Neutralizing Tm-Tnfα blocked the inflammatory signals and prevented growth failure, helped resolve jaundice and acholic stools by day 12 of life and promoted survival of RRVchallenged mice. Conclusions: Our results demonstrate a unique and early response of the neonatal immune system mediated by Tm-Tnfα responses regulating cholangiocyte cell death and epithelial injury and orchestrating the phenotype of experimental biliary atresia. Disclosures: Jorge A. Bezerra – Grant/Research Support: Molecular Genetics Laboratory, CHMC The following people have nothing to disclose: Pranavkumar Shivakumar, James E. Squires, Stephanie Walters Background: Hepatocellular accumulation

of phytosterols, a component of the lipid emulsion most commonly used in U. S. parenteral nutrition (PN) solutions, has Sotrastaurin research buy been implicated in the pathogenesis of PN associated cholestasis (PNAC). Hepatic macrophage activation

by endotoxin (LPS) absorbed from injured intestine and subsequent release of pro-inflammatory cytokines also promotes PNAC (Hepatology. 2012; 55: 151828). However, the interplay JAK cancer between phytosterol accumulation and LPS signaling in PNAC has not been clarified. The aim of this study was to determine if phytosterol- and LPS-activated macrophages play a role in hepatocellular accumulation of cholestatic phytosterols. Methods and Results: Wild type (WT) mice that were exposed to dextran sulfate sodium (to induce intestinal injury) and infused with phytosterol-containing PN solution for 14 days developed cholestasis, and had reduced hepatic mRNA levels of the sterol exporter, Abcg5/Abcg8, paralleled by increased mRNA for IL1β. To determine the effect of LPS on these pathways, WT mice were injected with intraperitoneal LPS (3-5mg/kg) for 24 hrs, which also reduced hepatic mRNA for Abcg5/8, and increased both IL1β and Tnfα mRNA. To determine if this was a direct effect on hepatocytes, HepG2 cells (human hepatocyte cell line) were exposed in vitro to either LPS (100-1000 ng/ml) or the cholestatic phytosterol, stigmasterol

acetate (Stig-Ac; 5-20 μM); mRNA expression of IL1β, TNFα, and ABCG5/8 was not altered by either in the HepG2 cells. However, when conditioned those media generated by LPS-activated human monocytes (U937 cell line) was transferred onto HepG2 cells, ABCG5/8 mRNA was significantly suppressed, suggesting a mediator from macrophages was involved. Therefore, recombinant IL-1β or TNF-α (10 ng/ml) was incubated with HepG2 cells and found to significantly suppress ABCG5/8 mRNA. Stig-Ac (5-20 μM) was also incubated with U937 monocytes and with mouse bone marrow derived macrophages (BMDMs) and found to significantly increase mRNA for IL1 p and TNFα in both cell lines. Incubating Stig-Ac (5-20 μM) with BMDMs from TLR4 mutant mice also induced cytokine transcription, thus this effect of Stig-Ac was independent of TLR4 signaling.

Correlation analysis showed that destination recall was significantly correlated with episodic recall in HD participants. Destination memory impairment in HD participants seems to be considerably influenced by their episodic memory performance. “
“The ‘beads task’ is used to measure the cognitive basis of delusions, namely the ‘Jumping to Conclusions’ (JTC) reasoning bias. find more However, it is not clear whether the task merely taps executive dysfunction – known to be impaired in patients with schizophrenia – such as planning

and resistance to impulse. To study this, 19 individuals with neurosurgical excisions to the prefrontal cortex, 21 unmedicated adults with Attention Deficit Hyperactivity Disorder (ADHD), and 25 healthy controls completed two conditions of the beads task, in addition to tests of memory and executive function

as well as control tests of probabilistic reasoning ability. The results indicated that the prefrontal lobe group GDC-0973 in vivo (in particular, those with left-sided lesions) demonstrated a JTC bias relative to the ADHD and control groups. Further exploratory analyses indicated that JTC on the beads task was associated with poorer performance in certain executive domains. The results are discussed in terms of the executive demands of the beads task and possible implications for the model of psychotic delusions based on the JTC bias. “
“Three studies are reported on the development of a four-disc version of the Tower of London test of planning ability. The first (n = 138) involved the selection of

items based on rational and empirical criteria to provide a short test of graded difficulty suitable for use with children and clinical populations. The second study (n = 480) checked the properties of the 10-item test Thalidomide on a new sample and in addition examined the internal consistency and factor structure of the test. The third study (n = 61) examined the test–retest reliability of the test over a period of 1 month. The difficulty level of the test remained relatively stable from sample to sample and was sensitive to linear trend in performance from age 5 years up to 30 years. Total score did not reflect the action of a single underlying construct but rather appeared to index a number of factors. Scores were reasonably stable over the 1-month period studied, at least for the children’s sample employed. The four-disc version is a promising method of assessing planning in children and adolescents in clinical situations. “
“Despite a recent upsurge of research, much remains unknown about the neurobiological mechanisms underlying synaesthesia. By integrating results obtained so far in Magnetic Resonance Imaging (MRI) studies, this contribution sheds light on the role of particular brain regions in synaesthetic experiences.

23 These preliminary data indicated that persistent virus replication such as HBV and HCV, at least in part, may be a contributing factor to Th17 expansion

in these patients. In addition, a fraction of Th17 cells coexpressing IFN-γ, IL-4, and FoxP3 was increased in CHB patients as compared to healthy controls. Although few data define the role of these double-positive cells at present, it is likely that they represent a subset of interim cells differentiating from Th1, Th2, or Tregs. Indeed, recent studies have confirmed that Th1, Th2, and Treg cells have the potential to differentiate into Th17 cells under certain conditions.36 In CHB patients, the increased Th17-related cytokines such as IL-1β and IL-6 as well as IL-23 may facilitate Th17 differentiation and expansion. It will be of interest to elucidate the factors that selectively facilitate Th17 differentiation HM781-36B nmr and expansion in CHB patients in the future. In summary, our findings demonstrate, for the first time, that peripheral and intrahepatic

Ensartinib clinical trial Th17 cells are preferentially increased in CHB patients, which might activate mDCs and monocytes to release inflammatory cytokines during chronic HBV infection. Thus, Th17 cells may participate in the immunopathogenesis of chronic HBV infection. We thank all HBV-infected individuals and healthy participants in this study. Additional Supporting Information may be found in the online version of this article. “
“The apical sodium-dependent bile acid transporter (ASBT, SLC10A2) mediates intestinal, renal, and cholangiocyte bile acid reclamation. Transcriptional regulation of ASBT is well described, whereas information on posttranscriptional regulation is limited. Prior studies suggested that ontogeny of

ASBT is controlled in part by changes in messenger RNA (mRNA) stability. We studied the role that Hu antigen R (HuR) and tristetraprolin (TTP) play in regulating the expression of mRNA that contains the 3′ untranslated region (UTR) of rat ASBT. The 3′UTR was incorporated into an SV-40 driven luciferase Florfenicol reporter (rASBT3-luciferase) for rapid screening of regulatory effects. Silencing HuR reduced luciferase reporter activity, whereas silencing TTP enhanced luciferase activity. Conversely, overexpression of HuR enhanced rASBT3-luciferase reporter activity. The same 3′UTR fragments of rat ASBT were incorporated into a beta-globin coding mRNA construct for analysis of mRNA stability (rASBT3-βglobin). mRNA half-life was progressively shortened by the incorporation of increasing sized fragments of the 3′UTR. Silencing HuR shortened the half-life of rASBT3-βglobin containing 0.3 kb of the rat ASBT 3′UTR. Gel shift assays revealed binding of HuR and TTP to rat ASBT 3′UTR.

In the current study, we sought selleck products to determine if RANK and RANKL were important in the hepatic response to I/R. Mice were subjected to partial hepatic ischemia followed by reperfusion. In

some experiments, mice received recombinant RANKL or neutralizing antibodies to RANKL 1 hour prior to surgery or at reperfusion to assess the role of RANK/RANKL signaling during I/R injury. RANK was constitutively expressed in the liver and was not altered by I/R. RANK was strongly expressed in hepatocytes and very weakly expressed in Kupffer cells. Serum RANKL concentrations increased after I/R and peaked 4 hours after reperfusion. Serum levels of osteoprotegerin (OPG), a decoy receptor find more for RANKL, steadily increased over the 8-hour period of reperfusion. Treatment with RANKL, before ischemia or at reperfusion, increased hepatocyte NF-κB activation and significantly reduced liver injury. These

beneficial effects occurred without any effect on cytokine expression or liver inflammation. Treatment with anti-RANKL antibodies had no effect on liver I/R injury. Conclusion: During the course of injury, endogenous OPG appears to suppress the effects of RANKL. However, exogenous administration of RANKL, given either prophylactically or postinjury, reduces liver injury in a manner associated with increased hepatocyte NF-κB activation. The data suggest that RANK/RANKL may be a viable therapeutic target in acute liver injury. (Hepatology 2012) Ischemia/reperfusion (I/R) injury of the liver is a major complication of hemorrhagic shock, liver resection, and transplantation.1,

2 It is widely accepted that there are two distinct phases in hepatic I/R injury. The first phase of injury Tyrosine-protein kinase BLK occurs during the initial few hours after reperfusion and is related to the production of reactive oxygen species from Kupffer cells, leading to mild hepatocellular injury.3, 4 The late phase injury is initiated by inflammatory mediators released by activated Kupffer cells and hepatocytes. These mediators, including interleukin (IL)-12/23, tumor necrosis factor-α (TNF-α), and IL-1, induce the expression of CXC chemokines and adhesion molecules that recruit activated neutrophils from the liver microcirculation to the parenchyma.5-10 These neutrophils then contribute to hepatocyte and vascular endothelial cell injury by releasing oxidants and proteases.4, 11 The expression of inflammatory mediators contributing to this response is largely controlled by the transcription factor nuclear factor kappaB (NF-κB). Based on a number of recent studies, it appears that the role of NF-κB in the hepatic response to I/R is cell-specific, such that NF-κB activation in Kupffer cells and endothelial cells promotes inflammatory gene expression, whereas activation in hepatocytes promotes cell survival.

All subjects enrolled in the study were native Italian speakers. All subjects gave informed consent to participate. Local ethics committee approval of the study was obtained. All patients were tested interictally at least 3 days after the last and before the next migraine attack. The following battery of neuropsychological tests assessing executive functions was administered to all subjects. Frontal Assessment Battery (FAB): consists of 6 subsets exploring different functions (conceptualization, mental flexibility,

motor programming, sensitivity to interference, inhibitory control, and environmental autonomy) related to the frontal lobes, originally designed for evaluating the frontal lobe function Erastin in neurodegenerative disorders;[17] The Trail Making Test (TMT): investigates visual attention and set shifting. It consists of 2 parts: A and B. The subject’s task is to connect with a line 25 consecutive targets on a sheet of paper in the shortest possible time. In TMT-A, the 25 targets are numbers (1, 2, 3, etc) while in TMT-B targets are both numbers and letters, and the subject must alternate them in ascending order (1, A, 2, B, etc). The performance measure taken into account is the time necessary to the subject to complete the task;[18] Controlled Oral Word Association Test (COWAT): this consists of 3

word-naming trials beginning with F, A, and S; it gives a measure of verbal fluency which is associated with frontal lobe functions;[19] Stroop Test: primarily measures executive selective attention, see more as the participant must ignore the distraction of the noncongruent color words during the

test phase. Both time of execution and number of errors were taken into account;[20] Boston Scanning Test: this is a letter cancellation test used to investigate attention; the subject has to mark all the letters A randomly arranged together with other letters;[21] Hamilton Depression Scale: the first version of this depression rating test was used.[22] Age and education adjusted scores according to Italian standardized normative data were used Acesulfame Potassium for the analysis of the neuropsychological results. In migraineurs, we used also the Migraine Disability Assessment Questionnaire (MIDAS) to assess the severity of disability related to migraine. It is a simple 5-item self-administered questionnaire, and it gives information on lost time from work or school, household work, and leisure activities. The MIDAS score is a sum of the number of lost days in these 3 domains. The validity of this tool was tested in a population-based sample of headache sufferers.[23] All patients and controls underwent MRI scans with a 1.5 Tesla (T) superconducting magnet system (GE, Milwaukee, WI, USA).

Loss of HNF6 results in normal apical-lateral localization of ZO-1, whereas loss of HNF1β results in very low levels of ZO-1 on the parenchymal side of forming bile duct lumen and improper apical localization of ZO-1 on the portal side. The postnatal consequences of these embryonic phenotypes that suggest loss of a cholangiocyte apical pole also differ between these two mouse models. Partial restoration of apical-basal polarity is observed when HNF6 is absent, but is not the case with HNF1β deficiency. Indeed, in patients with HNF1β mutations, ZO-1 was irregularly expressed in dysplastic ducts, and the observed DPM did not express ZO-1.

Absence of cystin-1 did not influence the apical marker osteopontin, but ZO-1 expanded to the apical surface of cholangiocytes, indicating that the basal and lateral poles were not established correctly. These phenotypes correspond PD0325901 ic50 to liver samples examined from ARPKD CT99021 datasheet fetuses. Because of the polarity defects observed during biliary tubulogenesis, the authors investigated whether cholangiocyte ciliogenesis was disrupted in these mouse models. Previously, HNF6 and HNF1β were implicated in either control of cilia formation or regulation of genes involved in cilia function in the pancreas and kidney, respectively.10, 11 Because of the

random distribution of centrioles ALOX15 observed in the absence of HNF6 or HNF1β, it is not surprising that embryonic cilia formation on cholangiocytes was significantly disrupted. The postnatal partial restoration of the apical-basal polarity in deficient HNF6 mice correlates with a few cilia present on cholangiocytes. However, the lack of cilia present on cholangiocytes remains as a postnatal defect in liver deficient for HNF1β. To determine if either HNF6 or HNF1β are involved in regulating the formation or function of cholangiocyte cilia, expression levels of candidate genes were examined in these two mouse models. Cystin-1 was the

only gene with reduced expression in both mouse models. Interestingly, in the cystin-1–deficient (cpk−/−) mouse model, the presence of a cilium is observed on some cholangiocytes. Therefore, reduced expression of cystin-1 in liver deficient in HNF6 and HNF1β is not the explanation for the reduced or absence of cilia in these two mouse models. Notably, and an avenue for further research, is the observation that the HNF1β targets in the kidney (Pkhd1, polycystic kidney and hepatic disease 1; Pkd2, polycystic kidney disease 2; Nphp1, nephronophthisis 1; IFT88, intraflagellar transport 88 homolog; and Kif12, kinesin family member 12) were not changed in HNF1β deficient liver, which indicates that HNF1β regulates a divergent transcriptional landscape for cilia in cholangiocytes versus kidney.

44 We further demonstrated that hCRP may impair insulin signaling through activation of the MAPK signaling pathway. Activation of MAPKs has been linked to the development of insulin resistance.2, 45, 46 p38 MAPK plays a key role in hepatic glucose metabolism,13 and ERK1/2 see more activation stimulates IRS-1 Ser612 phosphorylation

and thereby inhibits insulin signaling.47 Consistent with reported hCRP activation of p38 MAPK and ERK1/2 in endothelial cells and macrophages,10, 48 we found that hCRP increased phosphorylated p38 MAPK and ERK1/2 ex vivo in liver tissues and in vitro in hepatocytes. No activation of JNK by hCRP was observed in rat liver or hepatocytes in our study, which was contrary to the reports that CRP activates

the JNK pathway in endothelial cells.9, 10 The discrepancy could be attributed to tissue differences (liver versus extrahepatic), the different time course or source of CRP as recombinant hCRP used in previous studies may have affected the JNK pathway, the latter due to contamination. It has been suggested that ERK1/2 inhibits insulin signaling at the level of IRS proteins in adipocytes to a greater extent than JNK and p38 MAPK.44 Our in vitro study suggests that ERK1/2 plays a more important role than the other MAPKs in hCRP-mediated hepatic insulin resistance. In summary, we have find more provided the first in vivo evidence that hCRP induces hepatic insulin resistance accompanied by a defect in the IRS/PI3K/Akt pathway, suggesting a causative link between hCRP

and insulin resistance. Furthermore, in vitro evidence has implicated ERK1/2 as the primary MAPK that plays a role in hCRP-impaired insulin signaling, providing a molecular mechanism for such effect of hCRP. The current study suggests that hCRP, in addition to being a biomarker for inflammation, may be a potential target for treatment and prevention of hepatic insulin resistance. CRP gain and loss of function studies in humans are required to determine its relevance to the development of insulin resistance in humans. We thank Mark Dekker for comments on the article and for Methisazone technical assistance. Additional Supporting Information may be found in the online version of this article. “
“In hepatocellular carcinoma (HCC), intrahepatic metastasis frequently correlates with epithelial to mesenchymal transition (EMT) of malignant hepatocytes. Several mechanisms have been identified to be essentially involved in hepatocellular EMT, among them transforming growth factor (TGF)-β signaling. Here we show the upregulation and activation of the receptor tyrosine kinase Axl in EMT-transformed hepatoma cells.

As shown in Table 2, the P buy RG7204 values were quite

similar (P = 2.70 × 10−11 to 0.003) for 11 SNPs located at HLA-DP, while rs11752643 remained nonsignificant. For 11 significant SNPs, we examined the association of genotype frequencies between cases and controls (both clearance and healthy combined), and also between cases and clearance controls only. Table 3 presents the genotype distribution in each group: OR with 95% CI and P values for carriers versus controls, and carriers versus clearances. As illustrated in Fig. 1, the first five SNPs showed minor alleles (four in HLA-DPA1 and one adjacent within HLA-DPB1) associated with decreasing risk/protection of HBV chronic infection (Table 3; OR = 0.33 to 0.66, P = 6.7 × 10−7 to 0.045 for homozygote, OR = 0.50 to 0.77, P = 4.6 × 10−7 to 0.036 for heterozygote). The first four SNPs located in HLA-DPA1 formed haplotype block 1 (Fig. 1). The last six variants located on gene HLA-DPB1 had minor alleles significantly associated with increasing risk/susceptibility of HBV chronic infection (OR = 2.46 to 3.34, P = 5.7 × 10−12 to 7.0 × 10−7 for homozygote, OR = 1.56 to 2.36, P = 6.0 × 10−9 to 0.004 for heterozygote). These six SNPs with susceptibility selleck compound minor alleles

formed haplotype block 2 (Fig. 1). Similar significant associations were observed when we compared HBV carriers with HBV clearances (Table 3; columns 8, 9). Next we examined haplotype association for block 1, block 2, and the two blocks combined. Table 4 lists the haplotype frequencies in cases and controls, OR with 95% CI and P values for block 1 and block 2. The haplotype AACT, which retains all rare protective alleles of block 1, was significantly associated with decreasing risk of chronic hepatitis B infection (OR = 0.54, P = 8.73 × 10−7). The haplotype GAGATT (which retains

all rare susceptible alleles of block 2) and GGGGTC (which retains three rare susceptible aminophylline alleles of block 2) were significantly associated with increased the risk of chronic hepatitis B infection (OR = 1.98, P = 1.37 × 10−10 for GAGATT; OR = 1.7 P = 0.002 for GGGGTC). Table 5 presents a combination of haplotype block 1 and block 2 considered together. The combined protective haplotypes of block 1 (AACT) and block 2 (AGTGCC) were very strongly associated with decreased risk of chronic hepatitis B (OR = 0.36, P = 3.0 × 10−11). The protective haplotype of block 2 (AGTGCC) combined with other haplotypes of block 1 were also significantly associated with decreased risk of chronic hepatitis B infection (OR = 0.56 to 0.65, P = 0.002 to 0.0002). In this study, 12 SNPs that were previously reported to be associated with chronic hepatitis B18, 19 were interrogated in 521 persistent chronic HBV carriers and 819 controls in a Han Chinese population from northern China. Eleven SNPs located within HLA-DPA1 and HLA-DPB1 were strongly significantly associated with persistent chronic HBV carrier status (Table 2).

12, 13 CLDNs are critical components of TJs

that regulate paracellular permeability and polarity and have a tetraspanin topology with four transmembrane domains, two extracellular and one intracellular loops, and N- and C-terminal cytoplasmic domains.14 CLDN1 extracellular loop 1 (EL1) is required for HCV entry9 and is involved in barrier function and contributes to pore formation between polarized cells.15 Mutagenesis studies in nonpolarized 293T cells SP600125 mw demonstrate that CLDN1 enrichment at cell–cell contacts may be important for HCV entry.16 We17, 18 and others16, 19, 20 using a variety of imaging and biochemical techniques reported that CLDN1 associates with CD81. However, due to the lack of neutralizing anti-CLDN1 antibodies targeting extracellular epitopes, the exact role of CLDN1 in the viral entry process is poorly understood. BC, bile canalicular surface; CLDN1, claudin-1; CMFDA, www.selleckchem.com/products/Roscovitine.html 5-chloromethylfluorescein diacetate; EL1 and 2, extracellular loops 1 and 2; FRET, fluorescence resonance energy transfer; HCV, hepatitis C virus; HCVcc, cell culture-derived HCV; HCVpp, HCV pseudoparticles; IgG, immunoglobulin G; PBS, phosphate-buffered saline; SD, standard deviation; SR-BI, scavenger receptor class B type I; TJ, tight junction. Human Huh7,5 Huh7.5.1,21 HepG2,18 293T,5 Bosc,22 Caco-2,23 and rat BRL-3A

cell lines24 were propagated in Dulbecco’s

modified Eagle’s medium/10% fetal bovine serum. 293T/CLDN1 cells were obtained by stable transfection of 293T cells with a pcDNA3.1 vector encoding CLDN1. Dimethyl sulfoxide–mediated differentiation of Huh7.5.1 cells was performed as described.25 Primary human hepatocytes were isolated from liver resections from patients at the RVX-208 Strasbourg University Hospitals with approval from the Institutional Review Board.26, 27 In brief, liver specimens were perfused with calcium-free 4-(2-hydroxyethyl)-1-piperazine ethanesulfonic acid buffer containing 0.5 mM ethylene glycol tetraacetic acid (Fluka) followed by perfusion with 4-(2-hydroxyethyl)-1-piperazine ethanesulfonic acid containing 0.05% collagenase (Sigma) and 0.075% CaCl2 at 37°C. Following washing of cells with phosphate-buffered saline (PBS) and removal of nonviable cells by Percoll (Sigma) gradient centrifugation, freshly isolated hepatocytes (3 × 105 cells/well) were plated in 24-well plates precoated with collagen (Biocoat, BD Biosciences) and allowed to adhere in William’s E medium (Sigma-Aldrich) containing 1% Glutamax (Gibco), 1% insulin transferrin selenium (Gibco), 10−7 M dexamethasone (Sigma), 0.15% bovine serum albumine (Sigma), and 10% fetal bovine serum (PAN Biotec). Anti-CLDN1 antibodies were raised by genetic immunization of Wistar rats using a human CLDN1 complementary DNA expression vector.

The maximal delay from HCV contamination to diagnosis of acute hepatitis C was <3 months in 31 cases and <1 year in 13 cases. selleck chemicals The patients included in the follow-up study did not differ from those who were not included (data not shown) in terms of age, HIV infection (CD4 count, Centers for Disease Control and Prevention

clinical stage, treatment status), the presence of jaundice, concomitant sexually transmitted infections, the type of acute hepatitis C (acute symptomatic, seroconversion). Acute hepatitis C was diagnosed in these patients because of jaundice (n = 6) and/or other clinical symptoms (n = 13, mainly asthenia) and/or because of recent high-risk

sexual intercourse (n = 15) and/or elevated ALT levels (n = 39). Mean (± SD) ALT elevation at diagnosis was 484 ± 67 IU/L (11.1 ± 1.8 times the upper limit of normal). Acute hepatitis C was associated with another sexually transmitted disease in 20 (38%) patients, primarily syphilis (n = 14). Three patients also had positive hepatitis B surface this website antigenemia. In one case, acute hepatitis C was concomitant with HIV primoinfection. The CD4 count was above 500/mm3 in 29 patients, between 350 and 500/mm3 in 14 patients, between 200 and 350/mm3 in eight patients, and below 200/mm3 in two patients. Antiretroviral therapy was ongoing in 42 (79.2%) patients, and 31 patients had an undetectable HIV viral load. Of the 49 patients with an available HCV genotype, 28 (57.1%) 14 (28.6%), and 7 (14.3%) were infected with HCV genotype 4, 1, and 3, respectively. The mean HCV viral load was 5.8 ± 1.1 log10 IU/mL at the time of acute hepatitis C diagnosis. Among the 53 patients in the present study, eight experienced spontaneous clearance. The mean delay between

acute hepatitis C diagnosis and last negative HCV RNA in cases of spontaneous clearance was 25.9 ± 15.0 months. The cumulative rate of spontaneous HCV clearance was 8.3% 1 month after the diagnosis of acute CHIR-99021 price HCV infection, 11.0% at 3 months, and 16.5% at 6 months. The only difference observed between the patients with spontaneous HCV clearance and those without was the HIV viral load (3.54 ± 1.97 versus 2.43 ± 1.30 log10 copies/mL; P = 0.05) at the diagnosis of acute hepatitis C. No other difference was observed, particularly regarding the CD4 strata (P = 0.41) or the HCV viral load (5.58 ± 1.87 versus 5.86 ± 0.90 log10 IU/mL; P = 0.54). Overall, 13 patients were not treated for HCV. The characteristics of patients who were treated and those who were not are presented in Table 1.