[92, 93] An Asian study of IFN therapy regimens lasting six to te

[92, 93] An Asian study of IFN therapy regimens lasting six to ten months identified therapeutic benefits six months after the end of therapy in 30% of cases, compared to just 7% in the control group.[94] An even longer therapy regimen of 24 months achieved sustained quiescence of hepatitis in 30% of cases and 18% HBsAg elimination after six years.[95] In light of these findings, continued administration of IFN is recommended overseas for patients with HBeAg negative

chronic hepatitis B. IFN therapy has also been shown to selleck compound library suppress carcinogenesis and deliver improved life expectancies in HBeAg negative patients with chronic hepatitis B, as with HBeAg positive patients.[96] Recommendation IFN therapy has been shown to produce significant improvements in HBeAg positive chronic HBV patients with respect to HBeAg negative conversion, HBeAg seroconversion, HBV DNA negative conversion and ALT normalization, compared to an untreated control group. Pegylated IFN is available as Peg-IFNα-2a (40kD branched strand PEG covalently bonded to IFNα-2a)

and Peg-IFNα-2b (12kD single strand PEG urethane bonded to IFNα-2a). In Japan, only Peg-IFNα-2a is approved by medical insurance for the treatment of chronic active hepatitis B. PEG is a neutral, water-soluble molecule with no inherent toxicity. The molecular weight is governed by the number of ethylene oxide subunits. Pegylation of IFN has two objectives: to alter the pharmacokinetics check details in the body, and to prevent IFN from being recognized

and rejected by the host’s immune system. The concentration of Peg-IFNα-2a in the blood remains within the therapeutic range for approximately 168 hours after administration, reaching the peak concentration (Cmax) 72 to 96 hours after administration.[97] A study in Asia comparing the therapeutic effects of Peg-IFNα-2a and conventional IFNα-2a reported a complete response (i.e. elimination of HBeAg, suppression of HBV DNA and normalization of ALT) in 28% of patients treated with Peg-IFNα-2a compared to 12% of patients treated with conventional IFNα-2a, a statistically significant difference (P = 0.036). The HBeAg seroconversion rate was also higher for Peg-IFNα-2a (33% versus 25%), indicating the superiority of the pegylated agent.[98] In an overseas comparative study, 814 HBeAg positive patients were divided into three groups: Clomifene the first was administered Peg-IFNα-2a for 48 weeks, the second Peg-IFNα-2a together with lamivudine for 48 weeks, and the third lamivudine only for 48 weeks.[8] While all three groups returned similar HBeAg seroconversion rates at the end of the treatment period (27%, 24% and 20% respectively), the Peg-IFNα-2a groups showed significantly better HBeAg seroconversion rates 24 weeks after the end of treatment (32%, 27% and 19%). Virological outcomes 24 weeks after treatment were also better in the Peg-IFNα-2a groups, with 32% of patients <5 log copies/mL HBV DNA, 14% < 400 copies/mL, and HBsAg seroconversion in 3%.

This hypothesis is strengthened by the fact that the two selected

This hypothesis is strengthened by the fact that the two selected substitutions, sS143T and sM197T, are located at the external side of HBsAg, within known immunodominant epitopes. However, this was noted in only 1 patient in this study. Adefovir dipivoxil is still widely used worldwide, alone or in combination with lamivudine. As shown in this study, variants with amino acid substitutions ABT-263 mw known to confer resistance to various nucleoside/nucleotide analogs, including adefovir, can be detected in a substantial proportion of treatment-naïve patients with CHB. Larger scale studies are now required to determine

whether baseline testing with UDPS will be useful to orientate HBV treatment strategies. selleck chemicals llc In addition, next-generation sequencing methods, such as UDPS, could be of considerable interest for early diagnosis of viral resistance during antiviral therapy. Indeed, with our approach, resistance could be diagnosed at approximately the same time as with cloning and sequencing (thus considerably earlier than with population sequencing), in a user-friendly and rapid way, compatible

with clinical practice (data not shown). This will be facilitated in the future when the costs are reduced and the technology becomes easily available through specialized platforms. In conclusion, using an original software package for analyzing viral sequences generated by UDPS and other next-generation sequencing methods in the context of antiviral resistance, (1) we showed that substitutions conferring HBV

resistance to nucleoside/nucleotide analogs preexist in patients who have never been exposed to these drugs, (2) we characterized the complex and heterogeneous dynamics of adefovir-resistant viral populations in a group of HBV-infected patients in whom resistance emerged during long-term adefovir therapy, and (3) we identified thus far unknown amino acid substitutions that appeared to play an important role in HBV resistance to adefovir. These findings will also be helpful for understanding resistance to tenofovir, which shows cross-resistance many with adefovir in vitro. Our findings imply that next-generation sequencing data analysis will have a number of applications in viral resistance assessment, as we recently reported with hepatitis C virus and human immunodeficiency virus.[29, 30] The authors thank Thierry Ravard for his help with mathematical modeling and Françoise Roudot-Thoraval for her help with statistical tests, as well as Katyna Borroto-Esoda and Manh-Tong Dao. Additional Supporting Information may be found in the online version of this article. “
“Invasive fungal infection (IFI) related to surgery in elderly patients is often associated with high morbidity and mortality.

Such predisposition to develop NAFLD was, again, driven by proinf

Such predisposition to develop NAFLD was, again, driven by proinflammatory gene expression driven by other innate immune receptors, since deletion of either TLRs 4 or 9, or the TNF-α receptor, were sufficient to ablate

the increased susceptibility to NAFLD conferred by loss of NLRP6. This increased susceptibility to developing NAFLD was associated with altered microbiota composition, namely, elevated levels of Prevotella and Porphyromonas species. Such alterations were deemed to play a functional role in driving disease, since co-housing of these genetically Vadimezan clinical trial altered mice with wild-type mice transferred both the elevations in these bacterial populations Hormones antagonist and the predisposition to develop

metabolic syndrome.[10] While transfer of bacteria among co-housed mice seems likely to be far more efficient than one would expect in cohabitating humans, especially since mice are coprophagic, it nonetheless supports the principal that predisposition to NAFLD may be spreading through the population in a manner analogous to a traditional infectious disease. A likely factor in altering gut microbiota composition and consequently playing a role in perturbing the host-microbiota dynamic in NAFLD is diet. Indeed, HFDs alter gut microbiota composition by altering phyla ratios and promoting growth of Proteobacteria, both of which can increase the microbiota’s proinflammatory potential.[51] Importantly, such alterations in the microbiota occur quickly and are independent of weight gain, suggesting they are not purely a consequence of inflammation. Considerable suspicion has also focused

on the Unoprostone role of fructose, whose consumption has greatly increased in a manner roughly paralleling the rise of NAFLD as a common disease. Fructose consumption, mainly by consumption of added sugars, can represent 10% of total energy intake in developed country.[52] Placing mice on a high-fructose diet robustly promotes lipid accumulation in the liver and alters microbiota composition, although the extent to which fructose promotes hepatic lipid accumulation in humans is far from clear.[52] It is speculated that, analogous to the case of the role of the HFD in metabolic syndrome, diets high in fructose might alter host-microbiota interactions to promote NAFLD by altering microbial metabolism or promoting low-grade inflammation. The notion that fructose alters the metabolic capability of the microbiota in a manner that promotes lipid uptake and deposition is based on observations that a high-fructose diet alters the mouse microbiota by shifting phyla ratios in a way that increases energy harvest.

92 [0 86-0 99]) Conclusions Among patients on liver transplant w

92 [0.86-0.99]). Conclusions Among patients on liver transplant waiting lists, those with a TIPS have lower waiting list mortality than those without TIPS. These findings suggest the possibility that patients with TIPS may have better survival than those without TIPS even among cirrhotic patients not listed for transplantation. Disclosures: The following people have nothing to disclose: Kristin Berry, George N.

Ioannou Background. Two randomized controlled studies have evaluated the effect of rVlla on variceal bleeding in cirrhosis without showing significant benefit. The aim of the present study was to perform a meta-analysis of the two trials, click here based on individual patient data with special focus on high risk patients with active bleeding at endoscopy. Methods. Access to individual data of the two studies was achieved and a meta-analysis hereof was performed. The primary outcome measure was the effect of rVlla on a composite five day endpoint: failure to control bleeding, 5-day rebleeding or death. Analysis was based on intention to treat. High risk was defined as active bleeding on endoscopy and Child-Pugh score>8. Results.497 patients were egligible for the meta-analysis with 308 (62%) having active variceal bleeding

at endoscopy (oozing or spurting) and 283 of these (57%) having a Child-Pugh score>8. The intention to treat analysis on the composite endpoint in all Selleck Poziotinib patients with bleeding from

esophageal varices did not show any treatment beneficial treatment effect. However, failure rate for the primary composite end-point was significantly lower in treated patients Branched chain aminotransferase with active bleeding at endoscopy (17%) compared to placebo (26%, p=0.049). This difference was highly significant in patients with Child-Pugh score>8 and active bleeding at endoscopy (rVlla 16%, placebo 27%; p=0.023). No significant treatment effect was found at 42 days. Five thromboembolic events occurred in rVlla treated patients compared to none in placebo treated patients. Conclusion. The current metaanalysis shows a beneficial effect of rVlla on the primary composite endpoint of control of acute bleeding, prevention of rebleeding day 1-5 and 5-day mortality in patients with advanced cirrhosis and active bleeding from esophageal varices at endoscopy. This treatment can be considered in patients with lack of control of bleeding after standard treatment. Disclosures: Jaime Bosch – Advisory Committees or Review Panels: Intercept pharma; Consulting: Chiasma, Gilead Science, Norgine, ONO-USA; Grant/Research Support: Gore The following people have nothing to disclose: Flemming Bendtsen, Gennaro D’Amico, Ea Rusch, Roberto De Franchis, Per K.

Prioritizing treatment toward those with more advanced fibrosis i

Prioritizing treatment toward those with more advanced fibrosis is associated with a decrease in total cost of $7.5 billion

and 59,035 fewer HCV-related complications. Total QALYs and complications click here avoided are maximized when treatment initiation occurs as soon as possible after testing. Conclusion: This study confirms that birth cohort testing is, on average, cost-effective. However, this remains true only when enough tested and HCV-positive subjects are treated to generate sufficient cost offsets and QALY gains. Given the practical and financial challenges associated with implementing birth cohort testing, the greatest return on investment is obtained when eligible patients are treated immediately and those with more advanced disease are prioritized. (HEPATOLOGY 2013) Hepatitis C virus (HCV) is a major global public health issue. In the United States, chronic HCV infection is the leading cause of hepatocellular carcinoma (HCC) and liver transplantation.1-5

It is estimated that 3.2 million people are living with chronic HCV in the United States,6 and between 45% and 85% of these people are unaware of their infection.7-10 Historically, the two principal modes of HCV transmission are blood transfusion and injection drug use11; however, after the introduction of routine blood www.selleckchem.com/products/icg-001.html testing in 1992, the predominant route of disease transmission in the United States is now among persons who inject drugs12; with an estimated 17,000 new infections occurring annually.13 In the absence of a robust HCV testing and treatment program in the United States, it is estimated that 1.76 million people with chronic

HCV will develop cirrhosis; 400,000 will develop HCC, and more than 1 million will die of an HCV-related death.14 CDC, Centers for Disease Control and Prevention; ESLD, end-stage liver disease; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; NHANES, National Health and Nutrition Examination Survey; QALYs, quality-adjusted life years; SVR, sustained virological response Risk-based testing guidelines to identify HCV infection were first published in 1998.15 These guidelines advocated testing for HCV in persons at high risk of infection, such as those with a history of injection drug use and those receiving a blood transfusion or organ transplant prior to comprehensive OSBPL9 blood screening. Recent modeling studies have presented compelling economic analyses demonstrating that birth cohort screening compared with risk-based screening in the United States is cost-effective.16-18 These findings have led to published Centers for Disease Control and Prevention (CDC) guidelines advocating one-time testing for HCV of all persons born between 1945 and 1965.13 Despite demonstrable cost-effectiveness, there are substantial financial and practical barriers to the widespread implementation of a comprehensive birth cohort testing program.

Immunodetection was performed using anti-Myc (Santa Cruz Biotechn

Immunodetection was performed using anti-Myc (Santa Cruz Biotechnology, Santa Cruz, CA), anti-α-tubulin (Sigma-Aldrich, St. Louis, MO), and anti-C-Jun (BD Biosciences, Franklin Lakes, NJ) Abs. HepG2 cells were transfected with different combinations of plasmids using FuGENE 6 reagent (Roche, Indianapolis, IN), according to the manufacturer’s protocol. Plasmids used included Myc/pcDNA3.1+ vector containing various forms of HBx, MMP10-WT/pGL3-Basic, MMP10-AP1-Mut/pGL3-Basic Selleckchem AZD1208 reporter constructs, and an internal control (pRL-SV40). The total amount of expression vectors was equalized with the empty vector. Twenty-four hours after transfection, luciferase and

Renilla luciferase activities were measured by the Dual Luciferase Reporter assay system (Promega, Madison, WI), according to the manufacturer’s protocol. Transfection efficiency was normalized with the Renilla luciferase activity. Experiments were done thrice Tanespimycin solubility dmso independently. Cells (3 × 106) were seeded 1 day before harvest and chromatin immunoprecipitation (ChIP) assay was performed. Cells were fixed with 1% formaldehyde for 10 minutes, and the reaction was neutralized by adding glycine to a final concentration of 125 mM in the mixture. Formaldehyde cross-linked

cells were collected by centrifugation, resuspended in membrane containing lysis buffer (5 mM of KOH [pH 8.0], 85 mM of KCL, 0.5% NP-40, 0.5% SDS, and 1×CompleteProtease Inhibitors), and incubated on ice for 30 minutes. Cell nuclei were collected by

centrifugation, and cross-linked DNA was digested by Micrococcal nuclease for 20 minutes, according to manufacturer’s protocol (New England Biolabs, Inc., Ipswich, MA). Digested DNA was released from nuclei by freeze-thaw 17-DMAG (Alvespimycin) HCl cycles and processed for ChIP assay according to the EZ-Chip assay kit (Millipore, Billerica, MA) protocol. The Ab against C-Jun protein was used (Santa Cruz Biotechnology), and the primer set (forward 5′-CAAACACAGAAATCATTTCCTGG-3′ and reverse 5′-AGATCACCAACAGTATGATTCATGC-3′) covering the putative AP-1-binding site on the MMP10 promoter was employed for standard PCR measurement in the ChIP assay. Clinicopathological features of HCC patients, including tumor size, cellular differentiation according to Edmondson’s grading, venous invasion into portal or hepatic venules, direct liver invasion, tumor microsatellite formation, tumor encapsulation, and number of tumor nodules, were analyzed using PASW Statistics 18 for Windows (SPSS, Inc., Chicago, IL). For clinicopathological correlation analysis, Fisher’s exact test was used for analysis of categorical data. For in vitro cell-invasion assay and reporter assay, the Student t test was used for continuous data. Results were considered significant if the P value was less than 0.05.

We describe the conventional MR imaging, perfusion MRI, proton MR

We describe the conventional MR imaging, perfusion MRI, proton MR spectroscopy (1H MRS), histopathology, immunohistochemistry, and chromosomal analysis in two cases of these tumors, with some features which have not been previously well described. Both tumor types demonstrated markedly elevated cerebral blood volume on perfusion MRI and had 1p19q chromosomal codeletions. Both tumor types showed an elevated Cho/Cr ratio, but extraventricular ganglioneurocytoma showed a preserved NAA/Cr ratio. These tumors should be considered in the differential diagnosis of intra-axial

brain tumors. “
“To report the brain imaging JNK phosphorylation features on magnetic resonance imaging (MRI) in inadvertent intrathecal gadolinium administration. A 67-year-old female with gadolinium encephalopathy from inadvertent high dose intrathecal gadolinium administration during an epidural steroid injection was studied with

multisequence 3T MRI. T1-weighted imaging shows pseudo-T2 appearance with diffusion of gadolinium into the brain parenchyma, olivary bodies, and membranous labyrinth. Nulling of cerebrospinal fluid (CSF) signal is absent Gemcitabine ic50 on fluid attenuation recovery (FLAIR). Susceptibility-weighted imaging (SWI) demonstrates features similar to subarachnoid hemorrhage. CT may demonstrate a pseudo-cerebral edema pattern given the high attenuation characteristics of gadolinium. Intrathecal gadolinium demonstrates characteristic imaging features on MRI of the brain and may mimic subarachnoid hemorrhage on susceptibility-weighted imaging. Identifying high dose gadolinium within the CSF spaces on MRI is essential to avoid diagnostic and therapeutic errors. “
“Postpartum cerebral angiopathy mostly occurs in the large or medium-sized cerebral arteries. In this Galeterone case, we aimed to report a case of postpartum cerebral angiopathy presented as an asymmetrical penetrating arterial territory infarct with severe surrounding vasogenic edema. A 26-year-old woman admitted because of sudden headache after an attack of seizure. On initial computerized tomography

(CT), hypodense lesion in the right basal ganglia was observed. The diffusion-weighted image on 5th day revealed focal acute ischemic infarction with surrounding extensive vasogenic edema in right basal ganglia. The CT angiography showed multifocal arterial narrowing of intracranial cerebral arteries that completely resolved on the follow-up study. This case suggested that asymmetrical small penetrating arterial territory infarct can occur as an atypical presentation of postpartum cerebral angiopathy. “
“To describe a case of successful intracranial angioplasty and stenting of a symptomatic middle cerebral artery (MCA) stenosis using a transcervical approach. A 73-year-old woman presented with several ischemic strokes in the left MCA distribution.

Although it is possible that these aspects are specifically deran

Although it is possible that these aspects are specifically deranged in the liver, we observed the morphological characteristics of VPA hepatotoxicity in human myoblasts,3 implicating the same mechanism in our in vitro model. Moreover, an elevated serum creatine kinase in patients with VPA toxicity points

to a similar direct toxic effect on skeletal muscle.11 Unlike mature skeletal muscle and brain, the liver can proliferate in response to damage, and there is clear evidence of hepatocyte proliferation in patients with AHS. We have shown that treatment with 2 and 10 mM VPA impairs cellular proliferation in vitro, and that p.Q1236H increases mtDNA mutability in yeast and may decrease mtDNA copy number in myotubes. The yeast system is a proven method to study the effects on mtDNA buy NVP-LDE225 of both strong and weak POLG mutations, such as p.E1143G, whose effects are very mild and cannot easily be observed in higher eukaryotes.14 After a limited number of cell divisions most yeast mitochondria are homoplasmic, as the heteroplasmic state is always transient in S. cerevisiae.14 Therefore, conditions that cause increased mtDNA mutability, even at a low extent, lead to an increase of respiratory

deficient cells (i.e., petite mutants) after only a few generations. For the p.Q1236H mutation we observed a small but significant increase PF-02341066 manufacturer in extended mtDNA mutability determined as an increase in petite frequency. Observation of this effect in a yeast model predicts that a similar effect would occur in human cells, resulting in mtDNA copy number reduction, as observed in myotubes harboring this mutation. This raises the possibility that both mechanisms independently compromise the regenerative capacity of the liver, thus inhibiting the endogenous capacity for liver repair in response to an external insult. Dipeptidyl peptidase For VPA, this could be through the inhibition of histone deacetylases, which regulate gene expression by relaxing chromatin structure and facilitating access to DNA by the transcriptional

machinery.19 In this study, over 50% (8/14) of patients with probable VPA hepatotoxicity had heterozygous POLG substitutions associated with >20-fold increased risk of VPA-induced liver injury, seven of whom harbored previously described single nucleotide polymorphisms; p.Q1236H and p.E1143G . Here we show that p.Q1236H is not phenotypically neutral, with histidine at position 1236 increasing both mtDNA deletion frequency and point mutability frequency in yeast. However, the phenotype of both substitutions is mild, explaining why these alleles are common throughout the world (p.Q1236H ≤8.6%, and p.E1143G ≤4%). This suggests p.Q1236H and p.E1143G are only disadvantageous in specific contexts, such as exposure to VPA. Screening for functional POLG substitutions will minimize the risk of fulminant liver failure in patients exposed to VPA. Global and Hispanic control data for p.Q1236H was kindly supplied by Dr. Andy Singleton, NIH, Bethesda, MD.

THIS WORK WAS supported by the National Natural Science Foundatio

THIS WORK WAS supported by the National Natural Science Foundation of China (30600575). We also thank Xu-Zhen Wang, PhD, for her constructive

suggestions and editorial assistance. “
“A 59-year-old female with a past history of oral contraceptive use presents with right upper quadrant pain. Her physical examination and liver biochemical tests are normal. The alpha-fetoprotein level is also within normal limits. The abdominal computed tomography (CT) scan shows a small mass in the kidney that raises the suspicion of renal cell carcinoma. Images through the liver show a vague mass with some peripheral hyperenhancement in the right lobe of the liver (Fig. 1A). What is the role of magnetic resonance imaging (MRI) in the characterization of indeterminate liver masses? Is there any benefit in using newer MRI contrast

selleckchem agents such as Eovist? CH, cavernous hemangioma; mTOR inhibitor CT, computed tomography; FL-HCC, fibrolamellar hepatocellular carcinoma; FNH, focal nodular hyperplasia; HA, hepatic adenoma; HCC, hepatocellular carcinoma; MRI, magnetic resonance imaging; NSF, nephrogenic systemic fibrosis. Improvements in imaging technology and more widespread utilization of imaging techniques have led to increased detection of liver masses. In many cases, a lesion can be diagnosed with certainty because of its characteristic appearance. However, the appearances may not always be typical. Hepatic masses may be enhanced more than, less than, or equally to normal hepatic parenchyma; this depends on the nature of the lesion, the timing of the scan with respect to the contrast bolus, and the attenuation of the liver during CT (e.g., normal attenuation versus low attenuation from fatty infiltration). Lesions that typically

show arterial phase hyperenhancement include cavernous hemangioma (CH), focal nodular hyperplasia (FNH), hepatic adenoma (HA), hepatocellular carcinoma (HCC), fibrolamellar hepatocellular carcinoma Pregnenolone (FL-HCC), and certain metastases (e.g., neuroendocrine tumors and breast cancer). The degree, pattern, and temporal appearance of the enhancement are all helpful in the characterization of these masses. CHs typically show nodular or globular, discontinuous peripheral enhancement with progressive centripetal filling over time. Small CHs may show more homogeneous flash filling during the early arterial phase. On MRI, the lesions are usually well defined with high signal intensity on T2-weighted images. On ultrasound, they are typically echogenic with through transmission, but they may be hypoechoic in a fatty liver. The typical appearance of FNH is a diffusely homogeneous, hyperenhancing, slightly lobulated mass during the arterial phase of imaging (Fig. 1B).

The data obtained from the staggerer mice are intriguing 22, 24,

The data obtained from the staggerer mice are intriguing. 22, 24, 31 These mice exhibit a phenotype that includes lower body weight and reduced adiposity; however, liver triglyceride levels were dramatically different across published reports: they were more than double in the staggerer mice in one experiment, but were only 50% of those of wild-type mice in another. The expression pattern of hepatic LXRα, SREBP-1c, and FAS in staggerer mice also varied greatly in these reports. The nature of this discrepancy in the lipid metabolism of staggerer mice is difficult to understand. The systemic sg mutation of RORα may induce substantial primary effects, as well as secondary effects, on lipid

metabolism after severe neurological and developmental defects. Targeted muscle-specific expression of truncated RORα1ΔDE, a dominant-negative RORα, affected the fatty acid learn more biosynthetic pathway by elevating pAMPK levels and decreasing the expression levels of LXRα and SREBP-1c. 26 Apparently these results are completely opposed to ours. However, we demonstrated clearly that expression of functional RORα suppressed lipid accumulation in vitro and inhibited hepatic steatosis in vivo. Interestingly, our finding that the truncated mutant lacking LBD was as effective as the wild-type RORα in the activation of AMPK and repression of LXRα (Supporting Fig. 3) suggests that the functionally

active domain in repressing hepatic lipogenesis does not reside in the LBD of RORα. Lumacaftor These data suggest the possibility that RORα1ΔDE is a positive effector, rather than a dominant-negative regulator Rebamipide in suppressing hepatic lipogenesis. Further studies using specifically controlled knockout of RORα, or transgenes of functional domains in the liver, may be useful for understanding the role of RORα in hepatic lipid metabolism. In conclusion, our study of the role of RORα in hepatic lipogenesis may provide a deeper insight not only into understanding the maintenance of energy homeostasis at the molecular level, but also into

the design of therapeutic strategies against hepatic steatosis and metabolic disturbances. Additional Supporting Information may be found in the online version of this article. “
“The high levels of interleukin 10 (IL-10) present in chronic hepatitis C virus (HCV) infection have been suggested as responsible for the poor antiviral cellular immune responses found in these patients. To overcome the immunosuppressive effect of IL-10 on antigen-presenting cells such as dendritic cells (DCs), we developed peptide inhibitors of IL-10 to restore DC functions and concomitantly induce efficient antiviral immune responses. Two IL-10-binding peptides (p9 and p13) were selected using a phage-displayed library and their capacity to inhibit IL-10 was assessed in a bioassay and in STAT-3 (signal transducer and activator of transcription 3) phosphorylation experiments in vitro.