Methods: Hepatocyte-specific keap-1 knockout mice (Keap1 Δhepa), that carry hepatic overexpression of the antioxidant

regulator Nrf2, were generated and fed a Methionine-Choline-Deficient (MCD) diet for 4 weeks in order to investigate the influence of Nrf2 activation on hepatic lipid metabolism, liver injury and inflammation as well as fibrosis initiation. Serum and liver samples were collected for biochemical, gene and protein expression analyses. Results: After 4 weeks of MCD treatment the liver/ body weight ratio of Keap1 Δhepa mice was significantly higher compared to controls with no differences in total body weight. Interestingly, liver histology (HE and ORO) revealed a dramatic reduction of lipid droplets in number and size confirmed by a decreased content of intra-hepatic triglycerides (TG) in Keap1 Δhepa. Accordingly, expression of the fatty acids transporter FABP1 and the lipid droplets-associated BMS-777607 cost protein G0S2 was down-regulated. Curiously, total circulating and hepatic levels of cholesterol were significantly increased in

the same group. Together with other antioxidant enzymes, Nrf2 target genes involved in the pentose phosphate pathway, G6PD and PGD, were significantly up-regulated compared to controls. Protein expression analysis showed an increased phosphory-lation of Akt and of its downstream target GSK-3beta. In line with these data, an enhanced glucose up-take seen in a glucose tolerance test in naïve Keap1 SAR245409 mw Δhepa hepatocytes GNAT2 indicates the functional importance of the pentose-phosphate pathway. TUNEL assay showed a reduced number of apoptotic cells without differences in proliferation (Ki67). However, no difference in inflammatory F4/80- and CD11b-positive cells was detected between the two groups as well as in pro-fibrogenic

expression of alphα-SMA and col1a1 genes. Conclusions: In this diet-induced NASH model, hepatocyte specific keap-1 deletion results in decreased TG accumulation and therefore reduces hepatic steatosis. This can possibly be attributed to Nrf2-dependent alternative metabolic substrate utilization, without affecting hepatic inflammation and fibrogenesis. These considerations should be taken in account in the development of targeted/specific Nrf2-activation in hepatocytes as therapeutic strategy for the treatment of fatty liver diseases. Disclosures: Christian Trautwein – Grant/Research Support: BMS, Novartis, BMS, Novartis; Speaking and Teaching: Roche, BMS, Roche, BMS The following people have nothing to disclose: Pierluigi Ramadori, Hannah K. Drescher, Fabienne Schumacher, Stephanie Erschfeld, Athanassios Fragoulis, Christoph Wruck, Daniela C. Kroy, Konrad L. Streetz Purpose: In human, needle biopsy is an established diagnostic technique, but not in experimental animals. The repeated use of this technique enables us to reduce the number of experimental animals as well as to evaluate the time course of the disease development and the effects of treatments.

2 These cells may be akin click here to the small hepatocyte-like progenitors (SHPCs) described by Gordon and colleagues.3 Cell foci resembling SHPCs have also been observed in retrorsine-treated hepatitis B surface antigen

(HBsAg) transgenic mice that have chronic liver injury.4 In the mouse, evidence has been proffered for a parenchymal stem cell niche close to the portal area. By labeling cells with bromodeoxyuridine after a necrogenic dose of acetaminophen, and then administering another dose 2 weeks later to induce several divisions of previously labeled cells, so-called label-retaining cells (LRCs), which are considered to be slowly dividing stem cells, were found, both as cholangiocytes of interlobular ducts and peribiliary hepatocytes and so-called null cells.5 Likewise, in human liver, rare putative stem cells that strongly AZD3965 datasheet express STAT3 (signal transducer and activator of transcription 3) and the embryonic

stem cell pluripotency-associated factors Oct4 (octamer 4) and Nanog are also located near portal tracts.6 Moreover, using mitochondrial DNA mutations as markers of clonality, we have also found clonally-derived populations of hepatocytes in human liver that also appear to have their origins close to portal areas.7, 8 A seemingly distinctively different stem cell compartment appears to be activated from within the smallest branches of the intrahepatic biliary tree in response to overwhelming liver injury, chronic

liver injury,9 or large-scale hepatocyte senescence,10 and can be demonstrated in a transgenic mouse model of fatty liver and DNA damage.11 This so-called “oval cell” or “ductular reaction” amplifies a cholangiocyte-derived (biliary) population before these cells differentiate into either hepatocytes or cholangiocytes. Oval cells are thought to be derived from the canal of Hering, and while in rodents this canal barely extends beyond the limiting plate, but in human liver, the canal of Hering extends to the proximate third of the lobule (Fig. 1B).12 So, would the liver be unique in having functionally distinct stem cell populations, one for “physiological growth” that maintains tissue homeostasis, and one (the biliary cell–derived HPCs) that acts as a back-up, Carbohydrate essentially for regenerative growth after tissue injury? A number of studies point to this state of affairs in many tissues.13, 14 This would include small intestine,15, 16 olfactory neuroepithelium,17 corneum,18 hair follicle,19 and the hematopoietic system.20 The recent article by Furuyama and colleagues now suggests the boundaries between the apparently distinct stem cell populations in the liver are somewhat blurred.21 This new study explored the role of the embryonic transcription factor Sox9 (sex determining region Y box 9) in three embryologically-related organs: liver, pancreas, and duodenum.

These include hepatocyte growth factors, platelet-derived serotonin, stem cell factor, complements, and the innate inflammatory response.1–4 Among these, the role BMS-777607 mouse of the innate inflammatory response has been extensively investigated.1–4 It is generally accepted that PHx leads to elevation of serum levels of bacterial endotoxin (lipopolysaccharide [LPS]),5 which stimulates Kupffer cells to produce tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). The

latter then targets the IL-6 receptor complex (gp80/gp130) in hepatocytes, triggering the activation of signal transducer and activator of transcription 3 (STAT3), which promotes hepatocyte survival and proliferation.1–4 However, a recent study suggests that MyD88 rather than LPS acting via Toll-like receptor 4 and CD14 contributes to IL-6/STAT3 activation after PHx, and the role of MyD88 in liver regeneration has been controversial.6, 7 IL-6 knockout (KO) mice display acute liver failure and impaired liver regeneration after PHx,8 although recent studies suggest that IL-6 may play a more important role in hepatoprotection during liver regeneration.9, 10 IL-6 activation of STAT3 also induces

expression of suppressor of cytokine signaling 3 (SOCS3), which in turn terminates STAT3 signaling and negatively regulates liver regeneration.11 Although mice with global knockout of IL-6 develop acute liver failure following PHx,8, 9 conditional deletion of the IL-6 downstream

signaling molecule gp130 or STAT3 in hepatocytes did not cause acute liver failure, resulting in either no effect or only impaired liver find more regeneration after PHx.10, 12 The more severe liver damage following IL-6 knockout may be due to STAT3-independent signaling of IL-6, to extrahepatic actions of IL-6, or both. After PHx, portal and systemic plasma concentrations of LPS are significantly elevated with peak levels reaching 140 pg/mL.5 Despite such high circulating Aldol condensation levels of LPS, hepatocyte apoptosis and hepatic and systemic inflammation remain minimal.1–3 For example, PHx reportedly induced only slight or no elevation of hepatocyte apoptosis,13 and even made hepatocytes resistant to Fas-induced and LPS-induced apoptosis.13, 14 PHx is associated with elevated serum levels of proinflammatory cytokines, but except for IL-6, these changes are minimal (Supporting Table 1),15 and there are no obvious inflammatory foci in the liver after PHx.1–3 At present, the mechanisms that temper liver inflammation and apoptosis post-PHx remain obscure. STAT3, a key signal for cell survival,16 is activated by PHx in the liver. However, deletion of STAT3 in hepatocytes only moderately impaired PHx-induced liver regeneration without inducing hepatocyte apoptosis.12 Here, we demonstrate for the first time that STAT3, an important anti-inflammatory signal,17 is also markedly activated in immune cells by PHx.

The three HP+ patient who were resistant to fluoroquilolones were HetEM (*2/*1).

Eradication with 14 days regime (PPI+clarithromycin+amoxycilin) was near 96%. Conclusion: More epidemiological data in Greek population are needed to establish the real prevalence of the CYP2C19 polymorphisms which, combined with the antibiotic resistant molecular test could be useful for difficult to treat patients. Key Word(s): 1. CYP2C19; 2. Helicobacter X-396 clinical trial pylori; 3. Resistance; 4. Eradication; Presenting Author: LIAOSHENG YIN Additional Authors: CHENJIAN YONG, HUJIAN FANG Corresponding Author: CHENJIAN YONG Affiliations: The People’s Hospital of JianXi Province; The People’s Hospital of JianXI Province; The People’s Hospital of Jianxi Province

Objective: To Study the gastric mucosal proteins expression in chronic gastictis rat with damp-heat selleck compound syndrome of spleen-stomach and investigate the pathogenesis related to the chronic gastictis. To observe the differential expression of gastric mucosal protein in chronic gastictis rat model with damp-heat syndrome of spleen-stomach after treatment with sanren decoction and investigate the mechanism of sanren decoction in chronic gastictis Methods: The rats models were reproduced by quantified method. Proteomic two-dimensional gel electrophoresis technique was used to separate total gastric mucosal protein. The two-dimensional gel electrophoresis maps were analysised to decect protein spots expressed differently by

PDquest 8.0 software, the protein spots expressed differently was identified by MALDI-TOF/TOF-MS. Results: the protein spots were 1025 ± 39, 994 ± 51, 1087 ± 33, deteced from two-dimensional gel electrophoresis profiles of normal control group, model group and sanren decoction group respectively. The protein spots of differential expression were 74 between model group and normal control group,30 spots up-regulated in model group while 44 spots down-regulated; The protein spots of differential expression were 75 between sanren decoction group and model group,49 spots up-regulated in sanren decoction group while 26 spots down- regulated. Dimethyl sulfoxide Five protein spots of differential expression were identified successfully. The identificated results are: heat shock protein 72, heat shock protein 60, protein disulfide-isomerase, malate dehydrogenase, unnamed protein Conclusion: The pathogenesis of chronic gastictis with damp-heat syndrome of spleen-stomach may be related to energy metabolism disorders and stress, the mechanism of sanren decoction in the chronic gastritis with damp-heat syndrome of spleen-stomach may adjust the differential expression of gastric mucosal protein. Key Word(s): 1. chronic gastritis; 2. Damp-heat syndrome; 3. proteome; 4. Sanren decoction; Presenting Author: YINGLIAN XIAO Additional Authors: FRÉDÉRIC NICODÈME, ZHIYUE LIN, SABINE ROMAN, PETER J.

15 In this study, the effects of possible confounders, including age, sex, race, and HBV and HCV infection status, were controlled with an individually matched design. In the stratified analysis, no significant interactive effects were found, suggesting that these factors should be effectually manipulated and not modify the correlation between the rs28383151 polymorphism and HCC related to AFB1 exposure. This study had several limitations. Because of the hospital-based study, potential selection bias might have occurred. Because the liver disease MK-2206 itself may affect the metabolism of AFB1 and modify the levels of AFB1 DNA adducts,

the increased risk with AFB1 exposure status noted in this study was probably underestimated. In spite of the relatively large sample sizes of our studies, the power to elucidate gene-environmental interactions was limited because of the very small magnitudes of the overall associations and the relatively low frequency of risk genotypes. Although the status of TP53M was investigated in cases of HCC, other mutations of the TP53 gene were not evaluated. Additionally, despite the analysis of 21 SNPs in the coding region of

XRCC4, we did not analyze the polymorphisms of other genes involved in the NHEJ pathway possibly being able to modify the risk of AFB1 for HCC.5, 34 Therefore, more genes deserve further Acalabrutinib molecular weight elucidation based on a large sample and the combination of genes and AFB1 exposure. In summary, this study is, to the best of our knowledge, the first report that describes XRCC4 polymorphisms and their associations with AFB1-related HCC risk and prognosis. Our study showed that the rs28383151 polymorphism

might modulate HCC risk and prognosis related to AFB1 exposure. Particularly, the association was stronger for gene-environmental interactions than for a single gene or environmental factor. Our findings might have prevention implications through identifying an at-risk population as well as add significant clonidine predictive value to the traditional predictors of cancer prognosis (e.g., stage and surgery) once these findings are replicated by other studies based on a larger scale or prospective studies. The authors thank Drs. Qiu-Xiang Liang, Yun Yi, and Yuan-Feng Zhou for their sample collection and management and Dr. Hua Huang for his molecular biochemical technique. The authors also thank all members of the Department of Medical Test and Infective Control, Affiliated Hospital of Youjiang Medical College for Nationalities, for their help. Additional Supporting Information may be found in the online version of this article. “
“Background and aims: IDX21437, a novel uridine nucleotide analog prodrug, is a potent and selective pangenotypic HCV NS5B inhibitor with a high in vitro barrier to resistance. In preclinical testing, IDX21437 produces high triphosphate levels in the liver and shows no evidence of genotoxicity, mito-chondrial or cardiotoxicity.

suis. Conclusions: K. heterogenica colonizes the stomach of Mongolian gerbils in exactly the same regions as gastric

Helicobacter species. The uncontrolled selleckchem presence of this yeast in the gerbil stomach can lead to an overestimation of the inflammation caused by Helicobacter in this animal model. “
“Background:  In this study, H. pylori-infected and noninfected children with gastritis were compared to a control group with respect to circulating CD4+ and CD8+ T lymphocytes expressing activation and differentiation markers. Additionally, the lymphocyte phenotypes of children with gastritis were correlated with the gastric inflammation scores. Materials and Methods: H. pylori infection status was assessed based on [13C]urea breath test, rapid urease test, and histology. Analysis of the lymphocyte surface molecule expression was carried ABT-199 datasheet out by triple-color flow cytometry. Results:  The group of H. pylori-infected children showed an elevated proportion of peripheral B cells with CD19low, along with a twofold increase in the percentage of memory (CD45RO+) CD4+ and CD8+ T-cell subsets (p < .05). Moreover, a positive correlation between the age and the percentage of these subsets was seen (r = .38, p = .04 and r = .56, p < .01, respectively). Children with gastritis but without infection had a slightly increased

percentage of CD8+ T cells and CD56+ NK cells, CD3high T cells and CD45ROhigh CD4+ T-cell subsets (p < .05). Both H. pylori-infected and noninfected children with gastritis were characterized by an increased percentage of memory/effector CD4+ T cells, the presence of NK cells with CD56high, memory T-cell subset Phospholipase D1 with CD4high, and naive, memory, memory/effector, and effector T-cell subsets with CD8high (p < .05). Gastric inflammation scores correlated positively with the percentage of CD4+ T lymphocytes in H. pylori-infected children (r = .42, p = .03). In noninfected children, gastric inflammation

scores correlated positively with the percentage of B cells (r = .45, p = .04). Conclusion:  In H. pylori-negative children, gastritis was associated with an increased percentage of activated NK and T cells, and intermediate-differentiated peripheral blood CD4+ T cells, which was more pronounced in H. pylori-positive children who also showed an increased B-cell response. However, increased inflammation was only associated with the elevation of CD4+ T-cell percentage in H. pylori-positive children as well as B-cell percentage in H. pylori-negative children with gastritis. “
“Background:  The 13C-urea breath test (13C-UBT) is a safe, noninvasive and reliable method for diagnosing H. pylori infection in adults. However, the test has shown variable accuracy in the pediatric population, especially in young children. We aimed to carry out a systematic review and meta-analysis to evaluate the performance of the 13C-UBT diagnostic test for H.

Using a dedicated gene microarray, we identified 69 deregulated genes, including 10 metallopeptidases, 3 TIMPs, and 9 members of the

serine protease inhibitor family, related to protease activities in fibrosis tissues, compared to a pool of 10 histologically healthy liver samples (Supporting Table 1). This approach, which yields a listing of candidate genes, was complemented by the integration of both DNA microarray data and array-independent literature mining. Forty-two genes were clustered after prefiltering for genes connected with at least two members of the input set, according to PubMed abstracts (Fig. 1; see Supporting Information for details). The network graph of gene connections showed two major nodes, MMP2 and ADAMTS1. MMP2 is a well-known MMP secreted by activated HSCs and associated with the fibrosis process,17 and we recently demonstrated its involvement Epigenetics Compound Library buy Erastin in CX3CL1 processing during chronic liver injury.8 In contrast, ADAMTS1 expression in the liver has been poorly documented and its role in fibrogenesis has never been investigated. To explore the possible role(s) of ADAMTS1,

we analyzed its expression in an independent set of 22 samples. Patients were 20 men and 2 women with a median age of 60.9 + 9.6 years; 3 were positive for HCV and 6 for hepatitis B virus (HBV). Steady-state ADAMTS1 mRNA levels in fibrotic tissues and control livers were measured by real-time PCR. ADAMTS1 mRNA levels were significantly increased in fibrotic liver samples, compared with healthy livers, and were correlated with grade of fibrosis: ADAMTS1 mRNA levels were significantly induced in cirrhotic (F4) livers, compared with F1-F3 livers (Fig. 2A). Moreover, up-regulation of ADAMTS1 was correlated with the known induction Paclitaxel purchase of MMP2 expression in chronic liver disease. To identify the cellular source of ADAMTS1 in the liver, we analyzed its expression in isolated hepatic cells. ADAMTS1 was highly expressed in activated HSCs, compared to hepatocytes and enriched Kuppfer cell

fractions (Fig. 2B). We further investigated ADAMTS1 expression during HSC activation, which reflects the transition from a quiescent to a myofibroblastic-like phenotype, a change that can be mimicked by culturing freshly isolated HSCs in uncoated tissue-culture plastic plates. qPCR analyses were performed on total RNA extracts from 1- to 11-day-old cultures and after 1-6 cell passages. The quiescent and activated status of HSCs was confirmed by analysis of the expression of specific markers, including peroxisome proliferator-activated receptors (PPAR), alpha-smooth muscle actin (α-SMA), and type I collagen (COL1A2) (Supporting Fig. 1). In agreement with previous reports,18-21 the three PPAR isoforms were expressed in isolated HSCs over the first 4 days, with a maximum increase of PPARβ at day 4.

143 Physicians should refer to the BTS guidelines for recommendations on predicting and preventing respiratory decompensation during air travel.57 As gas expands with decreasing barometric pressure, pneumatic splints are disallowed in most flights and plaster casts should be bivalved

if applied within the previous 48 h to avoid circulatory compromise.19 Patients who have recently undergone surgery are at risk of wound dehiscence and should not fly Smad inhibitor within a 10- to 14-day postoperative period.143 Air within feeding tubes, urinary catheters, and cuffed endotracheal or tracheostomy tubes should be replaced with water prior to air travel. Expansion of emphysematous bullae and abdominal gases may further compromise respiration selleck inhibitor in patients with COPD.57 All people traveling to altitude should know the precise details of their planned trip, train for physical demands, be familiar with standard ascent and acclimatization protocols, and recognize the symptoms of altitude-related

illness. For people with preexisting medical conditions, the risks of altitude exposure and removal from potential medical support are significant and must be taken seriously (Table 4). On the other hand, with proper planning and precautions, many people with preexisting medical conditions can safely take part in outdoor adventures at high altitude (Table 5). Ultimately, avoidance of potential risk must be carefully weighed against an individual’s desire to achieve personal goals. Physician and patient must work together to plan a rational and informed approach. The authors state they

have no conflicts of interest to declare. “
“Despite Nabilone high hepatitis B virus (HBV) endemicity in various resource-limited settings (RLSs), the impact of maternal HIV/HBV coinfection on infant health outcomes has not been defined. We aimed to assess the prevalence of HBV coinfection among HIV-infected pregnant women and its impact on HIV transmission and infant mortality. In this study, the seroprevalence of HBV coinfection was determined among HIV-infected pregnant women enrolled in the Six-Week Extended-Dose Nevirapine (SWEN) India trial. The impact of maternal HIV/HBV coinfection on mother-to-child transmission (MTCT) of HIV and infant mortality was assessed using univariate and multivariate logistic regression analysis. Among 689 HIV-infected pregnant Indian women, 32 (4.6%) had HBV coinfection [95% confidence interval (CI) 3.4%, 5.3%]. HBV DNA was detectable in 18 (64%) of 28 HIV/HBV-coinfected women; the median HBV viral load was 155 copies/mL [interquartile range (IQR) < 51–6741 copies/mL]. Maternal HIV/HBV coinfection did not increase HIV transmission risk [adjusted odds ratio (aOR) 1.06; 95% CI 0.30, 3.66; P = 0.93]. Increased odds of all-cause infant mortality was noted (aOR 3.12; 95% CI 0.67, 14.57; P = 0.15), but was not statistically significant.

143 Physicians should refer to the BTS guidelines for recommendations on predicting and preventing respiratory decompensation during air travel.57 As gas expands with decreasing barometric pressure, pneumatic splints are disallowed in most flights and plaster casts should be bivalved

if applied within the previous 48 h to avoid circulatory compromise.19 Patients who have recently undergone surgery are at risk of wound dehiscence and should not fly GDC-0199 nmr within a 10- to 14-day postoperative period.143 Air within feeding tubes, urinary catheters, and cuffed endotracheal or tracheostomy tubes should be replaced with water prior to air travel. Expansion of emphysematous bullae and abdominal gases may further compromise respiration RG7204 nmr in patients with COPD.57 All people traveling to altitude should know the precise details of their planned trip, train for physical demands, be familiar with standard ascent and acclimatization protocols, and recognize the symptoms of altitude-related

illness. For people with preexisting medical conditions, the risks of altitude exposure and removal from potential medical support are significant and must be taken seriously (Table 4). On the other hand, with proper planning and precautions, many people with preexisting medical conditions can safely take part in outdoor adventures at high altitude (Table 5). Ultimately, avoidance of potential risk must be carefully weighed against an individual’s desire to achieve personal goals. Physician and patient must work together to plan a rational and informed approach. The authors state they

have no conflicts of interest to declare. “
“Despite O-methylated flavonoid high hepatitis B virus (HBV) endemicity in various resource-limited settings (RLSs), the impact of maternal HIV/HBV coinfection on infant health outcomes has not been defined. We aimed to assess the prevalence of HBV coinfection among HIV-infected pregnant women and its impact on HIV transmission and infant mortality. In this study, the seroprevalence of HBV coinfection was determined among HIV-infected pregnant women enrolled in the Six-Week Extended-Dose Nevirapine (SWEN) India trial. The impact of maternal HIV/HBV coinfection on mother-to-child transmission (MTCT) of HIV and infant mortality was assessed using univariate and multivariate logistic regression analysis. Among 689 HIV-infected pregnant Indian women, 32 (4.6%) had HBV coinfection [95% confidence interval (CI) 3.4%, 5.3%]. HBV DNA was detectable in 18 (64%) of 28 HIV/HBV-coinfected women; the median HBV viral load was 155 copies/mL [interquartile range (IQR) < 51–6741 copies/mL]. Maternal HIV/HBV coinfection did not increase HIV transmission risk [adjusted odds ratio (aOR) 1.06; 95% CI 0.30, 3.66; P = 0.93]. Increased odds of all-cause infant mortality was noted (aOR 3.12; 95% CI 0.67, 14.57; P = 0.15), but was not statistically significant.

143 Physicians should refer to the BTS guidelines for recommendations on predicting and preventing respiratory decompensation during air travel.57 As gas expands with decreasing barometric pressure, pneumatic splints are disallowed in most flights and plaster casts should be bivalved

if applied within the previous 48 h to avoid circulatory compromise.19 Patients who have recently undergone surgery are at risk of wound dehiscence and should not fly click here within a 10- to 14-day postoperative period.143 Air within feeding tubes, urinary catheters, and cuffed endotracheal or tracheostomy tubes should be replaced with water prior to air travel. Expansion of emphysematous bullae and abdominal gases may further compromise respiration Trichostatin A in vivo in patients with COPD.57 All people traveling to altitude should know the precise details of their planned trip, train for physical demands, be familiar with standard ascent and acclimatization protocols, and recognize the symptoms of altitude-related

illness. For people with preexisting medical conditions, the risks of altitude exposure and removal from potential medical support are significant and must be taken seriously (Table 4). On the other hand, with proper planning and precautions, many people with preexisting medical conditions can safely take part in outdoor adventures at high altitude (Table 5). Ultimately, avoidance of potential risk must be carefully weighed against an individual’s desire to achieve personal goals. Physician and patient must work together to plan a rational and informed approach. The authors state they

have no conflicts of interest to declare. “
“Despite Interleukin-3 receptor high hepatitis B virus (HBV) endemicity in various resource-limited settings (RLSs), the impact of maternal HIV/HBV coinfection on infant health outcomes has not been defined. We aimed to assess the prevalence of HBV coinfection among HIV-infected pregnant women and its impact on HIV transmission and infant mortality. In this study, the seroprevalence of HBV coinfection was determined among HIV-infected pregnant women enrolled in the Six-Week Extended-Dose Nevirapine (SWEN) India trial. The impact of maternal HIV/HBV coinfection on mother-to-child transmission (MTCT) of HIV and infant mortality was assessed using univariate and multivariate logistic regression analysis. Among 689 HIV-infected pregnant Indian women, 32 (4.6%) had HBV coinfection [95% confidence interval (CI) 3.4%, 5.3%]. HBV DNA was detectable in 18 (64%) of 28 HIV/HBV-coinfected women; the median HBV viral load was 155 copies/mL [interquartile range (IQR) < 51–6741 copies/mL]. Maternal HIV/HBV coinfection did not increase HIV transmission risk [adjusted odds ratio (aOR) 1.06; 95% CI 0.30, 3.66; P = 0.93]. Increased odds of all-cause infant mortality was noted (aOR 3.12; 95% CI 0.67, 14.57; P = 0.15), but was not statistically significant.