been implicated in hepatocellular carcinoma (HCC) development in patients with chronic HCV infection, those with cryptogenic or known liver disease, and in patients with HBsAg seroclearance after chronic HBV infection. An increasing number of prospective studies and meta-analyses have reported a higher incidence of HCC in patients with HCV and OBI, as well as more advanced tumour histological grades and earlier age of HCC diagnosis, compared with patients without OBI. The proposed pathogenetic mechanisms of OBI-related HCC include the influence of HBV DNA integration on the hepatocyte cell cycle, the production of pro-oncogenic proteins (HBx protein and mutated surface proteins), and persistent low-grade necroinflammation (contributing to the development of fibrosis and cirrhosis). There remain uncertainties about exactly how, and in what order, these mechanisms drive the development of tumours in patients with OBI. [ABSTRACT FROM AUTHOR]

• Gaps remain in detection of early acute, late acute, and occult HBV infection. • A new Abbott ARCHITECT/Alinity HBsAg assay improves detection of HBV infection. • The new assay improved detection of early acute HBV by 36.4%. • The new assay detected late acute HBV infection longer than current assays. • The new HBsAg assay increased detection of occult HBV by 10.9%. Hepatitis B surface antigen (HBsAg) is the primary marker for diagnosis of acute and chronic hepatitis B. Although HBsAg assays have undergone continuous improvement, gaps remain in the detection of early and late acute infection and occult hepatitis B infection (OBI). The performance of a prototype, improved sensitivity HBsAg assay run on the ARCHITECT and Alinity instruments was evaluated for detection of early and late acute infection and OBI. Seventy seven early acute samples [positive only for hepatitis B viral DNA (HBV DNA)], twelve seroconversion panels spanning late acute infection, and 101 occult samples (HBsAg negative, positive for HBV DNA and anti-HBc) were tested with the prototype assay and ARCHITECT HBsAg Qualitative II. HBsAg gene sequencing was performed to determine genotype and mutations in the immunodominant region. Compared with ARCHITECT HBsAg Qualitative II, the prototype assay showed increased detection of NAT yield samples (28/77, 36.4%,), late acute samples (≥13 days longer detection of HBsAg for 6/12 panels), and OBI samples (11/101, 10.9%). HBsAg sequence data were obtained for 62 samples. Genotypes represented were A1, A2, B2, B4, C1, C2, C5, D3, E, and H. HBsAg escape mutations were found in 4.8% of NAT yield and 38.9% of OBI samples sequenced. Prototype assay values for 188 samples were equivalent on the ARCHITECT and Alinity instruments. The new prototype HBsAg assay will be of diagnostic value in providing improved detection of early acute, late acute, and occult HBV infections. [ABSTRACT FROM AUTHOR]

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Background and study aims Occult hepatitis B infection (OBI) is known to be mostly prevalent in chronic hepatitis C (CHC) patients and OBI reactivation might be life-threatening in patients undergoing interferon (IFN)-free direct acting antiviral (DAA) therapy. As previous studies have revealed a relationship between OBI and non-response to IFN-based antiviral therapy, the aim of the current study was to determine if there was a higher prevalence of OBI in IFN non-responders than responders. Patients and Methods This retrospective cross-sectional study was conducted in CHC patients who had previously received IFN-based antiviral therapy. Serum samples of 100 HBsAg negative CHC patients were tested for HBV DNA, anti-HBc IgG, anti-HBs, ALT and AST. The presence of OBI was compared between 50 IFN responders and 50 IFN non-responders. Patients with a history of previous HBV infection, patients with evidence of cirrhosis and patients who had received IFN therapy within the last one year were excluded from the study. Results Anti-HBc IgG positivity was determined in 53% of the patients. HBV DNA positivity, indicating OBI was determined in 1 (1%) patient. This patient was anti-HBc IgG positive, anti-HBs negative, ALT and AST levels were normal. The HBV DNA and anti-HBc IgG positivity rates were higher in the non-responder group than in the responder group, but the difference was not statistically significant ( p  = 0.31 and p  = 0.07 respectively). Conclusion According to the results of this study, the prevalence of OBI is lower than expected amongst CHC patients in Turkey and it may not be necessary to apply routine screening to IFN non-responders for OBI infection before DAA therapy. However, there is a need for multicentre studies with larger patient series. [ABSTRACT FROM AUTHOR]

Background/purpose: Occult hepatitis B infection (OHB) is not rare in countries that are endemic for hepatitis B virus (HBV) and in patients with chronic hepatitis C virus (HCV) infection. Notably, OHB has been shown to play a role in the progression of liver diseases, including the development of hepatocellular carcinoma (HCC); however, the data is inconsistent. We aim to clarify the contribution of concurrent OHB to the progression of liver diseases in a long-term cohort of patients with HCV infection and to investigate the value of total anti-hepatitis B core (anti-HBc) antibody as a surrogate OHB biomarker.Methods: We included 250 chronic anti-HCV-positive patients who had resolved HBV infection (anti-HBc positive and hepatitis B surface antigen negative). OHB was then detected using a sensitive commercial assay for serum HBV DNA with a low limit of detection of 6 IU/mL. Clinical outcomes, including the development of liver cirrhosis, HCC, and all-cause deaths, were compared between OHB-positive and OHB-negative patients.Results: At baseline, only 183 (73.20%) patients had positive HCV ribonucleic acid, and 56 (30.60%) of these 183 patients with active HCV infection had OHB. The presence of OHB did not correlate with any adverse clinical outcome in multivariate analyses. In addition, chronic hepatitis C patients with OHB did not have a higher level of serum total anti-HBc.Conclusion: OHB infection may not contribute to the development of adverse liver outcomes in patients with chronic HCV. [ABSTRACT FROM AUTHOR]

• Hepatitis B surface antigen seroclearance (SC) is regarded as functional cure of chronic hepatitis B infection. • Highly sensitive assays used in this study detected hepatitis B virus (HBV) surface and core-related antigens in >70% patients with SC. • This study reiterates the potential of using sensitive HBV antigen detection assays to detect low levels of viral activity in patients with SC or patients with occult hepatitis B infection. • Correlation between low levels of HBV antigens and disease progression deserved further investigations. This study aimed to evaluate the usefulness of two novel assays, namely the iTACT-hepatitis B surface antigen (iTACT-HBsAg) and iTACT-hepatitis B core-related antigen (iTACT-HBcrAg) assays, in chronic hepatitis B (CHB) patients with HBsAg seroclearance (SC) documented by standard assays. HBsAg and HBcrAg were measured by the two iTACT-assays in 556 serial sera collected from 96 CHB patients at 7 different time points spanning from 5 years before to 10 years after SC and 120 HBsAg-negative, anti-HBc-positive individuals. As controls, 60 seronegative individuals, who were negative for HBsAg, anti-HBc and anti-HBs, were tested. Using the iTACT-assays, HBsAg was detectable in 154/418 (36.8%) samples collected after SC. HBcrAg was detectable in 78.3% and 65.9% of samples collected before and after SC, respectively. The detectability rates of both HBsAg and HBcrAg progressively decreased over time after SC. At 10 years after SC, 20.4% and 64.5% of the patients still had detectable HBsAg and HBcrAg, respectively. 66 (71%) patients had detectable HBsAg and/or HBcrAg. Among the 120 HBsAg-negative, anti-HBc-positive individuals, 11 (9.2%) and 4 (3.3%) had detectable HBsAg and HBcrAg respectively. Both HBsAg and HBcrAg were undetectable in the controls. The iTACT assays detected a low level of HBsAg and/or HBcrAg in >70% of patients even at 10 years after SC, suggesting that CHB patients with SC still harbour a low level of HBV protein expression. The clinical significance of detectable viral proteins after SC with regard to disease progression and HBV reactivation deserves further investigations. [ABSTRACT FROM AUTHOR]

Hepatitis B virus (HBV) infection plays a major role in hepatocellular carcinoma (HCC) development. Much evidence suggests that HBV also maintains its pro-oncogenic properties in cases of occult HBV infection (OBI). Mutations of the beta-catenin and p53 genes ( CTNNB1 and TP53 , respectively) may be associated with HCC occurrence in patients with overt HBV infection, whereas such genetic mutations have not been investigated in HCC patients with OBI thus far. We investigated the genetic heterogeneity of CTNNB1 exon 3 and all of the TP53 exons in tumor DNA extracts from a unique cohort of 61 HCC patients (all previously tested for HBV DNA and for its integration into the host's genome), including 34 OBI-positive, 20 HBV surface antigen (HBsAg)/OBI-negative, and 7 HBsAg-positive cases. No CTNNB1 exon 3 mutations or TP53 mutations were detected in any case. The homo- or heterozygous TP53 R72P polymorphism was found in 18 of 61 cases (29.5%), although no differences in its prevalence between OBI and non-OBI cases as well as between cases with and without viral integration were revealed. In conclusion, CTNNB1 and TP53 somatic mutations seem to be a rare event in patients with HCC in our area and in cases with either overt or occult HBV infection. [ABSTRACT FROM AUTHOR]

Viral and host factors leading to occult hepatitis B virus (HBV) infection (OBI) are not fully understood. Whether HBV genotype may influence the occurrence and course of OBIs is unknown. Here, we describe the case of a patient infected with HBV genotype A2 who developed symptomatic acute hepatitis and did not seroconvert after loss of HBsAg and HBeAg. The acute phase of hepatitis B was followed by a period of more than 2 years during which the DNA of an intergenotypic HBV/A2/G recombinant was intermittently detected in serum. [ABSTRACT FROM AUTHOR]

Abstract: Background: The diagnosis of hepatitis B is routinely based on the detection of hepatitis B surface antigen (HBsAg) only. However, occult hepatitis B virus (HBV) infection (OBI), which is defined as infection with positive hepatitis B core antibody (anti-HBc) antibodies, positive DNA (deoxyribonucleic acid) PCR (polymerase chain reaction), and undetectable HBsAg, as well as anti-HBs antibodies in serum or plasma of HBV infected individuals, will remain undetected using this screening diagnostic approach of detecting HBsAg. The current study aims in studying the prevalence of the OBI amongst human immunodeficiency virus type 1 (HIV-1) infected individuals who have not been exposed to anti-retroviral therapy. Method: Estimation of HBsAg, anti-HBs, and anti-HBc total antibody status amongst 100 HIV-1 infected study participants was carried out using enzyme-linked immunosorbent assay (ELISA) kits. Detection of HBV-DNA was carried out by in-house qualitative PCR. CD4 + T lymphocyte counts were analysed using Becton Dickinson''s (BD) FACSCount™ system. Results: The median age of the HIV-1 infected study population was 35 years (range: 22-67), with the gender distribution being 53 males and 47 females. The mean CD4 T lymphocyte count of the study participants was 210/mm3. Overall, serological evidence of HBV infection was observed in 28% of the HIV-1 infected study participants. There was 5% seropositivity for HBsAg, of which 2% were additionally positive for HBV-DNA-PCR. “Anti-HBc alone” status was seen in 18% of study participants, this being statistically higher in those with CD4 T lymphocyte counts < 200/mm3. While there was a single specimen with co-positivity for anti-HBc total antibodies and HBV-DNA, 5% of the in the study population exhibited anti-HBs antibodies positivity, with one sample exhibiting dual positivity for HBsAg and anti-HBs antibodies. Conclusion: Occult HBV infections may contribute to chronic liver damage, and associ-ated reactivation amongst immunocompromised individuals, HIV-1 in-fected being a subset of them. “Anti-HBc” testing followed by HBV-DNA detection by PCR can be utilised for such populations to detect OBIs. Early detection of hepatitis B viraemia will be important for deciding the antiviral therapeutic protocol so as to avoid evolution of antiviral resistance in the circulating HBV strains in HIV-1 infected individuals harbouring OBIs. [Copyright &y& Elsevier]

Abstract: Background: Occult HBV infection is defined by detection of HBV DNA in the serum or liver tissue of patients who test negative for HBsAg. The prevalence of occult HBV is higher in hepatitis C virus (HCV) positive patients than HCV negative patients and may have an impact on their clinical outcome. In this study, we evaluated the role of occult hepatitis B virus infection in chronic hepatitis C patients with ALT flare. Methods: Sixty HBsAg negative patients with chronic hepatitis C virus infection were included. Patients were divided into 2 groups according to their ALT level: 30 patients with normal or slightly high ALT and 30 patients with ALT flare (≥5 times normal values). Patients in both groups were examined for the detection of anti-HBs, anti-HBc IgM, and anti-HBc IgG. HBV DNA was detected using semi-nested PCR technique. Results: In patients with normal or slightly high ALT, HBV DNA was detected in 4 (13.3%) patients, while in those with ALT flare, HBV DNA was detected in 19 (63.3%) patients (p<0.001). No association was found between the presence of HBV DNA and various serology markers of HBV infection. Conclusion: Presence of occult hepatitis B, with its added deleterious effect, must always be considered in chronic hepatitis C patients especially those with flare in liver enzymes; HBsAg should not be used alone for the diagnosis of HBV infection. [Copyright &y& Elsevier]

Background/Aims: It has been suggested that, in HIV–HCV co-infected patients, co-infections with other viruses may affect the response to HCV therapy. We aimed to assess the prevalence of GBV-C, SEN-V and occult HBV infections, their impact on HCV and HIV infections and on the response to HCV therapy in HIV–HCV co-infected patients. Methods: Three-hundred and sixty eight patients were tested before starting interferon–ribavirin for the presence of occult hepatitis B DNA, GBV-C RNA and SEN-V DNA by using real time PCR. Clinical, immunological, virological, histological characteristics and response to HCV therapy were compared according to the presence or not of each viral co-infection. Results: HBV DNA, GBV-C RNA and SEN-V DNA were found in 5 (1.4%, CI95%: 0.2–2.4%), 104 (29.9%, CI95%: 25.1–34.7%) and 209 patients (57.9%, CI95%: 52.8–63.0%), respectively. GBV-C positive patients had significantly higher CD4 count at baseline, during and after HCV therapy, even after stratification on antiretroviral treatment. No other significant difference was observed according to the presence or not of GBV-C or SEN-V co-infection, in particular regarding virological responses to HCV combination therapy. Conclusions: There is no reason to withhold HCV therapy in HIV infected patients who have access to HAART, because of occult HBV, GBV-C or SEN-V co-infections. [Copyright &y& Elsevier]

Abstract: Background: Occult hepatitis B (HBV) has been reported in numerous clinical settings, but it remains unclear whether occult HBV contributes to liver damage. Given that typical chronic HBV infections often have periodic flairs in viral replication and liver damage, we hypothesized that occult HBV may also have flares in viral replication that are associated with increased liver enzymes. Study design: We screened hepatitis B surface antigen negative injection drug users with untreated chronic hepatitis C viral (HCV) infection for unexplained ALT/AST flares. To further enrich for individuals with possible occult HBV flares, we studied those individuals whose flares were associated with IgM antibodies to hepatitis B core antigen. Serum samples were assayed for HBV DNA and serologies were performed in serum collected 6 months before, at the time, and 6 months after the flare. HCV RNA levels were also determined. Controls consisted of individuals who also had ALT/AST flares but who were negative for IgM antibodies to hepatitis B core antigen. Results: Seven study cases and eight control cases were identified. HBV DNA was detectable during the enzyme flares in 7/7 study cases versus 3/8 controls, p =0.026. HBV DNA levels during the flare were low, averaging 1943±2341copies/ml, but were higher in study cases versus controls, p =0.002. No change in HCV levels was associated with the flares. Conclusions: In this population at high risk for occult HBV, AST/ALT flares can be associated with detection of HBV DNA. These findings may link occult hepatitis B to liver injury. [Copyright &y& Elsevier]

Abstract: This was a retrospective, unmatched case control, laboratory-based study, investigating the impact of human immunodeficiency virus (HIV) infection on the outcome of routine laboratory detection of HBsAg and prevalence of active HBV infection in 295 samples from 167 HIV-positive and 128 HIV-negative patients. The samples were tested for HBV (HBsAg, anti-HBc, anti-HBs, HBeAg and anti-HBe) and anti-HIV 1 and 2 (Axsym assays, Abbott Laboratories), as part of routine diagnosis. A nested PCR assay, with detection limit of 800copies/ml and employing independent sets of primers to core and surface genes, was used to investigate HBV DNA. Quantification of HBV DNA was determined with the Cobas Amplicor HBV Monitor assay (Roche Diagnostics). Of the 295 samples, the frequency of anti-HBc was almost similar; 82% for the HIV-negatives and 85% for the HIV-positives, indicating that both groups were equally exposed to HBV infection. The HIV-positives had a higher rate of anti-HBs (76.0% versus 47.7%) and a lower rate of HBsAg carriage (16.2% versus 35.2%), suggesting that HIV-positive individuals are less likely to experience chronic HBV infection. However, analysis of HBV DNA indicated that many of the anti-HBs positives (20.5% versus 8.2%) and HBsAg-negatives (22.1% versus 2.4%) had active HBV infection in the HIV-positive group. There was a statistically significant difference in the prevalence of HBV DNA in the HBsAg-negatives between the two groups (Odds ratio: 11.52; chi-square: p =0.00006). Additionally, 33.3% (5/15) of sera with “anti-HBc alone” serological pattern were HBV viremic in the HIV-positive group, compared to 0% (n =31) in the HIV-negatives. Quantification of HBV DNA from HBsAg-negative/HIV-positive patients demonstrated low level HBV viremia (below 10,000copies/ml). In conclusion, these findings strongly support that HIV infection is a risk factor for occult HBV infections. [Copyright &y& Elsevier]

Background/Aims: Occult hepatitis B virus (HBV) infection [HBV-DNA detection in hepatitis B surface antigen (HBsAg)-negative individuals] may cause acute and/or chronic liver disease. The objective of this study was to document the prevalence of occult HBV in an isolated, North American Inuit community. Methods: Four hundred and eighty seven HBsAg negative sera (61% of the community population) were available for HBV-DNA testing by real time PCR. Of these, 80 (Group 1) had serologic evidence of resolved HBV infection and 407 (Group 2) were HBV-seronegative. Results: HBV-DNA was detected in 14/80 (18%) and S-variants in 12/14 (86%) samples from Group 1. In Group 2, HBV-DNA was detected in 33/407 (8.1%) and S-variants in 17/33 (52%). In all cases (Groups 1 and 2) viral loads were low (&#60;105 viral copies/ml) and clinical or biochemical features did not distinguish HBV-DNA positive from negative individuals. However, S-variants were more common (P&#60;0.0001) in older age groups. Conclusions: The results of this study indicate that in this community-based population; (1) the prevalence of occult HBV infection is 18% in those with serologic evidence of previous HBV infection and 8.1% in HBV seronegative individuals, (2) age, gender and liver biochemistry findings do not identify those with occult HBV and (3) S-variants are present in the majority of individuals with occult HBV. [Copyright &y& Elsevier]

Abstract: Background: Reactivation of occult hepatitis B virus (HBV) infection is a well-known complication of cytotoxic chemotherapy. Lamivudine prophylaxis is recommended to reduce the incidence and severity of hepatitis in this context. Case report: An HIV-infected patient positive for HBs antigen became positive for HBc antibody alone under lamivudine given as part of antiretroviral therapy. He was treated with chemotherapy for non-Hodgkin''s lymphoma while under lamivudine. Then, he developed HBV-related hepatitis that led to delay chemotherapy. He received adefovir that induced a dramatic decline in HBV DNA load and a normalisation of hepatic enzyme levels. However, the patient died of a relapse of lymphoma. Retrospective analysis of stored plasma samples showed evidence of lamivudine-resistant occult hepatitis before the onset of chemotherapy and reactivation of the HBV mutant. Conclusion: To our knowledge, this is the first report of occult hepatitis reactivation due to lamivudine-resistant mutant selected under lamivudine therapy in an HIV-infected patient. Our study underlines the need to carefully investigate lamivudine resistance in HIV-infected patients with occult infection under lamivudine therapy. Those patients should be monitored with the addition of anti-viral agents effective against the mutant strain. [Copyright &y& Elsevier]

Abstract: Occult hepatitis B is defined as the presence of hepatitis B virus (HBV) DNA in the absence of detectable HBs antigen. The prevalence of occult hepatitis B among patients HIV-infected is uncertain, varying between 0% and 89%, and the clinical consequences of the coinfection are poorly known. The aim of this study was to evaluate the frequency of occult hepatitis B among HIV-infected patients and determine risk factors. Methods: This retrospective study was conducted with plasma samples from 31HIV-infected patients untreated for HBV infection and for whom at least one sample was available. All patients were found to be carriers of isolated anti-HBc antibodies between 2000 and 2008, and HBV DNA was quantified in 51 samples (one to three per patient) by real-time PCR using the Qiagen® HBV PCR kit. Results: HBV DNA was found in samples from seven patients (22%). Occult hepatitis B seemed to be more frequent among patients coinfected with HCV (p =0,047). The number of CD4 cells was significantly less in samples containing detectable HBV DNA than in those with no detectable HBV DNA. Conclusion: The prevalence of occult hepatitis B seemed high, and HBV DNA titers were weak (< 20UI/mL), among patients infected with HIV and carrying isolated anti-HBc antibodies. These results would support screening HIV-infected patients for the presence of HBV DNA if confirmed with a larger patient population. [Copyright &y& Elsevier]