Acute Fulminant Hepatitis Research Articles

Autoimmune Hepatitis: Diagnostic Dilemma in the Setting of Suspected Iron Overload

Autoimmune hepatitis (AIH) is an inflammatory condition of the liver that has a multitude of clinical presentations from chronic hepatitis to acute fulminant hepatitis. AIH diagnosis is typically suspected after ruling out other causes of hepatitis (such as vial hepatitis, hemochromatosis, Wilson's disease, and primary biliary cirrhosis) through serological tests and by findings of high titers of certain autoantibodies (ANA and anti-SMA for type 1 AIH and anti-LKM-1 for type 2 AIH). AIH like most inflammatory conditions is associated with increased ferritin levels (acute-phase reactant) but typically near-normal transferrin saturation. The presence of excessive ferritin level in absence of high-transferrin saturation helps differentiate secondary iron overload from hemochromatosis where transferrin saturation is typically high. We herein describe a case of AIH that presented with high ferritin levels and transferrin saturation suggesting a diagnosis of hemochromatosis and needed arduous work-up to arrive at accurate diagnosis of AIH.

Are first line anti-retroviral therapies really toxic for children? A study from Eastern India

This research aims to study the incidence of drug induced toxicity during antiretroviral therapy (ART) among children from a tertiary care institute from Kolkata. This is a prospective study that consist of 100 children aged 2 to 14 years receiving first line ART [Stavudine (d4T), Lamivudine (3TC), Nevirapine (NVP)/Efavirenz (EFV)]; these children were followed up for 3 years (2007 to 2010). The results showed gastro-intestinal symptoms in 20% (n = 20), transient maculo-papular skin rashes in 10% (n = 10), clinical jaundice in 4% (n = 4) and peripheral neuropathy in 1% (n = 1). No death or life threatening conditions like Steven-Johnson syndrome, immune reconstitution syndrome (IRIS), acute fulminant hepatitis and pancreatitis were noted. d4T, 3TC and NVP/EFV are safe in HIV positive children even after 3 years of uninterrupted ART. Key words: Human immunodeficiency virus (HIV), highly active anti retroviral therapy (HAART), fixed dose combination (FDC).

Occupational Hazards and HBV infection among health care workers in Public Teaching Hospitals in Khartoum State, Sudan: A multiple Discriminant Analysis

Background: Infection with HBV leads to a wide spectrum of liver injury. It ranges from acute self-limited infection and fulminant hepatitis to chronic hepatitis.Objectives: To examine the prevalence of sero-epidemiologic markers of hepatitis B virus and to identify the risk factors of exposure to HBV among health care workers in Public Teaching Hospitals in Khartoum State, Sudan; in 2004.Methods: The study was a cross sectional, facility-based study. It was conducted on stratified two stage cluster sampling of 843 subjects. The study adopted multivariate statistical approach, using Multiple Discriminant Analysis (MDA) and some non-parametric tests.Results: Infection rate measured by Anti-HB core, carrier rate measured by HBs Ag, and a profile of high infectivity rate measured by HBe Ag was found to be high; while immunity rate measured by Anti-HBs was found to be low. Needle stick injury, contaminated sharp instruments injury andexposure to blood are the most significant occupational variables related to infection rate of HBV. Contaminated sharp instruments injury and exposure to blood, are the most significant occupational variables related to carrier rate. Date of needle stick injury, incidence and date of contaminated sharp instruments injury, incidence and date of exposure to blood have significant relation to immunity rate against HBV infection.Conclusion: The prevalence rate of HBV markers among HCWs in Public Teaching Hospitals in Khartoum State, Sudan, differs according to occupational hazard factors. With the exception of the HBeAg, seroprevalence of all HBV markers was found to be significantly correlated with occupational hazards (P<0.05).Key words: HBV markers, HCWs.

Pathogenesis and Treatment of Hepatitis E Virus Infection

Hepatitis E has been considered to be a travel-associated, acute, self-limiting liver disease that causes fulminant hepatic failure in specific high-risk groups only. However, hepatitis E virus (HEV) infection can also be acquired in industrialized countries-HEV genotype 3 infection is a zoonosis, with pigs and rodents serving as animal reservoirs. In recent years, cases of chronic HEV infection that were associated with progressive liver disease have been described in several cohorts of immunocompromised individuals, including recipients of organ transplants. The topic of hepatitis E is therefore re-emerging and has raised the following important questions: what is the risk for HEV infection in Western countries (eg, from eating uncooked meat)? How frequently does chronic hepatitis E develop among human immunodeficiency virus-infected patients and recipients of organ transplants? What are the treatment options? What is the current status of vaccine development? What do we know about the pathogenesis of HEV infection, and why does it have a more severe course in pregnant women? This review summarizes the current knowledge on the pathogenesis and treatment of HEV infection.

Histological and immunohistochemical features in fatal acute fulminant hepatitis E

Hepatitis E is being increasingly recognized as an emerging infection in developed countries. Data on histological findings and nature of inflammatory cell infiltrate in liver in this disease are quite sparse. This study was planned to study the histological features and the type of inflammatory infiltrate in liver biopsies of patients with acute fulminant hepatitis E. We retrieved postmortem liver biopsies of 11 Indian patients with fulminant hepatitis E, and compared these with biopsies from seven patients with fulminant hepatitis B. Biopsies from acute fulminant hepatitis E showed varying degrees of hepatocyte necrosis, mixed portal and lobular inflammation, accompanied by bile ductular proliferation, lymphocytic cholangitis, Kupffer cell prominence, cholestasis, apoptotic bodies, pseudo-rosette formation, steatosis, and presence of plasma cells in portal tracts. Interface hepatitis was more frequent in acute hepatitis B than in acute hepatitis E (100% vs 20%; P<0.05). These findings differ from those reported in cases with autochthonous hepatitis E in Europe. On immunohistochemistry, lymphocyte infiltrate consisted predominantly of CD3 + T cells in both hepatitis E and hepatitis B; these cells contained a predominant cytotoxic (CD8 + ) cell subpopulation in 81.8% of cases with hepatitis E and in 50% of cases with hepatitis B. Our findings suggest that histological changes in HEV infection may vary with geographical location because of prevalent HEV genotypes, and that CD8 + lymphocytes play a role in HEV-induced liver injury.

A Pediatric Case of Toxic Hepatitis Induced by Hovenia Dulcis

Toxic hepatitis is a rare but devastating disease in children. Herbs are widely used in oriental medicine to treat various symptoms in Korea, however, several herbs have been reported to induce liver injury. We report a case of toxic hepatitis induced by Hovenia dulcis in a 3-year-old boy. He complained of nausea, abdominal discomfort, and jaundice. The patient had consumed water boiled with hovenia dulcis for about 1 year prior to presentation. A diagnosis of toxic hepatitis was made based on his history, laboratory data, viral markers, ultrasonography, and biopsied liver tissue. We administered supportive management for acute fulminant hepatitis but his symptoms and liver function progressed. He was transferred to another hospital for further evaluation and consideration for liver transplantation. Because acute liver failure due to herbs or dietary supplement taken for a long time is often fetal, it is important to make early diagnosis and stop taking the drug as soon as drug induced liver injury is suspected. (Pediatr Gastroenterol Hepatol Nutr 2012; 15: 111∼116)

Acute Fulminant Hepatitis With Bone Marrow Failure in An Adult Due to Parvovirus B19 Infection

Acute Fulminant Hepatitis With Bone Marrow Failure in An Adult Due to Parvovirus B19 Infection

Is There Any Value to Hepatitis B Virus Genotype Analysis?

Hepatitis B may cause a varying spectrum of diseases ranging from an asymptomatic or mild anicteric acute illness, to severe or fulminant hepatitis. Similarly, the outcome of chronic hepatitis B is variable. Viral factors associated with outcome of chronic hepatitis B virus (HBV) infection include hepatitis B e antigen status, HBV DNA, genotype, and HBV variants. HBV genotypes and subgenotypes have been associated with differences in clinical and virological characteristics, indicating that they may play a role in the virus-host relationship. A total of ten hepatitis B virus genotypes have been defined with a distinct geographical distribution. Hitherto, genotypes A, B, C and D have been studied most extensively. The HBV genotype appears to influence not only the natural history of HBV related liver disease but also the response to HBV treatment. HBV genotypes are also linked with both core promoter and BCP mutations. Progression to chronic infection appears to occur more frequently following acute infection with genotypes A and D than with the other studied genotypes. Genotypes A and B appear to have higher rates of spontaneous HBeAg seroconversion. More advanced liver disease and progression to HCC is more often seen in chronic infection with genotypes C and D in contrast to genotypes A and B. More specifically, genotypes A1, C, B2-B5 and H appear to be associated with more serious complications than genotypes A2, B1 and B6. These observations suggest important pathogenic differences between HBV genotypes. Genotypes A and B have higher response rates to interferon based therapy than genotypes C and D. Knowledge of HBV genotype enables clinicians to identify those patients at increased risk of disease progression whilst aiding the selection of appropriate antiviral therapy. Genotyping and monoclonal subtyping can provide useful information for epidemiological studies. In conclusion, genotyping of chronic HBV infections can help practicing physicians identify those at risk of disease progression and determine optimal anti-viral therapy.

Fatal fulminant primary hepatitis B virus infections with G1896A precore viral mutants in southeastern France

Fulminant hepatitis has been shown to occur in about 1% of acute hepatitis B virus (HBV) infections, and its mortality rate is nearly 70%. Specific HBV genotypic features have been pointed out in fulminant acute hepatitis B worldwide, but these associations remain controversial. We describe all four primary HBV infections diagnosed in 2008 in our institution in Marseille, southeastern France, including two fatal cases. HBV genotypes were D or E. Precore G1896A HBV mutants were detected in both fatal fulminant primary HBV infections. Hepatitis B surface antigen and hepatitis B e antigen (HBeAg) were negative in two and three cases, respectively, despite HBV DNA detection. Primary HBV infection remains a cause of death in France. The impact of the precore G1896A mutation on the severity of AHB deserves to be assessed in larger studies in this country.

Echinacea Alkamides Prevent Lipopolysaccharide/d-Galactosamine- Induced Acute Hepatic Injury through JNK Pathway-Mediated HO-1 Expression

This study aimed to shed light on the anti-inflammatory and hepatoprotective effect of the major alkamides dodeca-2E,4E,8Z,10Z(E)-tetraenoic acid isobutylamides (Alk-8/9), isolated from Echinacea purpurea roots, against acute fulminant hepatitis induced by lipopolysaccharide/D-galactosamine (LPS/D-GalN) in mice. The results show that Alk-8/9 dose-dependently induced heme oxygenase (HO)-1 protein expression in LPS-stimulated murine macrophages that was likely regulated by the JNK-mediated pathway through increasing SAPK/JNK phosphorylation, c-jun protein expression, and phosphorylation, and transcription factor AP-1 binding consensus DNA activity. The HO-1 inhibitor or CO scavenger significantly reversed the inhibitory effect of Alk-8/9 on TNF-α expression, whereas N-acetyl-L-cysteine was observed to reduce Alk-8/9-induced HO-1 expression in LPS-treated macrophages. Furthermore, Alk-8/9 markedly induced c-jun and HO-1 protein expression and suppressed serum aminotransferase activities, TNF-α expression, and hepatocyte damage in liver tissues of LPS/d-GalN-treated mice. This paper suggests a new application of Echinacea, a top-selling herbal supplement, as a hepatoprotective agent.

Molecular detection and sequence analysis of hepatitis E virus in patients with viral hepatitis from North India

Viral hepatitis is a major cause of mortality and morbidity in developing countries. Hepatitis E virus (HEV) is responsible for both sporadic and epidemic outbreaks of viral hepatitis in India. Here a total of 843 samples were collected: 685 from patients with acute viral hepatitis (AVH), 70 from patients with fulminant hepatic failure (FHF), 53 from patients with chronic liver disease (CLD), 11 from patients with antituberculosis therapy (ATT)–induced jaundice, and 24 from pregnant women. When tested for anti-HEV IgM, 58.3% of the pregnant women, 41.4% of the patients with FHF, 38.6% of the patients with AVH, 9.4% of the patients with CLD, and 18.2% of the patients with ATT-induced jaundice tested positive. We found that 34% and 16% of the acute hepatitis patients and fulminant hepatitis patients, respectively, showed no reactivity to the existing viral hepatitis markers and were thus grouped as non A to E. Among the HEV IgM–positive cases, males outnumbered females (62.8% versus 37.1%). HEV RNA was found in 35% of fulminant and 9.4% of acute hepatitis patients. From phylogenetic analysis, we observed that all the isolates were clustered within genotype 1. Critical analysis placed the acute isolates along with strains under subtype Ia, while the fulminant isolates clustered along with the FHF strain (X98292) under subtype Ic. The segregation of HEV isolates from AVH and FHF patients into different subtypes raises interesting questions on the molecular basis of HEV disease severity.

Severe hepatotoxicity and probable hepatorenal syndrome associated with sulfadiazine

PURPOSE. The case of a patient who developed hepatorenal syndrome during treatment with sulfadiazine for toxoplasmosis retinitis is reported. A 20-year-old Caucasian woman weighing 59 kg was admitted to the infectious diseases ward of a hospital in May 2009 with nausea, vomiting, and jaundice. In March 2009, she was diagnosed with toxoplasmosis retinitis and received sulfadiazine 3 g daily, pyrimethamine 50 mg daily, leucovorin 15 mg daily, and prednisolone 75 mg daily; she continued these medications for three weeks. After the development of gastrointestinal symptoms, she stopped taking the prescribed medications (five days before hospital admission). One day before hospital admission, her skin appeared jaundiced. At the time of admission, the patient had high transaminase levels, hyperbilirubinemia, abnormal prothrombin time and International Normalized Ratio values, and clinical evidence of acute fulminant hepatitis complicated by hepatorenal syndrome. Autoimmune hepatitis was excluded as a cause of her hepatotoxicity, as was Wilson's disease, herpes simplex virus, cytomegalovirus, hepatitis A virus, hepatitis E virus, and Epstein-Barr virus. She was diagnosed with probable drug-related fulminant hepatitis, presumably caused by sulfadiazine treatment. Lactulose 20 g was started for the prevention of encephalopathy. She received phytonadione 10 mg daily for three consecutive days, ranitidine 50 mg thrice daily, ciprofloxacin 250 mg twice daily, and acetylcysteine 600 mg thrice daily. The patient underwent hemodialysis five times during her hospital stay. Her symptoms gradually improved, and she was discharged on hospital day 20. Probable hepatorenal syndrome requiring hemodialysis occurred in a patient receiving sulfadiazine for the treatment of toxoplasmosis retinitis.

Adaptive immune responses during acute uncomplicated and fulminant hepatitis E

Hepatitis E virus (HEV) infection is endemic in several developing countries. Clinical manifestations of this infection vary widely from asymptomatic infection to uncomplicated acute viral hepatitis and fulminant hepatic failure. The pathogenesis of this disease and the reason of varying disease severity remain unknown. In viral infections, tissue injury can be caused either by virus itself or by host immune responses directed against infected cells. We therefore studied adaptive immune responses to HEV antigens in patients with hepatitis E of varying disease severity and healthy controls. Cytokine secreting CD4+ T cells and antibody-producing B cells specific for HEV were enumerated through intracellular cytokine staining and enzyme-linked immunosorbent spot assay, respectively. Patients with fulminant hepatitis E had a less marked expansion of HEV-specific interferon-γ or tumor necrosis factor-a secreting CD4+ T cells than patients with uncomplicated hepatitis E and healthy controls. These patients also had fewer CD4+ T cells that produce γ-interferon or tumor necrosis factor-a upon in vitro polyclonal stimulation. In addition, patients with fulminant disease had a more marked expansion of B cells that can secrete immunoglobulin G anti-HEV than patients with uncomplicated infection and control patients. These findings suggest that less-marked antiviral cellular immune responses and heightened antiviral humoral responses are associated with a more severe disease during HEV infection.

General evaluation of hepatectomy and hepatocellular carcinoma cases

Although the clinical and histopathological findings of hepatocellular carcinoma are well described, there are few national studies. In this study, we aimed to investigate the relationship between these findings in total or partial hepatectomy specimens in our series. We first collected 190 cases of total or partial hepatectomies performed because of hepatocellular carcinoma, cirrhosis or other disorders from the archives of Pathology. After re-examining the histopathological and clinical features such as age, gender and etiology, the relationship between them and serology results were statistically analyzed using the chi square and Multiple Comparison Tests. Among 190 cases, there were 168 (88.5%) total and 18 (9.5%) partial hepatectomies and 4 (2%) tumorectomy or metastasectomy cases. After gross and microscopic examination, 170 (89.5%) cases had a diagnosis of cirrhosis, 85 (44.7%) hepatocellular carcinoma, 3 parasitic cyst, 7 metastasis, 1 hepatoblastoma, 1 hepatocellular adenoma, 2 cholangiocarcinoma, 2 Budd Chiari Syndrome, 1 focal nodular hyperplasia, 1 cavernous hemangioma, and 2 acute fulminant hepatitis. Among the hepatocellular carcinoma cases, 53 had Hepatitis B virus, 15 Hepatitis C virus , 3 Hepatitis B virus and Hepatitis C virus, and 3 Hepatitis B virus and Hepatitis delta virus etiology, while 6 were alcoholic and 4 were due to other causes. Among cirrhosis patients, 84 (49.4%) had hepatocellular carcinoma. The male to female ratio of hepatocellular carcinoma cases was 74/11. The mean age was 55 and the median age 56.7. The results of this study demonstrated that the most common hepatic disorder was cirrhosis due to Hepatitis B virus in the hepatectomy specimens of our series that mostly consisted of total hepatectomies performed for transplantation where 50% had hepatocellular carcinoma.

Hepatitis viruses: Not always what it seems to be

The classic hepatotropic viruses, hepatitis A through E, are not the only viral agents able to infect the liver. Other systemic viruses may cause hepatic injury that can range from mild and transient elevation of aminotransferases to acute hepatitis and occasionally acute liver failure and fulminant hepatitis. The clinical presentation may be indistinguishable from that associated with classic hepatotropic viruses. These agents include cytomegalovirus; Epstein-Barr virus; herpes simplex virus; varicella-zoster virus; human herpesvirus 6, 7, and 8; human parvovirus B19; adenoviruses among others. Wide spectrums of clinical syndromes are associated with cytomegalovirus disease. Unique clinical syndromes may present in neonates, young adults and immunocompromised hosts infected with cytomegalovirus. Cases of fulminant hepatitis have been reported in both immunocompromised and immunocompetent hosts infected with Epstein Barr virus. Occasionally, these patients with acute hepatic failure may need liver transplantation. Herpes simplex viruses may involve the liver in neonatal infections, pregnancy, immunocompromised hosts and occasionally, immunocompetent adults. Varicella-Zoster virus has also been associated with severe acute hepatitis and fulminant hepatitis in adults. The drug of choice for these conditions is intravenous acyclovir. These may also need liver transplantation in the more severe forms of clinical presentation. Typical liver biopsy findings can be useful in determining the diagnosis of these viral infections. Human herpesviruses 6, 7, and 8, human parvovirus B19, and adenoviruses can also be present with features of acute liver injury and occasionally as fulminant hepatitis. The clinical syndromes are less well delineated than those associated with herpesviruses. It is important to consider these viruses as possible etiologic agents in patients who have acute liver injury and their serologic markers for the classic hepatotropic viruses are not indicative of an active infection.

Hepatitis viruses: not always what it seems to be.

The classic hepatotropic viruses, hepatitis A through E, are not the only viral agents able to infect the liver. Other systemic viruses may cause hepatic injury that can range from mild and transient elevation of aminotransferases to acute hepatitis and occasionally acute liver failure and fulminant hepatitis. The clinical presentation may be indistinguishable from that associated with classic hepatotropic viruses. These agents include cytomegalovirus; Epstein-Barr virus; herpes simplex virus; varicella-zoster virus; human herpesvirus 6, 7, and 8; human parvovirus B19; adenoviruses among others. Wide spectrums of clinical syndromes are associated with cytomegalovirus disease. Unique clinical syndromes may present in neonates, young adults and immunocompromised hosts infected with cytomegalovirus. Cases of fulminant hepatitis have been reported in both immunocompromised and immunocompetent hosts infected with Epstein Barr virus. Occasionally, these patients with acute hepatic failure may need liver transplantation. Herpes simplex viruses may involve the liver in neonatal infections, pregnancy, immunocompromised hosts and occasionally, immunocompetent adults. Varicella-Zoster virus has also been associated with severe acute hepatitis and fulminant hepatitis in adults. The drug of choice for these conditions is intravenous acyclovir. These may also need liver transplantation in the more severe forms of clinical presentation. Typical liver biopsy findings can be useful in determining the diagnosis of these viral infections. Human herpesviruses 6, 7, and 8, human parvovirus B19, and adenoviruses can also be present with features of acute liver injury and occasionally as fulminant hepatitis. The clinical syndromes are less well delineated than those associated with herpesviruses. It is important to consider these viruses as possible etiologic agents in patients who have acute liver injury and their serologic markers for the classic hepatotropic viruses are not indicative of an active infection.

Characterization of a Variant Virus from Ascitic Fluid of Subacute Granulomatous Serositis in Interferon-γ-Deficient C57BL/6 Mice Persistently Infected with Murine Coronavirus Strain JHM

Previously, we showed that intraperitoneal infection with murine coronavirus strain JHM (JHMV) established a persistent infection with subacute granulomatous serositis in interferon-gamma-deficient C57BL/6 (B6-GKO) mice. Herein, we characterize a variant virus from B6-GKO mice persistently infected with JHMV. Viruses were isolated from ascites at 25 d post-infection and cloned by limiting dilution on DBT cells; one variant was named 25V16G. To compare pathogenicity in vivo, we inoculated 25V16G and JHMV intraperitoneally into 8- to 12-week-old B6-GKO mice. Whereas nearly all of the B6-GKO mice infected with JHMV survived over 14 d, all of those infected with 25V16G died by 9 d post-infection. Histopathological examination revealed that 25V16G induced acute fulminant hepatitis in B6-GKO mice, whereas JHMV caused severe but focal hepatitis. The virus titer of 25V16G in the liver was 50- and 250-fold higher than that of JHMV at 5 and 7 d post-infection, respectively. However, there was no significant difference in viral growth between 25V16G and JHMV in cell lines cultured in vitro. Nucleotide sequencing of the S gene of 25V16G and JHMV revealed a deletion of 29 amino acids encompassing S(511-539), which covers a major cytotoxic T lymphocyte (CTL) epitope in C57BL/6 mice, and two point mutations resulting in amino acid changes in the S protein of 25V16G. One explanation for the greater pathogenicity of 25V16G is that 25V16G escapes CTL-mediated protection in B6-GKO mice. This experimental model may be used to assess the role of IFN-gamma in viral persistence in vivo.

BRE over-expression promotes growth of hepatocellular carcinoma

BRE, also known as TNFRSF1A modulator and BRCC45, is an evolutionarily highly conserved protein. It is a death receptor-associated protein in cytoplasm and a component of BRCA1/2-containing DNA repair complex in nucleus. BRE was found to have anti-apoptotic activity. Over-expression of BRE by transfection promoted survival of cell lines against apoptotic induction; whereas depletion of the protein by siRNA resulted in the opposite. In vivo anti-apoptotic activity of BRE was demonstrated by significant attenuation of Fas-induced acute fulminant hepatitis in transgenic mice expressing the human protein specifically in the liver. BRE was also implicated in tumor promotion by the accelerated tumor growth of Lewis Lung carcinoma transfected with human BRE; and by high expression of BRE specifically in the tumoral regions of human hepatocellular carcinoma (HCC). The present study was to test directly if transgenic expression of BRE in livers could promote HCC development in neonatal diethylnitrosamine model. By 8 months after tumor induction, the maximal sizes of tumor nodules of transgenic mice were significantly larger than those of the non-transgenic controls, although the numbers of tumor nodules between the two groups did not significantly differ. Importantly, as in human HCC, the mouse endogenous BRE level was up-regulated in mouse HCC nodules. These results show that BRE over-expression can indeed promote growth, though not initiation, of liver tumors. Furthermore, the common occurrence of BRE over-expression in human and mouse HCC suggests that up-regulation of BRE is functionally important in liver tumor development.

Effective inhibition of hepatitis E virus replication in A549 cells and piglets by RNA interference (RNAi) targeting RNA-dependent RNA polymerase

RNA interference (RNAi) is a natural mechanism for suppressing or silencing expression of aberrant or foreign genes. It is a powerful antiviral strategy that has been widely employed to protect hosts from viral infection. Hepatitis E (HE) is an acute fulminant hepatitis in adults that has particularly high mortality in pregnant women. At this point in time, there is no vaccine or antiviral treatment that is effective against the infectious agent, HEV. The nonstructural polyprotein region possesses an RNA-dependent RNA polymerase (RdRp) that is responsible for the replication of the viral RNA genome. RdRp is therefore regarded as one of the most attractive candidates for RNA interference (RNAi). In the present study, the high efficiency and specificity of siRNA were evaluated by Real-Time quantitative PCR and Western blot assays. Protective effects against HEV infection were achieved in A549 cells and in piglets. In piglets treated with a shRNA-RdRp-1 expression plasmid prior to HEV inoculation, HEV antigens were significantly reduced in the liver, spleen, and kidneys, and the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBIL) were clearly decreased. These results suggested that RNAi is a potentially effective antiviral strategy against HEV replication and infection.

ROLE OF NUTRITION IN MEDICAL MANAGEMENT OF ACUTE FULMINANT HEPATITIS

Journal Article Role of Nutrition in Medical Management of Acute Fulminant Hepatitis Get access Nutrition Reviews, Volume 35, Issue 7, July 1977, Pages 167–169, https://doi.org/10.1111/j.1753-4887.1977.tb06580.x Published: 01 July 1977