There were 24 HBeAg-positive and 4 HBeAg-negative patients within the original 28 AdLF-CHB patients. At the end of 10 years lamivudine treatment, 20 of the 24 HBeAg-positive patients had HBeAg loss. HBeAg seroconversion was detected in 10 of these 20 HBeAg loss patients. HBsAg loss was observed

in 4 of the original 28 patients. Among these 4 HBsAg loss patients, 3 had HBsAg seroconversion. All patients achieved HBV DNA undetectable. Histopathology was evaluated between paired original and final liver biopsies among 19 patients as follows: 4/19 achieved complete liver fibrosis/cirrhosis regression; 9/19 improved in ishak fibrosis score; while 6/19 showed no fibrosis improvement. About 75% patients achieved inflammatory/fibrotic improvement. No significant disease progression was observed in 24/28 patients. Furthermore, no significant difference in histopathology improvement, cirrhosis regression, disease progression between non-resistance Roscovitine mw and rescue for resistance was observed. Long-term lamivudine therapy achieves regression of fibrosis/cirrhosis, improvement

of histological and disease progression in AdLF-CHB patients. “
“Failure of liver stiffness measurement (LSM) by transient elastography (TE, FibroScan) and unreliable results occur in ≈5% and 15% of patients, respectively, mainly due to obesity. In this multicenter study, we evaluated the feasibility and performance of the novel FibroScan XL probe in 276 patients with chronic liver disease (42% viral hepatitis, 46% nonalcoholic

fatty liver disease [NAFLD]) and a body mass index (BMI) ≥28 kg/m2. Patients underwent liver biopsy and TE with learn more the standard M and XL probes. TE failure was defined as no valid LSMs and unreliable examinations as <10 valid LSMs or an interquartile range (IQR)/LSM >30% or success rate <60%. Probe performance for diagnosing ≥F2 fibrosis and cirrhosis (F4) versus biopsy were examined using areas under receiver operating characteristic curves (AUROC). FibroScan failure was less frequent selleck kinase inhibitor with the XL probe than the M probe (1.1% versus 16%) and the XL probe was more often reliable (73% versus 50%; both P < 0.00005). Reliable results with the XL probe were obtained in 61% of patients in whom the M probe was unreliable. Among 178 patients with ≥10 valid LSMs using both probes, liver stiffness was highly correlated between probes (ρ = 0.86; P < 0.0005); however, median liver stiffness was lower using the XL probe (6.8 versus 7.8 kPa; P < 0.00005). The AUROC of the XL and M probes were similar for ≥F2 fibrosis (0.83 versus 0.86; P = 0.19) and cirrhosis (0.94 versus 0.91; P = 0.28). Conclusion: Compared with the M probe, the FibroScan XL probe reduces TE failure and facilitates reliable LSM in obese patients. Although the probes have comparable accuracy, lower liver stiffness cutoffs will be necessary when the XL probe is used to noninvasively assess liver fibrosis.

The objectives of this article include descriptions of diagnostic records and their impact on treatment success, and criteria clinicians should use to determine whether fixed or removable prostheses are the treatment of choice in any given situation. Specific criteria and clinical guidelines will be identified for use in the treatment planning process. Determination of optimal tooth positions and their relationships to residual ridges or extraction sites are one of the critical factors in determining designs for maxillary implant prostheses. Prosthetic designs (fixed or removable) should be determined by clinicians prior to

placing implants; removable prostheses should not be considered to be the “fall-back” treatment option if fixed treatments become unavailable secondary to loss of implants or other mTOR inhibitor clinical complications. Inherent differences between fixed and removable prosthetic treatments are critical for clinicians to understand, as they often include key points for clinicians explaining the features of fixed/removable-implant

prostheses to patients. Appreciation of the differences between fixed and removable prostheses is critical for patients and clinicians to make informed decisions. “
“This study was conducted to measure and compare the effect of the soldering method (torch soldering or ceramic furnace soldering) used for soldering bars to bar-retained, implant-supported DAPT concentration overdentures on the fit between the bar gold cylinder and implant transgingival abutment. Thirty-two overdenture implant bars were manufactured and screw retained into two Bränemark implants, which were attached to a cow rib. The bars were randomly distributed in two groups: a torch-soldering group and a porcelain-furnace

soldering group. Then all bars were cut and soldered using a torch and a ceramic furnace. The fit between the bar selleck products gold cylinders and implant transgingival abutments was measured with a light microscope on the opposite side to the screw tightening side before and after the bar soldering procedure. The data obtained were statistically processed for paired and independent data. The average misfit for all bars before soldering was 33.83 to 54.04 μm. After cutting and soldering the bars, the misfit increased up to a range of 71.74 to 78.79 μm. Both before and after the soldering procedure, the bars soldered using a torch showed a higher misfit when compared to the bars soldered using a porcelain furnace. After the soldering procedure, the misfit was slightly lower on the left side of the bars, which had been soldered using a ceramic furnace. According to our data, the soldering of bars using the torch or furnace oven soldering techniques does not improve the misfit of one-piece cast bars on two implants. The lower misfit was obtained using the porcelain furnace soldering technique.

As its impact on survival is considerable, reliable risk factors facilitating the early diagnosis need to be established. Several genetic polymorphisms of pattern recognition receptors such as Toll-like receptor (TLR)-subclasses

and nucleotide-binding oligomerization domain-containing protein 2 (NOD2) have been proven to independently increase the risk for SBP. Variants of mannose binding lectin 2 (MBL2), that is a soluble complement associated receptor, has been linked to the susceptibility to infections. We therefore investigated the association of receptor polymorphisms with the occurrence of SBP in a single center cohort. Methods Ascites sample (AS) collection was performed in the line of clinically indicated paracentesis for therapeutic CHIR-99021 concentration or diagnostic reasons. If multiple interventions were performed only the first paracentesis was chosen for analysis. A leukocyte count of >500/mm3 in AS was defined as SBP. Bacterial DNA (bactDNA) was detected by using 16S rRNA gene based PCR methods. Genetic polymorphisms (SNP) of receptors such as TLR (subtypes 1,2,4,6), CD14, NOD2 and MBL2 were identified by detecting and amplifying corresponding genes. Data were correlated with selleck clinical and laboratory results. Results: 173 AS of cirrhotic

patients (ASH 72.8%, NASH 8.1 %, viral 2.3%, others 16.2%) were collected between 02/2011 and 12/2012. Median MELD was 16.05 (SBP 16.12, no SBP 15.95, p=0.296). In total 13.3% (n=23) of patients had a SBP. The bilirubin-level (58.09 ± 62.4 vs. 112.74± 149.74, p=0.034) and the CrP-level this website (32.15±30.84 vs. 50.74±36.83, p=0.019) was significantly increased if infection occurred in ascites. BactDNA could

be detected in both, nonleukocytic AS (38.7%, median 707 copies/ml) as well as leukocytic AS (47.6% (p=0.439), median 11950 copies/ml (p=0.006)). In contrast only 13% of AS were positive using conventional culture techniques. SNPs of TLR-subclasses, CD14 and NOD2 showed no association with the occurrence of SBP in AS. But variants of two MBL2-SNPs increased the risk for infections in ascites, rs11003125 C/G (GG n=65, 7.7% SBP; CG/CC n=92, 18.5% SBP; p=0.058; OR 2.7 for C allel) and rs5030737 C/T (CC n=136, 11.8% SBP; CT/TT n=21, 28.6 % SBP; p=0.040; OR 3.0 for T allel) but not for bactDNA detection. Conclusion: Mannose binding lectin 2 is a soluble pattern recognition receptor of the complement system that might resemble a new genetic risk factor for infectious complications like SBP in cirrhotic patients. This marker needs to be evaluated in a large prospective cohort.

Louis, MO) containing 1 mg/mL of Mycobacterium tuberculosis strain H37RA, and was subsequently boosted every 2 weeks with 2OA-BSA in incomplete Freund’s adjuvant (Sigma-Aldrich). Additionally, mice received 100 ng of pertussis toxin Selleckchem AZD9291 (List Biological Laboratories, Campbell, CA) at the time of initial immunization with 2OA-BSA in Complete Freund’s Adjuvant. Peripheral blood samples from individual mice were obtained from the tail vein prior to the initiation of treatment with mAbs (baseline) and then at 2-week intervals. Sera was collected prior to mAb treatment, 1 week afterward, and thereafter every 4 weeks, and stored at −70°C until

use. Animals were sacrificed at 15 weeks of age. Serum titers of anti–PDC-E2 autoantibodies were measured by way of enzyme-linked immunosorbent assay using our well-standardized recombinant autoantigens.32 Peripheral blood mononuclear cells were isolated from heparinized murine blood using Accupaque (Accurate Chemical & Scientific Company, Westbury, CT) to assess levels of B cells. Cells were preincubated with anti-mouse FcR blocking reagent and then incubated at 4°C with a predetermined optimum concentration of antigen-presenting cell (APC)-conjugated anti–T cell receptor β (BioLegend), phycoerythrin-conjugated anti-mouse IgM

(Caltag), and fluorescein isothiocyanate–conjugated anti-CD19 selleck (BioLegend); B cell frequency was then determined by way of flow cytometry. The liver and spleens were collected from mice immediately following sacrifice, and single-cell mononuclear cell suspensions

were prepared for multicolor flow analysis as described.23 Immediately after sacrifice, liver and spleen tissues were harvested and fixed in 10% buffered formalin, embedded in paraffin, and cut into 4-μm sections for routine hematoxylin (DakoCytomation, Carpinteria, this website CA) and eosin (American Master Tech Scientific, Lodi, CA) staining. Evaluation under light microscopy and scoring of liver inflammation was performed on coded hematoxylin and eosin–stained sections of liver using a set of three indices by a blinded pathologist (K. T.); indices included degrees of portal inflammation, parenchymal inflammation, and bile duct damage.33 Phenotypic analysis of bile duct damage was performed as described.34 Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphate (ALP) levels were measured using the Roche Diagnostics COBAS INTEGRA 400 Plus (Indianapolis, IN). Serum levels of the proinflammatory cytokines interleukin (IL)-6, IL-10, monocyte chemotactic protein-1 (MCP-1), interferon-γ (IFN-γ), tumor necrosis factor α, and IL-12p70 were quantified using the BD Cytometric Bead Array Mouse Inflammatory Kit (BD Biosciences) as described.35 The serum samples were loaded onto the plate neat.

Louis, MO) containing 1 mg/mL of Mycobacterium tuberculosis strain H37RA, and was subsequently boosted every 2 weeks with 2OA-BSA in incomplete Freund’s adjuvant (Sigma-Aldrich). Additionally, mice received 100 ng of pertussis toxin BI 2536 price (List Biological Laboratories, Campbell, CA) at the time of initial immunization with 2OA-BSA in Complete Freund’s Adjuvant. Peripheral blood samples from individual mice were obtained from the tail vein prior to the initiation of treatment with mAbs (baseline) and then at 2-week intervals. Sera was collected prior to mAb treatment, 1 week afterward, and thereafter every 4 weeks, and stored at −70°C until

use. Animals were sacrificed at 15 weeks of age. Serum titers of anti–PDC-E2 autoantibodies were measured by way of enzyme-linked immunosorbent assay using our well-standardized recombinant autoantigens.32 Peripheral blood mononuclear cells were isolated from heparinized murine blood using Accupaque (Accurate Chemical & Scientific Company, Westbury, CT) to assess levels of B cells. Cells were preincubated with anti-mouse FcR blocking reagent and then incubated at 4°C with a predetermined optimum concentration of antigen-presenting cell (APC)-conjugated anti–T cell receptor β (BioLegend), phycoerythrin-conjugated anti-mouse IgM

(Caltag), and fluorescein isothiocyanate–conjugated anti-CD19 NVP-LDE225 supplier (BioLegend); B cell frequency was then determined by way of flow cytometry. The liver and spleens were collected from mice immediately following sacrifice, and single-cell mononuclear cell suspensions

were prepared for multicolor flow analysis as described.23 Immediately after sacrifice, liver and spleen tissues were harvested and fixed in 10% buffered formalin, embedded in paraffin, and cut into 4-μm sections for routine hematoxylin (DakoCytomation, Carpinteria, find more CA) and eosin (American Master Tech Scientific, Lodi, CA) staining. Evaluation under light microscopy and scoring of liver inflammation was performed on coded hematoxylin and eosin–stained sections of liver using a set of three indices by a blinded pathologist (K. T.); indices included degrees of portal inflammation, parenchymal inflammation, and bile duct damage.33 Phenotypic analysis of bile duct damage was performed as described.34 Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphate (ALP) levels were measured using the Roche Diagnostics COBAS INTEGRA 400 Plus (Indianapolis, IN). Serum levels of the proinflammatory cytokines interleukin (IL)-6, IL-10, monocyte chemotactic protein-1 (MCP-1), interferon-γ (IFN-γ), tumor necrosis factor α, and IL-12p70 were quantified using the BD Cytometric Bead Array Mouse Inflammatory Kit (BD Biosciences) as described.35 The serum samples were loaded onto the plate neat.

Fine marks may fade with time. Marks on young animals may also heal differently than those on older individuals. However, all marks that were observed at the start of this 2-year study, including those on subadults, were still visible at the end. Factors affecting lion-hunting success include prey size, the number of lions participating in the hunt, time of day and the amount of cover (Schaller, 1972; Funston et al., 2001; Hopcraft, Sinclair & Packer, 2005). Although solitary lions can attack adult giraffes (Pienaar,

Temozolomide mouse 1969), groups of lions are more successful at bringing down large prey (Schaller, 1972). During this 2-year study, we observed few lion-hunting attempts on giraffes, and none that resulted in contact. Coupled with the small number of claw marks acquired during the study, this suggests that attacks with contact are infrequent. We expected to find claw marks on giraffe learn more hindquarters

because lions regularly attack large prey from the rear, grasping with their forepaws (Schaller, 1972). Consistent with this, claw marks were predominantly located on giraffe rumps, hind legs and flanks, suggesting that most non-lethal attacks also occur from the rear. This finding also supports the hypothesis of Sathar et al. (2010) that thicker skin on the upper flank and rump of giraffes may protect against lion-inflicted wounds. Lions kill with a bite or hold to the nose or throat of their prey (Schaller, 1972) and are able to seize hold of the neck of a standing adult giraffe. Two adult females in our sample had claw marks on the upper neck region. A giraffe would be extremely vulnerable if brought to the ground, so these females presumably were not. Lions

rarely attack their prey from the front (Schaller, 1972), consistent with our finding that few giraffes had claw marks on the chest, neck and forelegs. Giraffes defend themselves with front and rear kicks (Schaller, 1972; Dagg & Foster, 1982), capable of maiming or even killing a lion, and lions risk significant injury during attacks on giraffes. The giraffe is not a preferred prey species of lions in Serengeti (Scheel & Packer, 1991), where smaller prey selleck inhibitor like zebras and wildebeest are abundant (Sinclair & Norton-Griffiths, 1979). Nevertheless, the giraffe’s size means that it can provide a large quantity of meat. Schaller (1972) estimated that although lions killed few giraffes, giraffes made up 27.5–32.5% of the lion’s annual diet in Serengeti in the late 1960s. Since then, wildebeest numbers in Serengeti have doubled (Mduma, Sinclair & Hilborn, 1999), while giraffe numbers have declined (Strauss, unpubl. data). Today, giraffes probably contribute substantially less to the lion’s diet. The lack of claw marks among giraffe calves suggests that calves are highly unlikely to survive attacks where contact is made.

56,76 This was followed by a flurry of reports on the ability of transplanted bone

marrow or cord blood progenitors to repopulate animal models of liver injury.77–80 The most notable of these used the mouse model of tyrosinemia,79 and demonstrated that the liver could be completely regenerated by bone marrow stem cells. This phenomenon was subsequently found to be predominantly due to fusion.81 While there continues to be controversy regarding whether bone marrow cells can transdifferentiate into hepatocyte-like cells under certain conditions,82 the weight of evidence suggests that the contribution of bone marrow to normal liver regeneration is insignificant.83,84 The observation that liver progenitor cells have mixed Pifithrin-�� clinical trial epithelial and mesenchymal markers72,73,85 and the ease by which mesenchymal stem cells can be converted to hepatocyte-like cells86–88 raised the possibility that they may arise from the mesenchymal

lineage via mesenchymal to epithelial transition. Sicklick et al.89 further proposed that progenitor cells may be derived from hepatic stellate cells, and that the sonic hedgehog pathway regulated this process. In a follow up study, Yang et al.90 used cell fate mapping to show that stellate cells could became oval cells when activated Regorafenib mouse in liver injury, and that these cells participate in ductular proliferation. The notion that there is a common schema within the stellate cell driving both fibrosis and regeneration by fluxing between epithelial check details and mesenchymal phenotypes91,92 is an attractive one, but has not been borne out by other investigations. Careful fate mapping studies failed to show any evidence of mesenchymal to epithelial transition or vice versa during liver injury.93,94 In light of conflicting evidence, the role of epithelial-mesenchymal transition and vice versa in liver injury and repair remains highly controversial.95,96 Nevertheless, taken in context with current evidence,

it is likely that the majority of liver progenitor cells are in situ cells that are descendants of the fetal ductal plate.75 The main strategy in attempting to augment regeneration in the clinical setting thus lies in increasing the numbers of these progenitor cells following liver injury, either by stimulating the stem cell niche to proliferate, or simply by transplanting more progenitor cells into the injured liver. The role of progenitor cell regeneration in normal liver physiology is still debated. These cells likely have no significant role in day-to-day liver turnover.97 The progenitor compartment is activated only in severe liver injury, and the belief that it plays an important role in regenerating the injured liver comes from three lines of evidence.

56,76 This was followed by a flurry of reports on the ability of transplanted bone

marrow or cord blood progenitors to repopulate animal models of liver injury.77–80 The most notable of these used the mouse model of tyrosinemia,79 and demonstrated that the liver could be completely regenerated by bone marrow stem cells. This phenomenon was subsequently found to be predominantly due to fusion.81 While there continues to be controversy regarding whether bone marrow cells can transdifferentiate into hepatocyte-like cells under certain conditions,82 the weight of evidence suggests that the contribution of bone marrow to normal liver regeneration is insignificant.83,84 The observation that liver progenitor cells have mixed Palbociclib ic50 epithelial and mesenchymal markers72,73,85 and the ease by which mesenchymal stem cells can be converted to hepatocyte-like cells86–88 raised the possibility that they may arise from the mesenchymal

lineage via mesenchymal to epithelial transition. Sicklick et al.89 further proposed that progenitor cells may be derived from hepatic stellate cells, and that the sonic hedgehog pathway regulated this process. In a follow up study, Yang et al.90 used cell fate mapping to show that stellate cells could became oval cells when activated selleck chemicals llc in liver injury, and that these cells participate in ductular proliferation. The notion that there is a common schema within the stellate cell driving both fibrosis and regeneration by fluxing between epithelial selleck chemicals and mesenchymal phenotypes91,92 is an attractive one, but has not been borne out by other investigations. Careful fate mapping studies failed to show any evidence of mesenchymal to epithelial transition or vice versa during liver injury.93,94 In light of conflicting evidence, the role of epithelial-mesenchymal transition and vice versa in liver injury and repair remains highly controversial.95,96 Nevertheless, taken in context with current evidence,

it is likely that the majority of liver progenitor cells are in situ cells that are descendants of the fetal ductal plate.75 The main strategy in attempting to augment regeneration in the clinical setting thus lies in increasing the numbers of these progenitor cells following liver injury, either by stimulating the stem cell niche to proliferate, or simply by transplanting more progenitor cells into the injured liver. The role of progenitor cell regeneration in normal liver physiology is still debated. These cells likely have no significant role in day-to-day liver turnover.97 The progenitor compartment is activated only in severe liver injury, and the belief that it plays an important role in regenerating the injured liver comes from three lines of evidence.

However, with increased use of marginal livers for therapeutic

transplant, availability of livers that yield high quality hepatocytes is becoming limited. Protein Tyrosine Kinase inhibitor We have developed a hypothermic machine perfusion (HMP) process that restores function to ischemia-damaged livers leading to improved survival of transplants in a rat model. We therefore tested if this system could improve isolation of hepatocytes from marginal donors. In rat studies, livers (n=6/group) were subjected to 120 min warm ischemia (WI) followed by either 24 hr simple cold storage (SCS) or 24 hr SCS + 5 hr perfusion with a recovery solution (HMP). Hepatocytes were then isolated by collagenase digestion. HMP improved yield by 50% and improved viability from 66. 6% to 86. 5% (p<0. 05). Isolated Tanespimycin in vivo cells were plated on collagen coated plates. Plateability of the cells was improved by HMP

from 38. 5% to 72. 2% vs. SCS. Function of the cells was tested by ethoxycoumarin O-deethylase (ECOD) activity and urea production. HMP cells showed improved both phase I and phase II ECOD activity (90 vs 51 pmole/106 cells/min) for phase II, HMP vs SCS, p<0. 05). Urea production by HMP cells was also more than double that of SCS (p<0. 05). These results suggested that HMP provides improved yield, viability and function of hepatocytes isolated from ischemia damaged rat livers. We then tested the procedure in a series of three human livers. Livers not accepted for transplant were obtained from an OPO with cold storage times of 16-24 hrs. They were divided into two segments with one digested immediately and the other placed on HMP for 3 hrs and then digested. On a grading scale in which a score of <6 is acceptable for cell isolation, the liver scores selleck were 5, 10 and 15. With a score of 5, HMP and SCS showed similar yield and viability but HMP cells had a 40% greater attachment after cryopreservation. The second liver (score of 10) was steatotic and 20 min WI. HMP improved yield (6 x 108 vs 1. 4 x 108 cells) and viability (73 vs 57%). HMP also improved ECOD activity

after cryopreservation (233 vs 77. 5 pmol/106 cells/min). The third liver had a WI of 60 min and >50% steatosis. SCS yielded no viable cells while HMP yielded 4. 3×108 cells from 500 g liver. Although plating efficiency was low after cryopreservation (10%) additional storage of cells in HMP solution increased it to 24%. The results demonstrate that HMP after the SCS process can improve cell isolation from both rat and human DCD livers. Also, additional hypothermic storage in the HMP solution improved viability and plating of human hepatocytes. Disclosures: Mark G. Clemens – Management Position: HepatoSys Inc; Stock Shareholder: HepatoSys Inc John W. Ludlow – Consulting: Zen Bio Inc. Charles Lee – Management Position: HepatoSys Inc. The following people have nothing to disclose: Cathy Culberson, Joshua D.

Methods: First we examined the effects of di-phosphoryl lipid A (representing the native form in wild type LPS) and mono-phosphoryl lipid A on macrophages and fibroblasts (RAW264.7, 3T3 and LX2 cells) in vitro. We then examined alkaline phosphatase and LPS-dephosphorylating activity in normal and fibrotic livers of CCL4- treated mice and human patients. We also studied the effect of a 2-week administration of Calf Intestinal AP (500 mU/mouse/injection) on macrophages and fibroblasts in mice with CCl4-induced established fibrosis (8 weeks model). Finally, intestinal AP knock-out C57BL/6 mice (iAP KO) were examined at 6 weeks of age and

compared to age-matched wild-type. Results: Whereas diphosphoryl find more Lipid A strongly activated RAW cells, 3T3 and LX2 cells as reflected by enhanced expression of pro-inflammatory cytokines, adhesion molecules and MHC Class II, monophosphoryl lipid A induced

no such activities in either cell type. Significant dephosphorylating activity of diphosphoryl lipid A and wild type LPS was found in fibrotic livers of both mice and man. This activity co-localized with intra-hepatic AP activity. CD68-positive macrophages and α-SMA-positive cells were found to express AP activity. Administration of AP to CCL4-exposed fibrotic mice significantly attenuated staining for desmin which was associated with a reduction in the expression of the M2 macrophage marker YM-1. In contrast, iAP KO mice displayed higher intrahepatic expression levels of fibrogenic markers (PAR-1, Collagen I) paralleled by an increase in YM-1 staining relative to http://www.selleckchem.com/products/BMS-777607.html WT. So, lack of intestinal AP stimulates fibrogenesis within the liver. Conclusions: Based on our in vitro studies it can be concluded that removal of just one phosphate from the Lipid A moiety of LPS abrogates many biological effects of LPS. The detection of LPS-dephosphorylating activity in fibrotic livers of mice and man may therefore represent the upregulation of a protective enzyme. The in vivo effects

of exogenous AP on fibroblasts and macrophages in fibrotic mice and our observations in i-AP KO mice further see more support the hypothesis that alkaline phosphatase activity attenuates LPS-mediated effects within the fibrotic liver. Disclosures: Klaas Poelstra – Consulting: BiOrion Technologies BV; Grant/Research Support: BiOrion Technologies BV; Stock Shareholder: BiOrion Technologies BV The following people have nothing to disclose: Marlies Schippers, Eduard Post, Aysegul Cetintas, Catharina Reker-Smit, Madhu S. Malo, Richard A. Hodin, Jose L. Millan, Leonie Beljaars Patients with HCV/HIV co-infection show a faster progression of hepatic fibrosis and more severe inflammation. The HIV envelope protein gp120 has been previously shown to modulate different aspects of hepatic stellate cell (HSC) biology, including directional migration and expression of profibrogenic cytokines.