Function can be measured either performance-based or self-reported. The latter is assessed by means of a generic or disease specific instrument, and only recently the hemophilia activities list (HAL) became the first disease specific questionnaire on haemophilia [99]. The functional independent scale of hemophilia (FISH) is the only performance-based instrument that evaluates whole tasks [100]. There are numerous examples of ‘functional tests’, often used in physiotherapy such as walking tests (e.g. 50 metre walking test at preferred speed), get up & go, shuttle walk and run tests etc. Unfortunately, none of them is used in haemophilia research for

extended follow-up tasks. When the management stratagems from different countries around the world for control of a chronic condition or see more disease are collated into one ideological framework, potential

discrepancies are likely to occur based in part on the myriad of health care systems and networks that are in existence. Perhaps this statement resonates more clearly with haemophilia than with any other disease state. When attempting to define management techniques as ‘state of the art’, variables outside of the control of the therapist such as economics, patient registries, levels of education and training of clinical staff, basic availability of dedicated staff to treat PWH, and political systems can have a significant Ku 0059436 and realistically MCE公司 limiting effect. The World Federation of Hemophilia has estimated that 75% of the global population of people with bleeding disorders receives either inadequate treatment or no treatment whatsoever [101]. Based purely on the financial cost of the most advanced medical and pharmaceutical technologies, this statistic seems unlikely to change. The clear advantage of excellence

in musculoskeletal management is the fact that it is far less expensive, and far more amenable to being taught to patients and caregivers to perform on their own at home. Measurable improvement of joint and muscle status of the global haemophilia community is an attainable goal. Although many factors related to haemophilia care vary from country to country, the anatomical structure of joints and muscles is constant. The critical component is thorough assessment, which becomes the touchstone for design of the treatment programme. The international community of physiotherapists represented in this study, who work with PWH, have carried this message consistently whether it be applied to flexibility training, strength, sensorimotor retraining, balance or functional exercise. Designing an effective exercise programme requires understanding of the cause of injury, functional anatomy, the science of the various elements of exercise and tissue healing, and perhaps most importantly – of the patient involved.

The objective of this systematic review was to evaluate the effect of adjuvant antiviral therapy on recurrence and survival after curative treatment of HCC. We conducted an extensive search strategy. All randomized controlled trials comparing adjuvant antiviral therapy versus placebo or no treatment were considered for this review. Results were expressed as hazard ratio for time-to-event

outcomes with 95% confidence intervals using RevMan 5. We included nine trials (three of low risk of bias and six of unclear risk of bias) with 954 patients. All the included studies used conventional interferon (IFN) as adjuvant antiviral therapy; none of them used pegylated IFN or nucleoside analogs. There were significant improvements for recurrence-free survival and overall survival in the adjuvant IFN group selleck screening library compared with the control group. Subgroup analysis also showed a significant Deforolimus mouse difference favoring IFN therapy in hepatitis C virus (HCV)-related HCC patients, but for hepatitis B virus (HBV)-related patients, the difference failed to reach statistical significance. A dose reduction was needed in 28.3% of patients and discontinuation of IFN therapy happened in 8.2% of patients due to moderate to severe side-effects. Our study suggested potential benefits of adjuvant IFN therapy following curative treatment of HCC, especially for HCV-related HCC. Further high-quality randomized controlled trials of more effective

adjuvant antiviral regimens, either used alone or in combination, for virus-related HCC, especially HBV-related HCC, are needed. “
“Acute liver injury is manifested by different degree of hepatocyte necrosis and may recover via the process of hepatocyte regeneration once the injury is discontinued. Most of the liver injury is associating with inflammatory cytokines.

Resveratrol (RSV) is a natural phytoalexin with powerful anti-inflammatory effects. The effects of RSV on cellular factors mediating liver damage and 上海皓元医药股份有限公司 regeneration in acute carbon tetrachloride (CCl4) liver injury were investigated. RSV decreased alanine aminotransferase, aspartate aminotransferase, necrosis, and 4-hydroxynonenal in the CCl4-injured liver. RSV decreased hepatocyte apoptosis by reducing caspase 8 and caspase 3 but not Bax and Bcl-xL. RSV reduced Kupffer cells recruitment, the expressions of tumor necrosis factor-α and interleukin-6, but not interleukin-10. RSV lowered the numbers of anti-5-bromon-2′-deoxyuridine and anti-Ki67-positive hepatocytes. Hepatic hepatocyte growth factor, c-Met and transforming growth factor-α expressions were reduced by RSV, while transforming growth factor-β1 and hepatic stellate cells activation were not changed. RSV reduced the injury-induced CXCL10 elevations in serum and liver in vivo. Besides, RSV inhibited CXCL10 release from CCl4-injured hepatocytes in vitro. In contrast, recombinant CXCL10 improved the viability of CCl4-injured hepatocytes. RSV therapy can be beneficial for acute toxic liver injury.

The objective of this systematic review was to evaluate the effect of adjuvant antiviral therapy on recurrence and survival after curative treatment of HCC. We conducted an extensive search strategy. All randomized controlled trials comparing adjuvant antiviral therapy versus placebo or no treatment were considered for this review. Results were expressed as hazard ratio for time-to-event

outcomes with 95% confidence intervals using RevMan 5. We included nine trials (three of low risk of bias and six of unclear risk of bias) with 954 patients. All the included studies used conventional interferon (IFN) as adjuvant antiviral therapy; none of them used pegylated IFN or nucleoside analogs. There were significant improvements for recurrence-free survival and overall survival in the adjuvant IFN group CT99021 cell line compared with the control group. Subgroup analysis also showed a significant C59 wnt clinical trial difference favoring IFN therapy in hepatitis C virus (HCV)-related HCC patients, but for hepatitis B virus (HBV)-related patients, the difference failed to reach statistical significance. A dose reduction was needed in 28.3% of patients and discontinuation of IFN therapy happened in 8.2% of patients due to moderate to severe side-effects. Our study suggested potential benefits of adjuvant IFN therapy following curative treatment of HCC, especially for HCV-related HCC. Further high-quality randomized controlled trials of more effective

adjuvant antiviral regimens, either used alone or in combination, for virus-related HCC, especially HBV-related HCC, are needed. “
“Acute liver injury is manifested by different degree of hepatocyte necrosis and may recover via the process of hepatocyte regeneration once the injury is discontinued. Most of the liver injury is associating with inflammatory cytokines.

Resveratrol (RSV) is a natural phytoalexin with powerful anti-inflammatory effects. The effects of RSV on cellular factors mediating liver damage and 上海皓元医药股份有限公司 regeneration in acute carbon tetrachloride (CCl4) liver injury were investigated. RSV decreased alanine aminotransferase, aspartate aminotransferase, necrosis, and 4-hydroxynonenal in the CCl4-injured liver. RSV decreased hepatocyte apoptosis by reducing caspase 8 and caspase 3 but not Bax and Bcl-xL. RSV reduced Kupffer cells recruitment, the expressions of tumor necrosis factor-α and interleukin-6, but not interleukin-10. RSV lowered the numbers of anti-5-bromon-2′-deoxyuridine and anti-Ki67-positive hepatocytes. Hepatic hepatocyte growth factor, c-Met and transforming growth factor-α expressions were reduced by RSV, while transforming growth factor-β1 and hepatic stellate cells activation were not changed. RSV reduced the injury-induced CXCL10 elevations in serum and liver in vivo. Besides, RSV inhibited CXCL10 release from CCl4-injured hepatocytes in vitro. In contrast, recombinant CXCL10 improved the viability of CCl4-injured hepatocytes. RSV therapy can be beneficial for acute toxic liver injury.

Methods: 19 HBeAg positive chronic HBV carriers were recruited in the trial including find more 15 males and 4 females aged 14-54 years.

PBMCs obtained from 50ml of heparinized peripheral blood through density gradient centrifuge and adherence method were proliferated under the induction by GM-CSF and IL-4, and sensitized with the stock of hepatitis B vaccine containing 30μg HBsAg on day 5 and with hepatitis B vaccine commercially available containing 20μg HBsAg on day 6. anti-HBV-DC vaccine was harvested on day 7 and injected, half hypodermically and half intravenously, to the patient once every two weeks for 12 practices applications totally. Lamivudine was taken 1 00mg daily, and thymosin-α1 1.6mg selleck screening library was injected hypodermically twice a week. Quantitative HBVM(TRFIA) and HBVDNA and hepatic functions

were evaluated at week 0, 4, 12, and 24. Results: Mean of HBsAg, HBeAg and HBVDNA decreased significantly, while mean of HBeAb increased after therapy of 4, 12 and 24 weeks. At week 4, 12 and 24, HBeAg negative conversion rate were 21.05%(4/1 9), 15.79(3/19) and 15.79%(3/19) respectively, HBeAb positive conversion rate were 10.53%(2/19), 21.05%(4/19) and 15.79%(3/19), HBeAg seroconversion rate were 1 0.53%(2/1 9), 15.79%(3/19) and 15.79%(3/19), HBVDNA negative conversion rate were 21.05%(4/19), 21.05%(4/19), and 36.84%(7/1 9), ALT abnormal increased rate were 5.26%(1/1 9), 1 0.53%(2/1 9) and 15.79%(3/19).The rate of adverse effect was 3.07% observed in re-infusion of anti-HBV-DC vaccine. Conclusions: anti-HBV-DC

vaccine in combination with lamivudine and thymosin-α1 can be considered as a safe approach for HBeAg positive chronic HBV carriers, which may effectively inhibit the viral replication, lower HBsAg, HBeAg and HBVDNA, improve the production of HBeAb, and increase the HBeAg seroconversion rate. Disclosures: The following people have nothing to disclose: 上海皓元 Bang-Fu Wu, Jiang-Ying Yang Background and Aims: A pilot study has shown that baseline quantitative hepatitis B core antibody (anti-HBc) level could pre- dict the treatment response in both interferon-treated and nucleos(t)ide analogues-treated cohorts but with limited sample size. Here, we tried to explore the value of quantitative anti-HBc at baseline in predicting treatment outcome at year 2 in a randomized controlled study (EFFORT study, NCT00962533). Methods: 606 patients with HBV DNA ≧10,000 copies/ml, ALT 2-10xULN and compensated HBeAg-positive CHB were enrolled in the study, receiving telbivudine or combined with adefovir for 104 weeks. Serum quantitative anti-HBc levels were measured by using a newly developed double-sandwich anti-HBc immunoassay validated by the WHO anti-HBc standards from baseline to week 52. A post-hoc multivariate analysis was conducted to investigate predictors for treatment outcome at week 104. Results: 599 patients of ITT population were included in the analysis.

Serum markers of antioxidant status such as total, reduced (GSH) and oxidized (GSSG) glutathione as well as ferric reducing antioxidant power (FRAP) were measured according to the procedures reported Selleckchem AZD6244 below. Ten percent formalin-fixed paraffin-embedded sections of liver samples were divided into 4-μm sections by using routine techniques and mounted onto slides with coverslips. Representative sections of each fixed sample were stained with standard hematoxylin-eosin and Sirius red/fast green according to standard protocols. All histological analyses were performed by an experienced histopathologist in a blinded manner. For the

detection and quantification of collagen, liver sections were stained with Picrosirius red solution. The extent of liver fibrosis was determined as the proportion of Picrosirius-stained area in each section. For each rat, 64 fields of a constant raster of 31 mm2 were analyzed at 100× final magnification. For semiautomated morphometry, a Sony 3CCD (model DXC-950P) videomicroscope equipped with a motor stage and the Quantimed 500MC (Leica, Germany) software were used. To detect the immunohistochemical

localization of adiponectin receptor 2 (adipo-R2), sections from formalin-fixed, paraffin-embedded specimens were deparaffinized and rehydrated in decreasing concentrations of ethyl alcohol. The detailed procedure, including antibody used selleck screening library and all material specificities and provenience, is provided in the Supporting Information. Western blot analyses in tissue lysates prepared and quantified

for protein content were performed as described in the Supporting Information. Semiquantitative reverse-transcription polymerase chain reaction amplification of messenger RNA liver extracts was performed using the procedure and primers described in the Supporting Information. Markers of antioxidant status such as total, reduced (GSH), and oxidized (GSSG) glutathione in serum and liver samples; glutathione transferase activity in the liver; and plasma FRAP were measured according to the protocols described in the Supporting Information. Tumor necrosis factor α (TNF-α), interferon-γ (IFN-γ), interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, and IL-10 were quantified MCE in liver samples through the xMAP technology developed by Luminex (Austin, TX) and using a rat multiplex bead-based assay Bio-Plex Suspension Array System (Bio-Rad Laboratories, Hercules, CA) according to the manufacturer’s instructions. Data were analyzed using Bio-Plex Manager version 3.0 (Bio-Rad Laboratories) with five parameter logistic regression algorithm curve fits. Detection limits for the cytokines were 2-32,000 pg/mL. A detailed protocol for tissue preparation is described in the Supporting Information.

(HEPATOLOGY 2011;.) Hepatocellular carcinoma (also called malignant hepatoma) is one of the most common malignant tumors and the third leading cause of cancer mortality worldwide.1 Despite many efforts to develop various classes of agents, systemic chemotherapy and hormone therapy have failed to significantly increase the survival of patients with advanced hepatoma. However, recent advances in the understanding of hepatoma progression have led to the development of novel molecularly targeted therapies.2 Because angiogenesis is pivotal for the development and progression of hepatoma,

key molecules Epacadostat in vivo regulating angiogenesis are regarded as promising targets for treating hepatoma.3 Hypoxia inevitably develops in rapidly growing tumors and is an important microenvironment that forces changes in tumor behavior. In particular, hypoxia activates hypoxia-inducible factor-1α (HIF-1α), which promotes the progression of malignancy by stimulating angiogenesis and by augmenting the ability of tumors to survive.4, 5 The roles of

HIF-1α have been extensively investigated in cancer patients and in tumor-bearing mice.6, 7 Consequently, HIF-1α is believed to be a valid target for the treatment of aggressive tumors, and many efforts have been made to identify suitable HIF-1α inhibitors.8 Chaetocin, which is produced by Chaetomium sp., is an antibiotic having the thiodioxopiperazine structure (a disulfide-bridged selleck products piperazine).9 Other thiodioxopiperazines are known to have antimicrobial, antiviral, immunosuppressive, and antiinflammatory activities,10, 11 but the biological activity of chaetocin has been reported in relatively few reports. In one such report, it was suggested that chaetocin inhibits the histone methyltransferase suv39H1.12 Recently, it was also demonstrated that chaetocin induces apoptosis of myeloma cells and retards the growth of myeloma xenografts.13 Mechanistically, it was

proposed that chaetocin produces oxidative damage in myeloma cells by inhibiting the antioxidant enzyme thioredoxin reductase.14 However, little is known about the effects of chaetocin on solid tumors, and thus we tested the anticancer activity of chaetocin against solid tumors. Here we demonstrated that chaetocin has 上海皓元医药股份有限公司 antiangiogenic and anticancer activities in hepatoma and fibrosarcoma grafts, and that these actions of chaetocin are due to HIF-1α down-regulation caused by the deregulation of HIF-1α premessenger RNA (pre-mRNA) splicing. ATP, adenosine triphosphate; CA9, carbonic anhydrase 9; EPO, erythropoietin; HIF, hypoxia-inducible factor; MEF, mouse embryonic fibroblast; PDK1, pyruvate dehydrogenase kinase 1; PHD, prolyl-hydroxylase domain protein; RCC, renal cell carcinoma; VEGF, vascular endothelial growth factor; VHL, von Hippel-Lindau.

This study was carried out with assistance of the National haemophilia organizations from Canada, France, the Netherlands, Poland and the UK. The authors stated that they had no interests which might

be perceived as posing a conflict or bias. “
“The immune response toward factor VIII (FVIII) presents several characteristics that make it unique. Antibodies to FVIII are made by healthy individuals, by patients BYL719 purchase suffering from hemophilia A, and by patients affected by some autoimmune diseases. FVIII is an autoantigen in the first and third of these situations. In the second instance, FVIII is administered intravenously and on a recurrent basis. The diverse characteristics make it essential to consider the immune response to FVIII from a general Wnt drug point of view, and not just as a peculiar response occurring in only a proportion of patients with hemophilia A. The purpose of this chapter is to review the current understanding of the homeostasis of the anti-FVIII response, to summarize information recently gathered from animal models, and to update data obtained from relevant clinical observations. “
“Inherited factor VII (FVII) deficiency

is one of the commonest rare bleeding disorders. It is characterized by a wide molecular and clinical heterogeneity and an autosomal recessive pattern of inheritance. Factor VII-deficient patients are still scarcely explored in Pakistan although rare bleeding disorders became quite common as a result of traditional consanguineous marriages. The aim of the study was to give a first insight of F7 gene mutations in Pakistani population. Ten unrelated FVII-deficient patients living in Pakistan were investigated (median FVII:C = 2%; range = 2–37%). 上海皓元 A clinical questionnaire was filled out for each patient and direct sequencing was performed on the coding regions, intron/exon boundaries and 5′ and 3′ untranslated regions of the F7 gene. Nine different mutations (eight missense mutations and one located

within the F7 promoter) were identified on the F7 gene. Five of them were novel (p.Cys82Tyr, p.Cys322Ser, p.Leu357Phe, p.Thr410Ala, c-57C>T, the last being predicted to alter the binding site of transcription factor HNF-4). Half of the patients had single mutations in Cys residues involved in disulfide bridges. The p.Cys82Arg mutation was the most frequent in our series. Six of seven patients with FVII:C levels below 10% were homozygous in connection with the high percentage of consanguinity in our series. In addition, we graded the 10 patients according to three previously published classifications for rare bleeding disorders. The use of the bleeding score proposed by Tosetto and co-workers in 2006 appears to well qualify the bleeding tendency in our series. “
“Summary.

This study was carried out with assistance of the National haemophilia organizations from Canada, France, the Netherlands, Poland and the UK. The authors stated that they had no interests which might

be perceived as posing a conflict or bias. “
“The immune response toward factor VIII (FVIII) presents several characteristics that make it unique. Antibodies to FVIII are made by healthy individuals, by patients NU7441 suffering from hemophilia A, and by patients affected by some autoimmune diseases. FVIII is an autoantigen in the first and third of these situations. In the second instance, FVIII is administered intravenously and on a recurrent basis. The diverse characteristics make it essential to consider the immune response to FVIII from a general http://www.selleckchem.com/products/Erlotinib-Hydrochloride.html point of view, and not just as a peculiar response occurring in only a proportion of patients with hemophilia A. The purpose of this chapter is to review the current understanding of the homeostasis of the anti-FVIII response, to summarize information recently gathered from animal models, and to update data obtained from relevant clinical observations. “
“Inherited factor VII (FVII) deficiency

is one of the commonest rare bleeding disorders. It is characterized by a wide molecular and clinical heterogeneity and an autosomal recessive pattern of inheritance. Factor VII-deficient patients are still scarcely explored in Pakistan although rare bleeding disorders became quite common as a result of traditional consanguineous marriages. The aim of the study was to give a first insight of F7 gene mutations in Pakistani population. Ten unrelated FVII-deficient patients living in Pakistan were investigated (median FVII:C = 2%; range = 2–37%). 上海皓元 A clinical questionnaire was filled out for each patient and direct sequencing was performed on the coding regions, intron/exon boundaries and 5′ and 3′ untranslated regions of the F7 gene. Nine different mutations (eight missense mutations and one located

within the F7 promoter) were identified on the F7 gene. Five of them were novel (p.Cys82Tyr, p.Cys322Ser, p.Leu357Phe, p.Thr410Ala, c-57C>T, the last being predicted to alter the binding site of transcription factor HNF-4). Half of the patients had single mutations in Cys residues involved in disulfide bridges. The p.Cys82Arg mutation was the most frequent in our series. Six of seven patients with FVII:C levels below 10% were homozygous in connection with the high percentage of consanguinity in our series. In addition, we graded the 10 patients according to three previously published classifications for rare bleeding disorders. The use of the bleeding score proposed by Tosetto and co-workers in 2006 appears to well qualify the bleeding tendency in our series. “
“Summary.

1, 3 Despite the Kasai portoenterostomy, which is performed at the time of diagnosis, BA usually leads to biliary cirrhosis and is the most common indication for pediatric liver transplantation. The etiology of this disease has yet to be elucidated. In 1974, Landing4 proposed that acquired BA could be caused by a virus infection. A leading theory of the pathogenesis of BA is that the bile duct damage is initiated by a virus infection followed by the release of altered “self” antigens that activate bile duct-specific autoreactive T cells, resulting in a chronic, inflammatory fibrosclerosing injury of the bile ducts.3, 5 Pathogenic

mechanisms of autoimmunity include this “bystander activation,” molecular mimicry, and loss of inhibition of autoimmunity see more due to defects in regulatory T cells (Tregs).6-9 Studies utilizing the rotavirus-induced selleck kinase inhibitor mouse model of BA have established evidence for this virus-induced, autoimmune-mediated pathway of bile duct injury.10-12 Here, autoreactive T cells specific to

bile duct epithelial proteins have been identified and contribute to bile duct injury.10, 11 Furthermore, a role for humoral autoimmunity in mouse and human BA was identified based on detection of high levels of α-enolase autoantibodies.12 BA patients at diagnosis have been tested for reovirus, rotavirus, cytomegalovirus (CMV), as well as other viruses in an attempt to identify the inciting virus infection associated with disease onset. Thus far, there have been conflicting results for all of these viruses. Studies on BA serum and liver tissue collected at the time of the Kasai portoenterostomy have identified increased incidences of reovirus,13-20

rotavirus,21 and CMV15, 22-30; however, other studies negate these findings.31-36 It is possible that the virus infection is short-lived, the virus damages bile duct cells and MCE is then cleared from the liver by the immune system, thus making it undetectable.3, 5 In support of this theory, virus is cleared within the first 2 weeks in the rotavirus-induced mouse model of BA, despite progression of inflammation and bile duct obstruction.37-39 We sought a different approach to answer the question of a possible perinatal virus infection associated with the onset of BA. If the neonate had a recent virus infection, then one would expect a liver T-cell response encompassing resident virus-specific memory T cells. The memory response is long-lasting and would be present even in the setting of viral clearance. It has been previously reported that the periductal inflammation at the time of diagnosis of BA includes activated T cells.40, 41 These T cells are oligoclonal in nature, suggesting antigen-specific T-cell activation; however, the inciting antigen(s) are not known.42 The aim of this study was to identify potential virus-specific liver T cells of infants with BA at the time of diagnosis, implicating the virus involved in early bile duct damage.

1, 3 Despite the Kasai portoenterostomy, which is performed at the time of diagnosis, BA usually leads to biliary cirrhosis and is the most common indication for pediatric liver transplantation. The etiology of this disease has yet to be elucidated. In 1974, Landing4 proposed that acquired BA could be caused by a virus infection. A leading theory of the pathogenesis of BA is that the bile duct damage is initiated by a virus infection followed by the release of altered “self” antigens that activate bile duct-specific autoreactive T cells, resulting in a chronic, inflammatory fibrosclerosing injury of the bile ducts.3, 5 Pathogenic

mechanisms of autoimmunity include this “bystander activation,” molecular mimicry, and loss of inhibition of autoimmunity KU57788 due to defects in regulatory T cells (Tregs).6-9 Studies utilizing the rotavirus-induced Obeticholic Acid ic50 mouse model of BA have established evidence for this virus-induced, autoimmune-mediated pathway of bile duct injury.10-12 Here, autoreactive T cells specific to

bile duct epithelial proteins have been identified and contribute to bile duct injury.10, 11 Furthermore, a role for humoral autoimmunity in mouse and human BA was identified based on detection of high levels of α-enolase autoantibodies.12 BA patients at diagnosis have been tested for reovirus, rotavirus, cytomegalovirus (CMV), as well as other viruses in an attempt to identify the inciting virus infection associated with disease onset. Thus far, there have been conflicting results for all of these viruses. Studies on BA serum and liver tissue collected at the time of the Kasai portoenterostomy have identified increased incidences of reovirus,13-20

rotavirus,21 and CMV15, 22-30; however, other studies negate these findings.31-36 It is possible that the virus infection is short-lived, the virus damages bile duct cells and medchemexpress is then cleared from the liver by the immune system, thus making it undetectable.3, 5 In support of this theory, virus is cleared within the first 2 weeks in the rotavirus-induced mouse model of BA, despite progression of inflammation and bile duct obstruction.37-39 We sought a different approach to answer the question of a possible perinatal virus infection associated with the onset of BA. If the neonate had a recent virus infection, then one would expect a liver T-cell response encompassing resident virus-specific memory T cells. The memory response is long-lasting and would be present even in the setting of viral clearance. It has been previously reported that the periductal inflammation at the time of diagnosis of BA includes activated T cells.40, 41 These T cells are oligoclonal in nature, suggesting antigen-specific T-cell activation; however, the inciting antigen(s) are not known.42 The aim of this study was to identify potential virus-specific liver T cells of infants with BA at the time of diagnosis, implicating the virus involved in early bile duct damage.