Clinical observations have demonstrated that excessive chronic alcohol use negatively affects human immuno- deficiency virus (HIV) infection and contributes to the liver manifestations of the disease, even in HIV mono...Clinical observations have demonstrated that excessive chronic alcohol use negatively affects human immuno- deficiency virus (HIV) infection and contributes to the liver manifestations of the disease, even in HIV mono- infection. HIV/hepatitis C virus (HCV) co-infection is as- sociated with increased progression of HVC liver disease compared to HCV infection alone, and both of these are negatively affected by alcohol use. Recent data suggest that alcohol use and HIV infection have common targets that contribute to progression of liver disease. Both HIV infection and chronic alcohol use are associated with increased gut permeability and elevated plasma levels of lipopolysaccharide; a central activator of inflammatory responses. Both alcoholic liver disease and HIV infec tionresult in non-specific activation of innate immunity, proinflammatory cytokine cascade upregulation, as well as impaired antigen presenting cell and dendritic cell functions. Finally, alcohol, HIV and antiretroviral therapyaffect hepatocyte functions, which contributes to liver damage. The common targets of alcohol and HIV infection in liver disease are discussed in this minireview.展开更多
AIM:To examine trends in and correlates of liver disease and viral hepatitis in an human immunodeficiency virus (HIV)-infected cohort. METHODS:The multi-site adult/adolescent spectrum of HIV-related diseases (ASD) fol...AIM:To examine trends in and correlates of liver disease and viral hepatitis in an human immunodeficiency virus (HIV)-infected cohort. METHODS:The multi-site adult/adolescent spectrum of HIV-related diseases (ASD) followed 29 490 HIVinfected individuals receiving medical care in 11 U.S. metropolitan areas for an average of 2.4 years,and a total of 69 487 person-years,between 1998 and 2004. ASD collected data on the presentation,treatment,and outcomes of HIV,including liver disease,hepatitis screening,and hepatitis diagnoses. RESULTS:Incident liver disease,chronic hepatitis B virus (HBV),and hepatitis C virus (HCV) were diagnosed in 0.9,1.8,and 4.7 per 100 person-years. HBV and HCV screening increased from fewer than 20% to over 60% during this period of observation (P < 0.001). Deaths occurred in 57% of those diagnosed with liver disease relative to 15% overall (P < 0.001). Overall 10% of deaths occurred among individuals with a diagnosis of liver disease. Despite care guidelines promoting screening and vaccination for HBV and screening for HCV,screening and vaccination were not universally conducted or,if conducted,not documented. CONCLUSION:Due to high rates of incident liver disease,viral hepatitis screening,vaccination,and treatment among HIV-infected individuals should be a priority.展开更多
To elucidate the molecular response of shrimp hepatopancreas to white spot syndrome virus(WSSV) infection, microarray was applied to investigate the differentially expressed genes in the hepatopancreas of ‘Huanghai N...To elucidate the molecular response of shrimp hepatopancreas to white spot syndrome virus(WSSV) infection, microarray was applied to investigate the differentially expressed genes in the hepatopancreas of ‘Huanghai No. 2'(Fenneropenaeus chinensis). A total of 59137 unigenes were designed onto a custom-made 60 K Agilent chip. After infection, the gene expression profiles in the hepatopancreas of the shrimp with a lower viral load at early(48–96 h), peak(168–192 h) and late(264–288 h) infection phases were analyzed. Of 18704 differentially expressed genes, 6412 were annotated. In total, 5453 differentially expressed genes(1916 annotated) expressed at all three phases, and most of the annotated were either up-or down-regulated continuously. These genes function diversely in, for example, immune response, cytoskeletal system, signal transduction, stress resistance, protein synthesis and processing, metabolism among others. Some of the immune-related genes, including antilipopolysaccharide factor, Kazal-type proteinase inhibitor, C-type lectin and serine protease encoding genes, were up-regulated after WSSV infection. These genes have been reported to be involved in the anti-WSSV responses. The expression of genes related to the cytoskeletal system, including β-actin and myosin but without tubulin genes, were down-regulated after WSSV infection. Astakine was found for the first time in the WSSV-infected F. chinensis. To further confirm the expression of differentially expressed genes, quantitative real-time PCR was performed to test the expression of eight randomly selected genes and verified the reliability and accuracy of the microarray expression analysis. The data will provide valuable information to understanding the immune mechanism of shrimp's response to WSSV.展开更多
Chronic consumption of ethanol has a dramatic effect on the clinical outcome of patients with hepatitis C virus (HCV) infection, but the mechanism linking these two pathologies is unknown. Presently, in vitro systems ...Chronic consumption of ethanol has a dramatic effect on the clinical outcome of patients with hepatitis C virus (HCV) infection, but the mechanism linking these two pathologies is unknown. Presently, in vitro systems are limited in their ability to study the interaction between a productive wild-type HCV infection and chronic ethanol exposure. Mouse models are potentially very useful in dissecting elements of the HCV-ethanol relationship. Experiments in mice that transgenically express HCV proteins are outlined, as are experiments for the generation of mice with chimeric human livers. The latter models appear to have the most promise for accurately modeling the effects of chronic ethanol intake in HCV-infected human livers.展开更多
To study the role of natural killer (NK) cells in T cell recruitment in murine liver infected with virus, mice were intravenously injected daily with anti-NK1.1 + antibody to deplete NK cells. Lymphocytes in the liver...To study the role of natural killer (NK) cells in T cell recruitment in murine liver infected with virus, mice were intravenously injected daily with anti-NK1.1 + antibody to deplete NK cells. Lymphocytes in the liver tissue of mice infected with type 5 adenovirus depleted in the E1 and E3 regions were assessed by fluorometric activated cell sorting (FACS). Expression of chemokine IP-10 and its receptor CXCR3 mRNA in the liver, hepatic lymphocytes and spleen tissue were examined by reverse transcription polymerase chain reaction (RT-PCR). Serum alanine aminotransferase (ALT) was measured as an indicator of liver injury. It was found that infection of adenovirus and anti-Fas monoclonal antibody (mAb) into mice caused liver injury and high expression of interferon-γ inducible protein-10 (IP-10) mRNA in the liver. Anti-NK1.1 + mAb, which was intraperitoneally injected into the mice infected with adenovirus, suppresses T cell recruitment and expression of IP-10 mRNA in the liver. Slighter liver injury was also observed. After virus infection, expression of CXCR3 mRNA in spleen and liver tissue was observed at different time. The results suggested that T cell recruitment was initiated by NK cell dependent chemokine IP-10, which induced activated T cells priming in the spleen to the liver of the mouse. NK cells played a key role in T cell recruitment in the liver of mouse infected with adenovirus.展开更多
文摘Clinical observations have demonstrated that excessive chronic alcohol use negatively affects human immuno- deficiency virus (HIV) infection and contributes to the liver manifestations of the disease, even in HIV mono- infection. HIV/hepatitis C virus (HCV) co-infection is as- sociated with increased progression of HVC liver disease compared to HCV infection alone, and both of these are negatively affected by alcohol use. Recent data suggest that alcohol use and HIV infection have common targets that contribute to progression of liver disease. Both HIV infection and chronic alcohol use are associated with increased gut permeability and elevated plasma levels of lipopolysaccharide; a central activator of inflammatory responses. Both alcoholic liver disease and HIV infec tionresult in non-specific activation of innate immunity, proinflammatory cytokine cascade upregulation, as well as impaired antigen presenting cell and dendritic cell functions. Finally, alcohol, HIV and antiretroviral therapyaffect hepatocyte functions, which contributes to liver damage. The common targets of alcohol and HIV infection in liver disease are discussed in this minireview.
文摘AIM:To examine trends in and correlates of liver disease and viral hepatitis in an human immunodeficiency virus (HIV)-infected cohort. METHODS:The multi-site adult/adolescent spectrum of HIV-related diseases (ASD) followed 29 490 HIVinfected individuals receiving medical care in 11 U.S. metropolitan areas for an average of 2.4 years,and a total of 69 487 person-years,between 1998 and 2004. ASD collected data on the presentation,treatment,and outcomes of HIV,including liver disease,hepatitis screening,and hepatitis diagnoses. RESULTS:Incident liver disease,chronic hepatitis B virus (HBV),and hepatitis C virus (HCV) were diagnosed in 0.9,1.8,and 4.7 per 100 person-years. HBV and HCV screening increased from fewer than 20% to over 60% during this period of observation (P < 0.001). Deaths occurred in 57% of those diagnosed with liver disease relative to 15% overall (P < 0.001). Overall 10% of deaths occurred among individuals with a diagnosis of liver disease. Despite care guidelines promoting screening and vaccination for HBV and screening for HCV,screening and vaccination were not universally conducted or,if conducted,not documented. CONCLUSION:Due to high rates of incident liver disease,viral hepatitis screening,vaccination,and treatment among HIV-infected individuals should be a priority.
基金the Central Public-interest Scientific Institution Basal Research Fund, CAFS (No. 2016HY-ZD04)the National Natural Science Foundation of China (No. 31372523)+2 种基金the Scientific and Technological Innovation Project Financially Supported by Qingdao National Laboratory for Marine Science and Technology (No. 2015ASKJ02-03)the Taishan Scholar Program For Seed Industry, the Shandong Provincial Natural Science Foundation (No. ZR2014CQ001)the Special Fund for Postdoctoral Innovative Project of Shandong Province, and Central Public-Interest Scientific Institution Basal Research Fund of the Yellow Sea Fisheries Research Institute (Nos. 2060302013036 and 20603022015013)
文摘To elucidate the molecular response of shrimp hepatopancreas to white spot syndrome virus(WSSV) infection, microarray was applied to investigate the differentially expressed genes in the hepatopancreas of ‘Huanghai No. 2'(Fenneropenaeus chinensis). A total of 59137 unigenes were designed onto a custom-made 60 K Agilent chip. After infection, the gene expression profiles in the hepatopancreas of the shrimp with a lower viral load at early(48–96 h), peak(168–192 h) and late(264–288 h) infection phases were analyzed. Of 18704 differentially expressed genes, 6412 were annotated. In total, 5453 differentially expressed genes(1916 annotated) expressed at all three phases, and most of the annotated were either up-or down-regulated continuously. These genes function diversely in, for example, immune response, cytoskeletal system, signal transduction, stress resistance, protein synthesis and processing, metabolism among others. Some of the immune-related genes, including antilipopolysaccharide factor, Kazal-type proteinase inhibitor, C-type lectin and serine protease encoding genes, were up-regulated after WSSV infection. These genes have been reported to be involved in the anti-WSSV responses. The expression of genes related to the cytoskeletal system, including β-actin and myosin but without tubulin genes, were down-regulated after WSSV infection. Astakine was found for the first time in the WSSV-infected F. chinensis. To further confirm the expression of differentially expressed genes, quantitative real-time PCR was performed to test the expression of eight randomly selected genes and verified the reliability and accuracy of the microarray expression analysis. The data will provide valuable information to understanding the immune mechanism of shrimp's response to WSSV.
文摘Chronic consumption of ethanol has a dramatic effect on the clinical outcome of patients with hepatitis C virus (HCV) infection, but the mechanism linking these two pathologies is unknown. Presently, in vitro systems are limited in their ability to study the interaction between a productive wild-type HCV infection and chronic ethanol exposure. Mouse models are potentially very useful in dissecting elements of the HCV-ethanol relationship. Experiments in mice that transgenically express HCV proteins are outlined, as are experiments for the generation of mice with chimeric human livers. The latter models appear to have the most promise for accurately modeling the effects of chronic ethanol intake in HCV-infected human livers.
文摘To study the role of natural killer (NK) cells in T cell recruitment in murine liver infected with virus, mice were intravenously injected daily with anti-NK1.1 + antibody to deplete NK cells. Lymphocytes in the liver tissue of mice infected with type 5 adenovirus depleted in the E1 and E3 regions were assessed by fluorometric activated cell sorting (FACS). Expression of chemokine IP-10 and its receptor CXCR3 mRNA in the liver, hepatic lymphocytes and spleen tissue were examined by reverse transcription polymerase chain reaction (RT-PCR). Serum alanine aminotransferase (ALT) was measured as an indicator of liver injury. It was found that infection of adenovirus and anti-Fas monoclonal antibody (mAb) into mice caused liver injury and high expression of interferon-γ inducible protein-10 (IP-10) mRNA in the liver. Anti-NK1.1 + mAb, which was intraperitoneally injected into the mice infected with adenovirus, suppresses T cell recruitment and expression of IP-10 mRNA in the liver. Slighter liver injury was also observed. After virus infection, expression of CXCR3 mRNA in spleen and liver tissue was observed at different time. The results suggested that T cell recruitment was initiated by NK cell dependent chemokine IP-10, which induced activated T cells priming in the spleen to the liver of the mouse. NK cells played a key role in T cell recruitment in the liver of mouse infected with adenovirus.