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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections with hepatitis B (HBV) and hepatitis C virus (HCV) are worldwide one of the most frequent causes for chronic liver disease, liver cirrhosis and hepatocellular carcinoma. The mechanisms responsible for the elimination or the persistence of the virus are not well understood. The immunopathogenesis of HBV and HCV infection is primarily mediated by virus specific CD4+- and CD8+-T-cells. During acute infection a strong and multispecific T-cell response against different viral epitopes can be detected and is associated with the clearance of the virus. In case of viral persistence virus specific T-cells contribute to liver inflammation. In this article we summarize the current concepts about the role of the virus specific T-cell response in acute and chronic HBV and HCV infection.
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PMID:[The role of the virus specific T-cell response in acute and chronic HBV and HCV infection]. 1499 2

Due to shared risk factors for transmission, coinfection with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is a very common event. The prevalence of HCV infection among HIV-positive patients averages about 35% in the United States and Europe, but in clinical populations where there is a great prevalence of intravenous drug use as a risk factor for acquiring HIV, this value may be as high as 80-90%. Several studies have confirmed that HIV coinfection accelerates the natural course of chronic hepatitis C and an increased risk of liver cirrhosis, hepatocellular carcinoma, and decompensated liver disease has been found in coinfected subjects. Other studies have shown an increased risk of progression to acquired immunodeficiency syndrome (AIDS) and AIDS-related death among HIV-HCV-positive persons, suggesting that HCV coinfection may accelerate the course of HIV disease. In addition, hepatitis C may affect the management of HIV infection, increasing the incidence of liver toxicity associated with the antiretroviral regimens. The optimal therapeutic approach to HCV infection in HIV coinfected patients is still uncertain, because of the complex pathogenesis of both infections, potential drugdrug interactions, and the poor literature and information available about safety and efficacy of an interferon (IFN) and ribavirin combination in this clinical population. Available data show that the sustained virological response rates in coinfected persons treated with standard IFN plus ribavirin range from 18-40%, and several studies with pegylated IFN plus ribavirin are ongoing.
Infection 2004 Feb
PMID:Human immunodeficiency virus and hepatitis C virus coinfection: epidemiology, natural history, therapeutic options and clinical management. 1500 41

Infections with hepatitis B virus (HBV) and human immunodeficiency virus (HIV) have similar risk factors and routes of transmission. It is estimated that 64 to 84% of HIV-infected individuals have positive markers for anti-HBc antibodies, with the chronic HBV infection rate approaching 16%. There is, however, a paucity of information on HBV/HIV coinfection, and its clinical implications remain unclear. We review the literature and report our recent experience with a 44-year-old man with HBV/HIV coinfection who developed metastatic hepatocellular carcinoma despite quiescent HBV and HIV disease courses. Highly active antiretroviral therapy has revolutionized HIV disease. As a result, morbidity and mortality from other underlying chronic, non-HIV-related diseases, such as the HBV infection and hepatocellular carcinoma reported here, will likely continue to increase in the HIV-infected patient population.
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PMID:Hepatocellular carcinoma in a patient with human immunodeficiency virus and hepatitis B virus coinfection: an emerging problem? 1510 38

The severe acute respiratory syndrome-associated coronavirus (SARS-CoV) causes severe pneumonia with a fatal outcome in approximately 10% of patients. SARS-CoV is not closely related to other coronaviruses but shares a similar genome organization. Entry of coronaviruses into target cells is mediated by the viral S protein. We functionally analyzed SARS-CoV S using pseudotyped lentiviral particles (pseudotypes). The SARS-CoV S protein was found to be expressed at the cell surface upon transient transfection. Coexpression of SARS-CoV S with human immunodeficiency virus-based reporter constructs yielded viruses that were infectious for a range of cell lines. Most notably, viral pseudotypes harboring SARS-CoV S infected hepatoma cell lines but not T- and B-cell lines. Infection of the hepatoma cell line Huh-7 was also observed with replication-competent SARS-CoV, indicating that hepatocytes might be targeted by SARS-CoV in vivo. Inhibition of vacuolar acidification impaired infection by SARS-CoV S-bearing pseudotypes, indicating that S-mediated entry requires low pH. Finally, infection by SARS-CoV S pseudotypes but not by vesicular stomatitis virus G pseudotypes was efficiently inhibited by a rabbit serum raised against SARS-CoV particles and by sera from SARS patients, demonstrating that SARS-CoV S is a target for neutralizing antibodies and that such antibodies are generated in SARS-CoV-infected patients. Our results show that viral pseudotyping can be employed for the analysis of SARS-CoV S function. Moreover, we provide evidence that SARS-CoV infection might not be limited to lung tissue and can be inhibited by the humoral immune response in infected patients.
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PMID:S protein of severe acute respiratory syndrome-associated coronavirus mediates entry into hepatoma cell lines and is targeted by neutralizing antibodies in infected patients. 1516 6

Parvovirus B19 (B19 virus) can persist in multiple tissues and has been implicated in a variety of diseases, including acute fulminant liver failure. The mechanism by which B19 virus induces liver failure remains unknown. Hepatocytes are nonpermissive for B19 virus replication. We previously reported that acute fulminant liver failure associated with B19 virus infection was characterized by hepatocellular dropout. We inoculated both primary hepatocytes and the hepatocellular carcinoma cell line Hep G2 with B19 virus and assayed for apoptosis by using annexin V staining. Reverse transcriptase PCR analysis and immunofluorescence demonstrated that B19 virus was able to infect the cells and produce its nonstructural protein but little or no structural capsid protein. Infection with B19 virus induced means of 28% of Hep G2 cells and 10% of primary hepatocytes to undergo apoptosis, which were four- and threefold increases, respectively, over background levels. Analysis of caspase involvement showed that B19 virus-inoculated cultures had a significant increase in the number of cells with active caspase 3. Inhibition studies demonstrated that caspases 3 and 9, but not caspase 8, are required for B19 virus-induced apoptosis.
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PMID:Parvovirus B19-induced apoptosis of hepatocytes. 1522 Apr 51

Infection with hepatitis C virus (HCV) is a global public health issue. More than 200 million people in the world are infected with HCV. Hepatitis C is considered one of the main causes of chronic hepatitis, cirrhosis, hepatocellular carcinoma and liver transplantation. The identification of the viral genome quickly allowed delineation of genomic organization, and the structure and biochemical characterization of the proteins of HCV. However, it has been difficult to study its life cycle, as well as the development of antiviral agents due to the lack of a system of permissible culture. Numerous attempts have been reported to establish an in vitro system for the study of HCV. Recently, a system of efficient culture was established that allows replication of subgenomic molecules of HCV in a cell line of human hepatoma. In this revision, after a brief description of the molecular biology, means of transmission and clinical characteristics of hepatitis C, some of the experimental models are described that have been developed to date, focusing mainly on the subgenomic replicon system and their use in the development of new antiviral treatments.
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PMID:Experimental models for hepatitis C virus (HCV): new opportunities for combating hepatitis C. 1525 47

Hepatitis C virus (HCV), an RNA and a hepatotropic virus, is the leading cause of viral hepatitis worldwide. Infection with this virus causes a repertoire of liver diseases that include acute hepatitis, chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC), in addition to a number of extra-hepatic manifestations such as lichen planus, oral cancer, etc. At present, patients infected with this virus are treated with interferon either alone or in combination with ribavirin, a guanosine-like nucleoside analog. However, response to this treatment has been rather disappointing. For about a decade, lack of an alternative animal model other than chimpanzee, and an efficient cell culture system that could support long-term replication of the virus, hampered research on HCV. Despite this, a significant amount of information with regard to the molecular biology of the virus is available using bacterial cloning-expression systems, and based on computer predictions and analysis. Recent discovery of a cellular receptor to which the virus binds, identification of efficient cell culture/cell-free systems, HCV replicons and the development of a chimeric mouse model, provide a platform to verify the existing knowledge about this virus in the coming years. Additionally these developments aid the researchers in identifying novel therapeutic agents, apart from allowing us to reassess the efficiency of the currently available therapeutics. Presented in this article are a review of existing information with regard to the molecular biology of the virus, immunodiagnostic assays, genomic heterogeneity and the role of the virus in hepatocellular carcinoma. Likely therapeutic strategies other than those currently available are also introduced.
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PMID:Hepatitis C virus (HCV)--a review molecular biology of the virus, immunodiagnostics, genomic heterogeneity and the role of virus in hepatocellular carcinoma. 1526 99

Hepatocellular carcinoma is one of the most common cancers worldwide. Infection with hepatitis B virus and exposure to aflatoxins in the diet act synergistically to amplify risk. From a public health perspective, hepatitis virus vaccination programs and efforts to both reduce aflatoxin exposures and to attenuate the toxicological consequences of unavoidable exposures should have major impacts on the global incidence of this disease. Experimentally, aflatoxin-induced hepatocarcinogenesis can be inhibited by over a score of different chemopreventive agents with multiple mechanisms of action. One agent, oltipraz, is a potent inducer of phase 2 enzymes involved in the detoxication of carcinogens including aflatoxin. A second agent, chlorophyllin, impedes the bioavailability of carcinogens by forming molecular complexes and enhances their elimination in the fecal stream. This review highlights the findings of recent randomized clinical trials with oltipraz and chlorophyllin conducted in individuals exposed to dietary aflatoxins and at high risk for development of liver cancer. Both chemopreventive agents modulated levels of aflatoxin biomarkers in the study participants in manners consonant with protection. Although pharmacological approaches establish proof of principle and help identify key molecular targets for interventions, food-based approaches that also use these molecular targets may be the most practical for widespread application in high-risk populations.
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PMID:Chemoprevention of hepatocellular carcinoma in aflatoxin endemic areas. 1550 99

Infection by the hepatitis B virus (HBV) is a significant cause of morbidity and mortality, mainly due to evolvement to cirrhosis and hepatocellular carcinoma. The prevalence and genotypic distribution of HBV infection has marked geographic differences. HBV infection is a very dynamic process, with a phase of immune tolerance and high viral replication, followed by HBeAg clearance, not always accompanied by complete suppression of HBV replication. The latter situation corresponds to negative HBeAg hepatitis, which represents a group relatively resistant to therapy. The three approved drugs for the treatment of HBV infection (interferon alpha, lamivudine and adefovir) have limited efficacy. Relapses are more common with lamivudine and adefovir, requiring often long-term treatment. While the selection of lamivudine resistance mutations is frequent, adefovir has a high genetic barrier. HIV infection negatively impacts on HBV disease, requiring these coinfected patients strategies aimed to manage both viruses.
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PMID:[Advances in the diagnosis and treatment of the infection by the hepatitis B virus]. 1551 95

Hepatitis C virus (HCV) is the main cause of hepatocellular carcinoma in industrialized countries. HCV-HIV-1 co-infection occurs frequently among users of illicit intravenous drugs, thereby increasing the severity of HIV disease and the evolution of chronic active hepatitis towards cirrhosis and hepatocellular carcinoma. The present work shows that THP-1 monocytoid cells are susceptible to HCV infection, of strain 1b, and that this strain can induce cellular modifications in this cell line. Infection of HCV was demonstrated by positivity for the E2 antigen within THP-1 cells and by indirect immunofluorescence; moreover, HCV-RNA was detected in supernatants of THP-1 cells from day 7 post-inoculation. Cell shape and membrane surface antigens varied upon viral infection, which is also capable of inducing oxygen radicals. In particular we underline the relevant intracellular accumulation of ferritin that paralleled an increase of cell surface expression of the transferrin receptor. Evaluation of cellular events upon HCV infection in THP-1 cells may represent a useful tool with which to identify alteration in monocytes metabolism and to study therapeutic approaches for such alterations.
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PMID:Effect of HCV infection on THP-1 monocytoid cells. 1551 25


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