The model is also useful for studying the effect of drugs without the influence of cytokines and cytotoxic T lymphocytes. Nonetheless, the model is insufficient to study carcinogenesis of hepatitis viruses, because non-parenchymal cells in mouse liver are of mouse origin and do not support inflammation and fibrosis, which are probably closely related

to carcinogenesis. The lack of human immune cells also www.selleckchem.com/products/BIBW2992.html limits the study of inflammation and immunity. Furthermore, the availability of human hepatocytes is limited. Despite these limitations, the current model shows great potential as a mouse model for the study of hepatitis viruses. Development of a small animal model with or without human immunity using stem cells or iPS cells would be an ideal model in the future. This work was supported in part by Grants-in-Aid for scientific research and development from the Ministry of Education, Culture, Sports, Science and Technology, and the Ministry of Health, Labor and Welfare, Government of Japan. “
“Sirtuin 1 (SIRT1) has been implicated in telomere maintenance find more and the growth

of hepatocellular carcinoma (HCC). Nevertheless, the role of other sirtuins in the pathogenesis of HCC remains elusive. We found that sirtuin 2 (SIRT2), another member of the sirtuin family, also contributes to cell motility and invasiveness of HCC. SIRT2 is up-regulated in HCC cell lines and in a

subset of human HCC tissues (23/45). Up-regulations of SIRT2 in primary HCC tumors were significantly correlated with the presence of microscopic vascular invasion (P = 0.001), a more advanced tumor stage (P = 0.004), and shorter overall survival (P = 0.0499). Functional studies by short hairpin RNA–mediated suppression of SIRT2 expression in HCC cell click here lines revealed significant inhibition of motility and invasiveness. Depletion of SIRT2 also led to the regression of epithelial-mesenchymal transition (EMT) phenotypes, whereas the ectopic expression of SIRT2 in the immortalized hepatocyte cell line L02 promoted cell motility and invasiveness. Mechanistic studies revealed that SIRT2 regulates the deacetylation and activation of protein kinase B, which subsequently impinges on the glycogen synthase kinase-3β/β-catenin signaling pathway to regulate EMT. Conclusions: Our findings have uncovered a novel role for SIRT2 in HCC metastasis, and provide a rationale to explore the use of sirtuin inhibitors in HCC therapy. (HEPATOLOGY 2013;) Hepatocellular carcinoma (HCC) is the fifth-most common malignancy worldwide and the second-leading cause of cancer death in Asia, generally, and in China, in particular.

The model is also useful for studying the effect of drugs without the influence of cytokines and cytotoxic T lymphocytes. Nonetheless, the model is insufficient to study carcinogenesis of hepatitis viruses, because non-parenchymal cells in mouse liver are of mouse origin and do not support inflammation and fibrosis, which are probably closely related

to carcinogenesis. The lack of human immune cells also 3-MA cell line limits the study of inflammation and immunity. Furthermore, the availability of human hepatocytes is limited. Despite these limitations, the current model shows great potential as a mouse model for the study of hepatitis viruses. Development of a small animal model with or without human immunity using stem cells or iPS cells would be an ideal model in the future. This work was supported in part by Grants-in-Aid for scientific research and development from the Ministry of Education, Culture, Sports, Science and Technology, and the Ministry of Health, Labor and Welfare, Government of Japan. “
“Sirtuin 1 (SIRT1) has been implicated in telomere maintenance MG 132 and the growth

of hepatocellular carcinoma (HCC). Nevertheless, the role of other sirtuins in the pathogenesis of HCC remains elusive. We found that sirtuin 2 (SIRT2), another member of the sirtuin family, also contributes to cell motility and invasiveness of HCC. SIRT2 is up-regulated in HCC cell lines and in a

subset of human HCC tissues (23/45). Up-regulations of SIRT2 in primary HCC tumors were significantly correlated with the presence of microscopic vascular invasion (P = 0.001), a more advanced tumor stage (P = 0.004), and shorter overall survival (P = 0.0499). Functional studies by short hairpin RNA–mediated suppression of SIRT2 expression in HCC cell this website lines revealed significant inhibition of motility and invasiveness. Depletion of SIRT2 also led to the regression of epithelial-mesenchymal transition (EMT) phenotypes, whereas the ectopic expression of SIRT2 in the immortalized hepatocyte cell line L02 promoted cell motility and invasiveness. Mechanistic studies revealed that SIRT2 regulates the deacetylation and activation of protein kinase B, which subsequently impinges on the glycogen synthase kinase-3β/β-catenin signaling pathway to regulate EMT. Conclusions: Our findings have uncovered a novel role for SIRT2 in HCC metastasis, and provide a rationale to explore the use of sirtuin inhibitors in HCC therapy. (HEPATOLOGY 2013;) Hepatocellular carcinoma (HCC) is the fifth-most common malignancy worldwide and the second-leading cause of cancer death in Asia, generally, and in China, in particular.

The primary purpose of endotherapy is to control the jaundice and sepsis effectively and to improve the patients’ general condition promptly. The ultimate goal of endoscopic treatment, however, is to get rid of the narrowing of bile duct averting further surgery. There are several crucial steps when handling benign stricture endoscopically, i.e. the access, dilation and sustentation of the stenosis. For bile duct injury, early intervention with aggressive dilation followed by maximal number of stents placement is principal. The stents should be exchanged on schedule and keep in site for up to twelve months. For anastomotic stricture after liver

transplantation, proper endotherapy should be adopted according the stage and grade of the stricture. A single stent (without dilatation) would be inserted in patients within first month of transplant. This would be followed by serial balloon dilatation followed AZD3965 by multiple stents placement until at least three stents were successfully implanted. The stents were kept in site for at least six months and removed if cholangiogram demonstrated

no evidence of stricture and laboratory test revealed resolution of cholestasis. Methods: Between April 2004 and December 2010, a consecutive of 133 cases with BBS duo to various etiologies underwent 204 endoscopic procedures in our unit. A mean of 2.8 (range 2–6) plastic stents were placed with mean total size of 22.8 (range 14–42) Fr. The stents were persisted for mean time of 13.4 GDC-0199 mw (range 1–53) months. Up to now, stricture resolution was achieved in 87.2% (82/94) of follow-up patients. Results: The use of removable metal stent has showed promoting selleckchem outcome for the resolution of localized BBSs with relatively simple manipulation and short treatment duration. With collaboration with a domestic company, we developed a novel short fully-covered SEMS (FCSEMS) with a retrieval lasso. The stent could be

endobiliary placed with the lasso left outside duodenal papilla. Up to now, the novel stent was successfully placed in 45 patients. The median stenting duration was 8.1 (range 2–15.5) months. Subsequent stent removal was successful in 38/38 patients. Stent migration occurred in 3/34 patients (8.8%). During a mean (SD) follow up of 18.9 (12.3) months after stent removal, recurrent stricture was found in 2/31 (6.5%) of patients and was successfully treated with a second stent. Overall, the strictures resolved in 31/34 (91.2%) patients. Our result reveals that Intraductal placement of a short FCSEMS is suitable for the treatment of extrahepatic BBS. This new removable design offered prolonged stenting and drainage for BBS for up to one year with minimal complications. Conclusion: Recently, we had adopted radio-frequency ablation (RFA) to the treatment of refractory BBS. A consecutive 9 patients with BBS (surgical injury4, liver transplant 3, and chronic inflammation 2) underwent 1 to 5 sections of RFA therapy.

Liver steatosis is strongly associated with poor graft function after liver transplantation. Liver with more than 40–50% macrosteatosis should not be used. However, at present the quantity of fatty livers lack accepted standards. The computerized image analysis programs should be used to automate the determination of fat content in liver biopsy specimens. Liver grafts from anti-HBc positive donors can be safely used, preferentially in hepatitis B surface antigen (HBsAg) positive or anti-HBc/anti-HBs positive recipients. HCV positive allografts free from fibrosis or severe inflammation are a safe option for HCV positive recipients. The procurement team should consider liver biopsy to evaluate

these HCV positive allografts. Donor serum sodium over 150 mm may predict a higher rate of graft primary non-functions. Recently, however, some investigators reported the sodium level likely has little BAY 57-1293 order clinical impact on post-transplant liver function. The incidence of hepatic artery variations has been reported to be approximately

Navitoclax supplier 30%. To avoid injuries, it is very important to know and identify these variations with precision at the time of organ procurement. THE SUCCESSFUL RESULTS of liver transplantation (LT) have been followed by an increased number of patients on waiting lists. Organ shortage is a major problem in LT. The current era of organ shortage has promoted attempts to expand the donor pool, including the use of expanded criteria donors (ECD). ECD are currently defined as tumor, drug abuse, meningitis, hepatitis B or C, donor age greater than 65 years, intensive care unit stay greater than 7 days, high body mass index, steatosis, hypernatremia and high levels of liver enzymes or bilirubin. If any of these parameters apply, a donor is considered an ECD.[1] Use of ECD is an alternative to overcome the organ shortage. However, patients receiving ECD are at higher risk of impaired

graft function or increased early mortality after LT.[2] Therefore, to assess the quality of an organ is of critical importance for the outcome of the transplantations. In order to predict outcome after LT, Feng et al.[3] developed a quantitative donor risk index (DRI). They used data from adult deceased donor liver transplants in the USA to identify factors associated selleck kinase inhibitor with allograft failure. The original report identified that seven donor characteristics – including donor age (>40 years), donation after cardiac death, split/partial grafts, African-American race, less height, cerebrovascular accident and “other” causes of brain death, and cold ischemic time – were significantly associated with liver allograft failure. As the DRI increased from the baseline risk index group (0.0–1.0) to the highest risk index group listed (2.0), the frequency that the graft would be discarded was significantly higher, rising from 3.1% to 12.5%. After that, several studies have been performed by using risk models based on donor and transplant factors.

4). We hypothesized that retrograde flow from the vena cava (Fig. 4A, gray arrow) would enter the liver lobule through the central vein and deposit cells in the pericentral area. In contrast, cells seeded through

the portal vein, in the direction of physiologic flow, would enter the lobule through the portal triad and be deposited in the periportal area (Fig. 4A, purple arrow). The results of the seeding experiments confirmed that the distribution of the cells was consistent with these predictions (Fig. 4B-D). In Fig. 4B, fluorescent EC were seeded via vena cava and then cultured under constant medium perfusion for 3 days. Fluorescent microscopy showed that the labeled EC were distributed throughout the larger vessels

concentrating in regions Alvelestat nmr corresponding to central veins (Fig. 4B) and in smaller branches and capillary-size vessels. In the reciprocal experiment (Fig. 4C), GFP-labeled Dorsomorphin mouse EC seeded through the portal vein were distributed throughout the bioscaffold, with higher concentration of cells in the periportal areas of the liver lobule. Interestingly, some of these cells were observed aligning with the flow direction of the perfused culture medium (Fig. 4C, inset). In either seeding approach the EC lined the vascular network, ranging from the larger vessels to the capillary size. In order to test whether cells could be seeded throughout the entire vascular network, we first injected the bioscaffold with EC via portal vein and subsequently injected red fluorescent beads via the vena cava. Fluorescent microscopy was used to visualize the DAPI-stained EC and the red fluorescent check details beads within the vasculature. The image in Fig. 4D clearly shows that portal vein-seeded ECs were predominantly deposited in the periportal regions of the liver lobule (Fig. 4D, hexagon), whereas vena cava–perfused beads were concentrated in the region of the central vein (Fig. 4D, dashed circle). The resolution of the fluorescent microscopy (Fig. 4C) did not allow us to determine if the EC were able to completely cover

the entire luminal surface of the vascular channels in the bioscaffold. Transmission electron microscopy (TEM) was used to achieve high-resolution analysis of ECs inside the vasculature lumen within the bioscaffold. In one section we observed 3 ECs covering the entire luminal surface of a vessel (Fig. 4E). Higher magnification showed formation of cellular junctions between two adjacent ECs (Supporting Information Fig. 3A), indicating active spreading and formation of cell-cell junctions. ECs coverage of the vascular lumen predicts a nonthrombogenic surface and we tested this hypothesis by perfusing seeded and unseeded bioscaffolds with fresh rat heparinized blood. Platelet adhesion and aggregation to the scaffold’s matrix was analyzed by immunostaining with anti-integrin αIIb antibodies (Supporting Information Fig. 3B,C).

4). We hypothesized that retrograde flow from the vena cava (Fig. 4A, gray arrow) would enter the liver lobule through the central vein and deposit cells in the pericentral area. In contrast, cells seeded through

the portal vein, in the direction of physiologic flow, would enter the lobule through the portal triad and be deposited in the periportal area (Fig. 4A, purple arrow). The results of the seeding experiments confirmed that the distribution of the cells was consistent with these predictions (Fig. 4B-D). In Fig. 4B, fluorescent EC were seeded via vena cava and then cultured under constant medium perfusion for 3 days. Fluorescent microscopy showed that the labeled EC were distributed throughout the larger vessels

concentrating in regions Alpelisib purchase corresponding to central veins (Fig. 4B) and in smaller branches and capillary-size vessels. In the reciprocal experiment (Fig. 4C), GFP-labeled VX-770 clinical trial EC seeded through the portal vein were distributed throughout the bioscaffold, with higher concentration of cells in the periportal areas of the liver lobule. Interestingly, some of these cells were observed aligning with the flow direction of the perfused culture medium (Fig. 4C, inset). In either seeding approach the EC lined the vascular network, ranging from the larger vessels to the capillary size. In order to test whether cells could be seeded throughout the entire vascular network, we first injected the bioscaffold with EC via portal vein and subsequently injected red fluorescent beads via the vena cava. Fluorescent microscopy was used to visualize the DAPI-stained EC and the red fluorescent selleckchem beads within the vasculature. The image in Fig. 4D clearly shows that portal vein-seeded ECs were predominantly deposited in the periportal regions of the liver lobule (Fig. 4D, hexagon), whereas vena cava–perfused beads were concentrated in the region of the central vein (Fig. 4D, dashed circle). The resolution of the fluorescent microscopy (Fig. 4C) did not allow us to determine if the EC were able to completely cover

the entire luminal surface of the vascular channels in the bioscaffold. Transmission electron microscopy (TEM) was used to achieve high-resolution analysis of ECs inside the vasculature lumen within the bioscaffold. In one section we observed 3 ECs covering the entire luminal surface of a vessel (Fig. 4E). Higher magnification showed formation of cellular junctions between two adjacent ECs (Supporting Information Fig. 3A), indicating active spreading and formation of cell-cell junctions. ECs coverage of the vascular lumen predicts a nonthrombogenic surface and we tested this hypothesis by perfusing seeded and unseeded bioscaffolds with fresh rat heparinized blood. Platelet adhesion and aggregation to the scaffold’s matrix was analyzed by immunostaining with anti-integrin αIIb antibodies (Supporting Information Fig. 3B,C).

Methods:  A rat model selleckchem of segmental hepatic ischemia in which the bilateral median and left lateral lobes were made ischemic

by clamping the blood vessels was employed. Indocyanine green (ICG), infrared spectroscopy, and compartmental kinetic analysis, were used to indirectly monitor the movement of bile acids across hepatocytes in situ. Rates of bile flow were measured gravimetrically. Results:  In control livers (not subjected to ischemia), the movement of ICG from the blood to bile fluid could be described by a three compartment model comprised of the blood, a rapidly-exchangeable compartment, and the hepatocyte cytoplasmic space. In livers subjected to continuous clamping, the rates of ICG uptake to the liver, and outflow from the liver, were greatly reduced compared with those in control livers. Intermittent clamping (three episodes of 15 min clamping) compared with continuous clamping substantially increased the rate of ICG uptake from the blood but had less effect on the rate of

ICG outflow from hepatocytes. Conclusions:   It is concluded that intermittent ischemia promotes post reperfusion bile flow in the early phase of ischemia reperfusion injury principally by enhancing the movement of bile acids from the blood to hepatocytes. 2012 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd “
“Aim:  The aim of this study was to compare the clinical applicability of quantitative serum hepatitis B surface antigen (HBsAg), hepatitis B e-antigen (HBeAg) and hepatitis B virus (HBV) DNA for predicting virological learn more response (VR) to pegylated interferon (PEG-IFN) therapy. Methods:  Thirty HBeAg-positive chronic hepatitis B patients who received PEG-IFN-α-2b for 48 weeks were enrolled. Quantitative HBsAg, HBeAg and HBV DNA were measured before, during and after the therapy. Paired liver biopsies selleck chemicals llc were performed before and after treatment for covalently closed circular (ccc)DNA and intrahepatic HBV DNA analysis. Results:  VR at 48 weeks post-treatment, defined as HBeAg seroconversion and HBV DNA

less than 10 000 copies/mL was achieved in 10 (33.3%) patients. Responders had significantly lower baseline HBsAg, HBeAg, cccDNA and intrahepatic HBV DNA levels than non-responders. Baseline and reduced levels of log10 HBsAg and log10 HBeAg correlated well with those of log10 cccDNA and log10 total intrahepatic HBV DNA. Responders showed consistent decrease in serum HBsAg, HBeAg and HBV DNA levels during therapy. HBeAg level of 2.0 log10 sample to cut-off ratio at week 24 on therapy provided the best prediction of sustained virological response, with sensitivity and negative predictive values of 85% and 92%, respectively. One patient (3.3%) who cleared HBsAg at follow up exhibited a more rapid decline in serum HBsAg during therapy than those who developed VR without HBsAg clearance.

Hematoxylin

and eosin (H&E) stainings of 3-μm paraffin sections were used to evaluate basic histomorphology of the specimens, especially the portal and lobular amount of inflammatory cells (score 0-3 for negative to strong infiltration) and signs of regeneration/degeneration of hepatocytes (e.g., cytoplasmic volume, nuclear polymorphism, and thickness of liver cell plates as well as hepatic apoptotic bodies).23 Content of extracellular collagen was measured by the amount of chromotrope-aniline blue (CAB) in the portal tract and hepatic lobule (score 0-3 for negative to strong staining).24 Proliferating Raf inhibitor cell nuclear antigen (PCNA) and desmin staining were performed on an autostainer system (Dako), using the EnVision Detection System (Dako, Glostrup, Denmark), and developed using diaminobenzidine as the chromogen substrate (Roche Molecular Biochemicals, Mannheim, Germany), according to the manufacturer’s instructions. To highlight neutrophil granulocytes in liver tissue, naphtol AS-D chloroacetate esterase enzyme (NASD) histochemistry was used.25 Liver slices were stained for cluster of differentiation (CD)3 and forkhead box protein 3 (Foxp3) and developed with the PolapKit (Zytochem, Las Condes, Chile). Images were evaluated per mm2 (PCNA) or high-power field (400× magnification) using ImageAccess Enterprise software (version

9; Imagic, Glattbrugg, Switzerland). Histological quantification PLX-4720 supplier was performed by a pathologist. Results were analyzed using the Student’s t test, if two groups were compared; in addition, for analysis of real-time RT-PCR, logarithmized data and Welch’s t test were used. All data click here in this study are expressed as a mean ± standard error of the mean. P ≤ 0.05 was considered significant. HO-1 induction or overexpression have been shown to interfere with liver damage in mouse models of acute inflammation and apoptosis.7, 8 We have investigated the effects of HO-1 induction on chronic hepatic inflammation and fibrosis in Mdr2ko mice. Nine weeks of HO-1 induction in Mdr2ko mice (weeks 5-14 of lifespan) decreased plasma ALT levels, which increased over the first 22 weeks of lifespan (Fig. 1A, open bars). Significant

improvement was observed for at least 8 weeks beyond treatment (Fig. 1A, closed bars). HO-1 induction by CoPP in liver tissue was detectable on messenger RNA (mRNA) (Supporting Fig. 1A) and protein level (Supporting Fig. 1B) and did not alter hematocrit values (Supporting Fig. 1C). Likewise, isolated PHs and HSCs of Mdr2ko mice showed HO-1 induction after CoPP incubation (Supporting Fig. 1D). IHC staining of liver samples obtained at 12 weeks of age revealed reduced periportal and lobular inflammation in CoPP-treated mice (Fig. 1B). HO-1 induction significantly reduced the expression of TNFR1 and 2, whereas TNF expression in whole liver tissue was increased in Mdr2ko mice, compared to FVB background control (data not shown), but was not altered by HO-1 induction (Fig. 1C).

This scenario decreased prevalent infections by 36,980 (93%) and decreased liver-related deaths by 1,400 (70%) by 2030. HCV-related liver cancer cases decreased by 72%, and decompensated cirrhosis decreased by 77%, as compared to the base case. Conclusions: While HCV prevalence in New Zealand has plateaued, advanced liver disease and deaths continue to grow. A scenario that increased the treated population and reduced new cases had a markedly LY2109761 larger impact on future disease burden as compared to a scenario considering only increased SVR. The potential impact of scenarios can

inform strategies for diagnosis, treatment and control of HCV infection in New Zealand. Disclosures: Edward J. Gane – Advisory Committees or Review Panels: Novira, AbbVie, Novartis, Gilead Sciences, Janssen Cilag, Vertex, Achillion, Tekmira, Merck, Idenix; Speaking and Teaching: AbbVie, Novartis, Gilead Sciences, Janssen Cilag Chris Estes – Consulting: Gilead Homie Razavi – Management Position: Center for Disease Analysis Catherine A. Stedman – Advisory

Committees or Review Panels: Jansen, MSD; Speaking and Teaching: Gilead The following people have nothing to disclose: Cheryl R. Brunton, Charles Henderson, John Hornell, Sarah Radke Background & Aim: The treatment paradigm for hepatitis C virus (HCV) infection is expected to change over the next five years, and recent estimates of total infections is required to develop strategies to eliminate HCV infections. This study aimed to Nutlin-3a concentration update HCV prevalence focusing on the RNA positive (viremic) population. Methods: A comprehensive literature search was conducted excluding studies published prior to 2000 as well as those in high-risk populations. Inclusion and scoring of studies was based on sample size, time of data collection, and representativeness of selleck the general population. Available country estimates were used to develop regional and global estimates. Results: The global prevalence of anti-HCV among adults (individuals aged ≥15 years) was estimated at 2.0% (1.7-2.2%), corresponding to 105 (89-118) million infections. However, viremic

HCV prevalence was substantially lower (see table). Despite a moderate regional prevalence (1.1%), an estimated 45% of the global viremic population resides in Asia since this region accounts for 60% of the world’s adult population. China, Pakistan and India accounted for 22.8 million infections or 67% of infections in Asia. The highest viremic prevalence was found in Africa (3.7%) with 25.7 million infections. Nigeria, Egypt, Republic of Congo and Ghana accounted for 15.6 million or 61% of the region’s infections. The Americas and Europe had a similar profile. The United States, Brazil and Mexico accounted for 5.4 million (68%) of viremic infections in the Americas; while Russia, Ukraine, Italy, Romania and Spain accounted for 5.1 million (66%) of viremic infections in Europe. Australia and New Zealand accounted for 240 thousand or 92% of viremic infections in Australasia.

This scenario decreased prevalent infections by 36,980 (93%) and decreased liver-related deaths by 1,400 (70%) by 2030. HCV-related liver cancer cases decreased by 72%, and decompensated cirrhosis decreased by 77%, as compared to the base case. Conclusions: While HCV prevalence in New Zealand has plateaued, advanced liver disease and deaths continue to grow. A scenario that increased the treated population and reduced new cases had a markedly Selleckchem PD0325901 larger impact on future disease burden as compared to a scenario considering only increased SVR. The potential impact of scenarios can

inform strategies for diagnosis, treatment and control of HCV infection in New Zealand. Disclosures: Edward J. Gane – Advisory Committees or Review Panels: Novira, AbbVie, Novartis, Gilead Sciences, Janssen Cilag, Vertex, Achillion, Tekmira, Merck, Idenix; Speaking and Teaching: AbbVie, Novartis, Gilead Sciences, Janssen Cilag Chris Estes – Consulting: Gilead Homie Razavi – Management Position: Center for Disease Analysis Catherine A. Stedman – Advisory

Committees or Review Panels: Jansen, MSD; Speaking and Teaching: Gilead The following people have nothing to disclose: Cheryl R. Brunton, Charles Henderson, John Hornell, Sarah Radke Background & Aim: The treatment paradigm for hepatitis C virus (HCV) infection is expected to change over the next five years, and recent estimates of total infections is required to develop strategies to eliminate HCV infections. This study aimed to selleck products update HCV prevalence focusing on the RNA positive (viremic) population. Methods: A comprehensive literature search was conducted excluding studies published prior to 2000 as well as those in high-risk populations. Inclusion and scoring of studies was based on sample size, time of data collection, and representativeness of find more the general population. Available country estimates were used to develop regional and global estimates. Results: The global prevalence of anti-HCV among adults (individuals aged ≥15 years) was estimated at 2.0% (1.7-2.2%), corresponding to 105 (89-118) million infections. However, viremic

HCV prevalence was substantially lower (see table). Despite a moderate regional prevalence (1.1%), an estimated 45% of the global viremic population resides in Asia since this region accounts for 60% of the world’s adult population. China, Pakistan and India accounted for 22.8 million infections or 67% of infections in Asia. The highest viremic prevalence was found in Africa (3.7%) with 25.7 million infections. Nigeria, Egypt, Republic of Congo and Ghana accounted for 15.6 million or 61% of the region’s infections. The Americas and Europe had a similar profile. The United States, Brazil and Mexico accounted for 5.4 million (68%) of viremic infections in the Americas; while Russia, Ukraine, Italy, Romania and Spain accounted for 5.1 million (66%) of viremic infections in Europe. Australia and New Zealand accounted for 240 thousand or 92% of viremic infections in Australasia.