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Background Little is known about molecular characteristics of HBV strains circulating in Algeria and there are few data regarding HDV infection. Objectives The aim of this study is to describe the genetic diversity of HBV and HDV strains existing in Algeria and to determine the seroprevalence of HDV infection. Study design Plasma samples from 134 patients were analyzed by enzyme immunoassay method for HBV and HDV serological markers. Genotyping of HBV and HDV strains were performed using direct sequencing followed by phylogenetic analyses of the PreS1 and R0 region of the HBV and HDV genome respectively. Results The PreS1 gene was successfully amplified in 119 patients (82 males and 37 females). Phylogenetic analysis of HBV strains revealed the presence of genotypes D (86.5%) and A2 (11.76%). The subgenotypes D are distributed as follows: HBV/D7 (43.5%), HBV/D3 (24.75%), HBV/D1 (16.8%) and HBV/D2 (14.85%). A recombinant between genotypes A, E and D was found. The seroprevalence of HDV infection among HBV carriers was less than 5.35%. Only one isolate of HDV genotype 1 was identified. Conclusions Our data indicate the predominance of HBV subgenotype D7 and a low prevalence of HDV infection.

Algeria is the largest country of Africa, with a population of 40 million inhabitants living in disparate environments from the Sahara to the large cities of the Mediterranean coast. The molecular epidemiology of hepatitis B virus (HBV) variants has been partially described, but variations in the seroprevalence of HBV surface antigen (HBsAg) throughout the Algerian territories are still poorly described. We analyzed demographic features of new cases of chronic infection collected in 41 administrative regions (covering 92% of the population) in 2013. The mean age of the 1876 HBsAg(+) patients was 36.8 ± 14.2 years, with a slight excess of males (54%). The seroprevalence of HBV early antigen (HBeAg) was 9.3%, and the mean virus load was 3.2 ± 1.8 log IU/ml. A subset of 15.2% of patients was already cirrhotic at disease discovery. An important heterogeneity was observed throughout the country, with nine regions displaying a significant excess of cases. These regions formed four distinct foci located in distant parts of the country: Adrar-Bechar (southwest), El-Oued-Tebessa (east), M’Sila-Setif (north central) and Oran-Ain Temouchent (northwest). An excess of cases was found as well in the national capital Algiers. Patients from southern regions with an excess of cases (Bechar, Adrar, El Oued) were significantly younger (32.0 ± 10.7 years), as were patients from the regions of Bejaia and Bouira (32.1 ± 10.6). The southwestern regions were also marked by a significant imbalance of the sex ratio (58 vs 39% of female cases, P = 4.5 E-5). The highest HBeAg seroprevalence was observed in Setif (26.4 vs. 7.6%, OR = 4.3, 95% CI 2.6-6.5, P = 1.1 × 10−11) in accordance with the higher virus loads observed in the patients (3.9 ± 2.3 vs. 3.1 ± 1.6, P = 0.0002). In conclusion, we observed heterogeneity in HBsAg seroprevalence, demographic traits, and disease evolution in Algeria. Further studies are now warranted to shed light on these differences, which are presumably due to variability in transmission routes or in the infectivity of viral isolates.

Budd-Chiari syndrome (BCS) is a rare cause of portal hypertension and liver failure. This condition is characterized by an impaired hepatic venous drainage. The diagnosis of BCS is based on imaging, which helps initiate treatment. Imaging findings can be categorized into direct and indirect signs. Direct signs are the hallmarks of BCS and consist of visualization of obstructive lesions of the hepatic veins or the upper portion of the inferior vena cava. Indirect signs, which are secondary to venous obstruction, correspond to intra- and extrahepatic collateral circulation, perfusion abnormalities, dysmorphy and signs of portal hypertension.

Algeria is the largest country of Africa, peopled with populations living a range of traditional/rural and modern/urban lifestyles. The variations of prevalence of chronic active hepatitis care poorly known on the Algerian territory. We conducted a retrospective survey on all patients (n = 998) referred to our institution in 2012 and confirmed by us for an active hepatitis C. Half of the hepatitis C virus (HCV) isolates were genotyped. Forty Algerian regions out of the 48 were represented in our study. Three geographical clusters (Ain-Temouchent/SidiBelAbbes, Algiers, and a large Eastern region) with an excess of active hepatitis C were observed. Patients coming from the Eastern cluster (Batna, Khenchela, Oum el Bouaghi, and Tebessa) were strongly over-represented (49% of cases, OR = 14.5, P

International audience; Background & aims: Hepatitis B virus (HBV) RNA can undergo alternative splicing, but the relevance of this post-transcriptional regulation remains elusive. The mechanism of HBV alternative splicing regulation and its impact on liver pathogenesis were investigated.Methods: HBV RNA-interacting proteins were identified by RNA pull-down, combined with mass spectrometry analysis. HBV splicing regulation was investigated in chemically and surgically induced liver damage, in whole HBV genome transgenic mice and in hepatoma cells. Viral and endogenous gene expression were quantified by quantitative reverse transcription polymerase chain reaction, Western blot and enzyme-linked immunosorbent assay. Resident liver immune cells were studied by fluorescence-activated cell sorting.Results: HBV pregenomic RNA-interacting proteins were identified and 15% were directly related to the splicing machinery. Expression of these splicing factors was modulated in HBV transgenic mice with liver injuries and contributed to an increase of the HBV spliced RNA encoding for HBV splicing-generated protein (HBSP). HBSP transgenic mice with chemically induced liver fibrosis exhibited attenuated hepatic damage. The protective effect of HBSP resulted from a decrease of inflammatory monocyte/macrophage recruitment through downregulation of C-C motif chemokine ligand 2 (CCL2) expression in hepatocytes. In human hepatoma cells, the ability of HBSP to control CCL2 expression was confirmed and maintained in a whole HBV context. Finally, viral spliced RNA detection related to a decrease of CCL2 expression in the livers of HBV chronic carriers underscored this mechanism.Conclusion: The microenvironment, modified by liver injury, increased HBSP RNA expression through splicing factor regulation, which in turn controlled hepatocyte chemokine synthesis. This feedback mechanism provides a novel insight into liver immunopathogenesis during HBV infection. Lay summary: Hepatitis B virus persists for decades in the liver of chronically infected patients. Immune escape is one of the main mechanisms developed by this virus to survive. Our study highlights how the crosstalk between virus and liver infected cells may contribute to this immune escape.

International audience; AIM: To assess the role of the major risk factors for hepatocellular carcinoma (HCC) development in the western part of North Africa. METHODS: A multicenter case control study was conducted in Tunisia, Morocco and Algeria in collaboration with Pasteur Institutes in these countries. A total of 164 patients with HCC and 250 control subjects without hepatic diseases were included. Prevalences of HBsAg, anti-hepatitis C virus (HCV) and diabetes were assessed. HCV and HBV genotyping were performed for anti-HCV and HBsAg positive patients. RESULTS: The mean age of patients was 62 ± 10 years old for a 1.5 M:F sex ratio. Sixty percent of HCC patients were positive for anti-HCV and 17.9% for HBsAg. Diabetes was detected in 18% of cases. Odd ratio (OR) and 95% confidence intervals (CI) were 32.0 (15.8 - 65.0), 7.2 (3.2 - 16.1) and 8.0 (3.1 - 20.0) for anti-HCV, HBsAg and diabetes respectively. Multivariate analysis indicated that the three studied factors were independent. 1b HCV genotype and D HBV genotype were predominant in HCC patients. HCV was the only risk factor significantly associated with an excess of cirrhosis (90% vs 68% for all other risk factors collectively, P = 0.00168). Excessive alcohol consumption was reliably established for 19 (17.6%) cases among the 108 HCC patients for whom data is available. CONCLUSION: HCV and HBV infections and diabetes are the main determinants of HCC development in North Africa. An active surveillance and secondary prevention programs for patients with chronic hepatitis and nutrition-associated metabolic liver diseases are the most important steps to reduce the risk of HCC in the region.

International audience; The molecular pathogenesis of hepatocellular carcinoma, a tumour characterized by a vast clinical heterogeneity, remains unexplored outside Europe and Eastern Asia. We analysed by direct sequencing or loss of heterozygosity assay, the common targets of genomic alterations in 42 hepatocellular carcinomas collected in western North-Africa. Overall, genomic instability was uncommon, allelic losses affecting mostly chromosomes l p, 4q, 8p and 17p (24-28% of cases). CTNNBI and TP53 were infrequently mutated (9 and 17% of cases, respectively). Surprisingly. TP53 mutation R249S, diagnostic of aflatoxin B1 exposure, usually frequent in Africa, was exceptional (one case), indicating that in western North-Africa, hepatocellular carcinoma genetics differs markedly from that of the remainder of the continent. (C) 2007 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.