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The project is studying ways to stop live castration of pigs in organic farming. To this end, an overview of farming practices (30 surveys) and castration (10 surveys) has been drawn up. When castration is stopped, the major obstacle to the development of whole male pig farming is the presence ofunpleasant odours linked to the deposit of androstenone and skatole in the meat...; Étude sur les modalités de l’arrêt de la castration à vif des porcs en élevage biologique. Un panorama des pratiques d’élevages (30 enquêtes) et de castration (10 enquêtes) a été dressé dans ce but. En cas d’arrêt de la castration, le frein majeur au développement de l’élevage de mâle entier est la présence d’odeurs désagréables liées au dépôt androsténone et de scatol dans les viandes...

In Gabon, a central African country, human immunodeficiency virus (HIV) and hepatitis B virus (HBV) are endemic. In a recent study, conducted in a semi-urban area (Franceville, Gabon), HBV infection was found to be more prevalent among HIV infected individuals. This study aims to investigate the prevalence and genetic diversity of hepatitis B virus infection among HIV infected individuals, predominantly under antiretroviral therapy, living in fully urbanized area: Libreville, capital of Gabon. Serological and molecular tests were performed to detect HBV infection among patients living with HIV/AIDS (PLHA). We used Monolisa HBsAg ULTRA, Anti-HBc Plus and Anti-HBs Plus EIA kits for serological analyses. HBV DNA viral load (HBV DNA VL) was determined by real time PCR and molecular characterization of HBV strains was performed by sequencing and phylogenetic analysis of partial HBV surface and core genes. At all, 70.2% of patients were under antiretroviral therapy. The prevalence of HBsAg was 8.8% (43/487). Detectable HBV DNA was found in 69.7% (30/43) of HBsAg positive patients and in 17.5% (24/137) HBsAg negative patients. HBV DNA VL was significantly higher among patient with CD4 cell counts less than 200 cells/mm3 than those with CD4 cell counts greater than 500 cells/mm3 (p = 0.008). We confirmed the presence of HBV sub-genotypes QS-A3 (40%), and A4 (20%) and HBV-E genotype (40%). The percentage of resistance to Lamivudine was high (40%) and varied according to the M204V/I motif. Occult hepatitis B infection (OBI) was found in patients with isolated HBcAb and among patients who had completed their HBsAg seroconversion. We detected HBV DNA for one patient without any HBV serological marker. This study provides a new landmark for the comprehension of HBV infection in PLHA in urban areas. OBI enhances HBV DNA prevalence and should be investigated in all HBsAg negative individuals.

HBV genotyping was performed by sequencing and phylogenetic analyses of the surface (S) and core (C) fragments. Briefly, HBV DNA was first extracted from 400 µL of plasma and eluted in 100 µL of pure water, using the QIAamp Viral DNA Mini Kit (QIAGEN, Courtaboeuf, France) followed by semi-nested PCR amplification of the S (930 bp) and C (1010 bp) gene fragments using MP Taq Core Kits 25 (MP Biomedical Diagnostic, Europe). The S fragment amplification was performed as described elsewhere. (Hu X, et al., 2000 [PMID:10677515] ; Makuwa M et al., 2006 [PMID: 16847965]; Olinger CM et al.,2006 [PMID: 16603517]) The first round was performed using primers sets 58P (5’-CCT GCT GGT GGC TCC AGT TC-3’) and 979 (5’-ATT GGA AAG TAT GTC AAA GAA TTG TGG GTC TTT TG-3’). The 50 µL final reaction mixture contained 31.4 µL of RNase DNase Free water, 5 µL of buffer 10X with MgCl2 (25 mM), 0.4 µL of dNTPs (25 mM), 1.5 µL of each primer (10 µM), 0.2 µL of Taq polymerase (5 U/µL) and 10 µL of extracted DNA. The second round PCR used the 58P/Mc2r (5’-TGGAAGTTGGGGATCATTGCC-3’) primer on a 50 µL final reaction mixture containing 36.4 µL of RNase DNase Free water, 5 µL of buffer 10X with MgCl2 (25 mM), 0.4 µL of dNTPs (25 mM), 1.5 µL of each primer (10 µM), 0.2 µL of Taq polymerase (5 U/µL), and 5 µL of first round PCR product. The PCR program was the same for the first and second round PCRs including denaturation at 94°C for 5 min followed by 40 cycles of denaturation at 94°C for 1 min, annealing at 55°C for 30 s and elongation at 72°C for 1 min, followed by final elongation at 72°C for 5 min. For the C fragment amplification, the couplet of primers BCP1F (5’-GCA TGG AGA CCA CCG TGA AC-3’) / 2853N (5’-TCA CCA TAT TCT TGG GAA CA-3’) was used for the first round and the couplet BCP2F(5’-CAT AAG AGG ACT CTT GGA CT-3’) / 2853N for the second round. The amplification conditions were the same as for the S fragment. The PCR products were purified using QIAquick PCR Purification Kit (Qiagen, Courtaboeuf, France) and submitted for sequencing at Macrogen Inc (Meibergdreef, Netherlands).

HBV DNA Real Time Quantification according to ARNS 12187 project Using the Arrow extractor (NorDiag, Biotrin International, Ireland), DNA was extracted from 240 μl of plasma, pre-treated with10 μl of proteinase K, using the Arrow Viral NA extraction kit, according to the manufacturer’s instructions during 45 min. Template DNA was eluted into 60 μl of kit elution buffer. Besides clinical samples, quantification standard (Acrometrix HBV Panel, Acrometrix, Menica, CA, USA) was also extracted for each run with the same protocol and1:10 diluted (from 50,000,000IU/mL to50IU/mL). For amplification, we used a primers/probe set designed under the auspices of “Agence Nationale de Recherches sur le SIDA et les hépatites virales” (ANRS 12187 project) and targeting a conserved region in the HBVS gene (nucleotide (nt) positions, 379–426). All runs were performed in a 50-μl volume containing DNA extract (10 μl), Master Mix (Platinum UGD, USA) (25 μl), pure water (HyClone Pure Water, Thermo Fisher Scientific, Waltham, MAUSA)(12.5 μl), forward primHBV1 (5’-GTGTCTGCGGCGTT TTATCA-3’) and reverse primHBV2 (5’-AGGCATAGCAGCAGGAT GAA-3’) primers at 10 μM (1μl each) and probe (5’FAM-TGCGGCGTTTTATCAT-MGB3’) at 5μM (0.5 μl). Each reaction consisted of: 2min at50°C and 10min at95°C; followed by 50 cycles of 15sec at 95°C and 1 min at 60°C each. The lower limit of quantification (LLOQ) of our technique was 100IU/mL and the lower limit of detection (LLOD) was 50IU/mL.

L’acces aux antiretroviraux a permis de prolonger l’esperance de vie des patients vivant avec le VIH. Toutefois, les co-infections VIH-hepatites virales, dans les pays endemiques pour ces infections, constitue un probleme pour une bonne prise en charge. Afin de connaitre l’ampleur de telles co-infections au Gabon, nous avons recherche, par technique ELISA, les marqueurs d’infection par les virus des hepatites B, C, et E chez 762 adultes infectes par le VIH-1. La quantification de l’ADN plasmatique du VHB (CV VHB) a ete effectuee par PCR en temps reel. Les amplifications des ARN VHC et VHE ont ete effectuees par RT-PCR et PCR nichees. La seroprevalence de l’infection a hepatite B chronique etait de 9,3 %. Parmi les patients avec des profils AcHBc isoles, la prevalence de l’infection a hepatite B occulte etait de 26,7 %, soit une prevalence reelle (CV-VHB detectables) de 17,3 % sur la population totale. La seroprevalence VHC etait de 8,8 %. Parmi les 67 patients seropositifs, 76,1 % avaient des profils replicatifs (ARN VHC detectables), soit une prevalence globale de 6,7 % sur la population totale. Pour l’hepatite E la seroprevalence etait de 3,5 %. Aucune infection chronique VHE n’a ete retrouvee. En conclusion, cette etude met en evidence un fort taux de co-infections VIH-Hepatites B, C et E au Gabon. Par ailleurs, nous montrons l’interet de rechercher les infections chroniques (profils replicatifs) chez les patients infectes par le VIH au Gabon. La mise en place de plateaux techniques pour ce type de recherche, accessible aux pays a revenus intermediaires s’impose.

Integrated data on hepatitis B virus (HBV) patterns, HBV genotypes and mutations are lacking in human immunodeficiency virus type 1 (HIV-1) co-infected patients from Africa. This survey was conducted in 2010-2013 among 762 HIV-1-positive adults from Gabon who were predominantly treated with 3TC-based antiretroviral treatment. HBV patterns were identified using immunoassays detecting total antibody to hepatitis B core antigen (HBcAb), hepatitis B surface antigen (HBsAg), IgM HBcAb, hepatitis B e antigen (HBeAg), antibody to HBsAg (HBsAb) and an in-house real-time PCR test for HBV DNA quantification. Occult hepatitis B (OBI) was defined by the presence of isolated anti-HBc with detectable serum HBV DNA. HBV genotypes and HBV mutations were analyzed by PCR-direct sequencing method. Seventy-one (9.3%) patients tested positive for HBsAg, including one with acute hepatitis B (0.1%; 95% CI, 0.0%-0.2%), nine with HBeAg-positive chronic hepatitis B (CHB) (1.2%; 95% CI, 0.6%-2.2%), 16 with HBeAg-negative CHB (2.1%; 95% CI, 1.2%-3.3%) and 45 inactive HBV carriers (5.9%; 95% CI, 4.4%-7.8%). Sixty-one (8.0%; 95% CI, 6.2%-10.1%) patients showed OBI. Treated patients showed similar HBV DNA levels to those obtained in untreated patients, regardless of HBV patterns. Around 15.0% of OBI patients showed high (>1,000 UI/mL) viremia. The mutation M204V/I conferring resistance to 3TC was more common in HBV/A (47.4%) than in HBV/E isolates (0%) (P = .04). Our findings encouraged clinicians to promote HBV vaccination in patients with no exposure to HBV and to switch 3TC to universal TDF in those with CHB.

Simian immunodeficiency virus (SIV) infection in African nonhuman primate (NHP) natural hosts is usually nonpathogenic, despite high levels of virus replication. We have previously shown that chronic SIV infection in sooty mangabeys (SMs) and African green monkeys (AGMs) is associated with low levels of immune activation and bystander T cell apoptosis. To compare these features with those observed in another natural host, the mandrill (MND), we conducted a cross-sectional survey of the 23 SIV-infected and 25 uninfected MNDs from the only semifree colony of mandrills available worldwide. Viral loads (VLs) were determined and phenotypic and functional analysis of peripheral blood- and lymph node-derived lymphocytes was performed. We found that mandrills chronically infected with SIVmnd-1 or SIVmnd-2 have similar levels of viral replication, and we observed a trend toward lower CD4 + T cell counts in chronically SIVmnd-2-infected MNDs than SIVmnd-1-infected MNDs. No correlation between CD4 + T cell counts and VLs in SIV-infected MNDs could be established. Of note, the levels of T cell activation, proliferation, and apoptosis were comparable between SIVmnd-1- and SIVmnd-2-infected MNDs and to those observed in uninfected animals, with the only exception being an increase in tumor necrosis factor alpha-producing CD8 + T cells in SIVmnd-2-infected MNDs. Overall, these findings recapitulate previous observations in SIV-infected SMs and AGMs and lend further evidence to the hypothesis that low levels of immune activation protect natural SIV hosts from disease progression.

Terra Nova, 23, 162–170, 2011 Abstract Most fault-related pseudotachylytes in the Val Sesia area, Ivrea zone, NW Italian Alps, occur in two areas: near the Canavese Line in the Kinzigite Formation paragneisses and in an elongate belt in the Mafic Complex gabbros away from the Canavese Line. 40Ar/39Ar dating indicates that pseudotachylytes from the Kinzigite Formation were formed in the late Eocene, likely during the early stages of the collision between the NW corner of the Adriatic indenter and the European margin. Pseudotachylytes from the Mafic Complex were formed under a transpressive strain regime, as suggested by kinematic indicators, and yield Early Cretaceous (Albian) 40Ar/39Ar ages. Their formation is possibly related to shortening during the inception of the tectonic inversion of the Adriatic passive margin.

Background Gabon is an endemic area for human immunodeficiency virus (HIV) and hepatitis C virus (HCV) and the risk of co-infection is high. Method Between November 2015 and April 2016, we conducted retrospective study on HCV infection among people living with HIV/AIDS (PLHA). A total of 491 PLHA were included in this study and tested for the presence of HCV infection. HIV viral loads were obtained using the Generic HIV viral Load® assay and the CD4+ T cells count was performed using BD FACSCount™ CD4 reagents. HCV screening was performed using the MP Diagnostics HCV ELISA 4.0 kit. HCV genotypes were determined by sequence analysis of NS5B and Core regions. The Mann-Whitney test was used to compare the groups. Chi-2 test and Fisher's Exact Test were used to compare prevalence. Results HCV seroprevalence was 2.9% (14/491), (95% confidence interval (CI):1.4-4.3%). The percentage of HCV viremic patients, defined by the detection of HCV RNA in plasma, was 57% (8/14), representing 1.6% of the total population. HCV seroprevalence and replicative infection were not statistically differ with gender. The percentage of co-infection increased with age. No correlation with CD4+ T cells count and HIV viral load level was registered in this study. Identified HCV strains were predominantly of genotype 4 (87.5%) including 4k, 4e, 4g, 4p, 4f and 4c subtypes. Only one strain belonged to genotype 2 (subtype 2q). Analysis of the NS5B region did not reveal the presence of resistance-associated substitutions for sofosbuvir. Conclusion A systematic screening of hepatitis C is therefore strongly recommended as well as genotyping of HCV strains in order to adapt treatments for the specific case of people living with HIV/AIDS in Central Africa.

We consider differential games with incomplete information. For special games with dynamics independent of the state of the system and linear payoffs, we give a representation formula for the value similar to the value of repeated games with lack of information on both sides. For general games, this representation formula does not hold and we introduce an approximation of the value: we build a sequence of functions converging to the value function.

The prevalence of hepatitis B virus (HBV) surface antigen was significantly higher in urban (12.9%) than in rural (7.6%) populations ( P = 0.003), but no difference was found in the prevalence of hepatitis delta virus (HDV), which was high in both populations. Phylogenetic analysis showed the circulation of HBV-A3 and -E genotypes and the presence of HDV-1, HDV-7, and HDV-8 clades.