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| 1 | HCV-RNA positivity in peripheral blood mononuclear cells of patients with chronic HCV-infection: does it really mean viral replication?显示文摘AIM To analyze the association of HCV-RNA with peripheral blood mononuclear cells (PBMC)and to answer the question whether HCV-RNA positivity in PBMC is due to viral replication,METHODS HCV-RNA was monitored in serumand PBMC preparations from 15 patients with chronic HCV infection before, during and after an IFN-α therapy using a nested RT/ PCRtechnique. In a second approach, PBMC from healthy donors were incubated in HCV positive plasma.RESULTS In the IFN-α responding patients,HCV-RNA disappeared first from total RNApreparations of PBMC and then from serum. In contrast, in relapsing patients, HCV-RNAreappeared first in serum and then in PBMC. A quantitative analysis of the HCV-RNAconcentration in serum was performed before and after transition from detectable to nondetectable HCV-RNA in PBMC-RNA and vice versa. When HCV-RNA was detectable in PBMCpreparations, the HCV concentration in serum was significantly higher than the serum HCV-RNA concentration when HCV-RNA in PBMC was not detectable. Furthermore, at no time during the observation period was HCV specific RNA observed in PBMC, if HCV-RNA in serum was under the detection limit. Incubation of PBMCfrom healthy donors with several dilutions of HCV positive plasma for two hours showed a concentration-dependent PCR-positivity for HCV-RNA in reisolated PBMC.CONCLUSION The detectability of HCV-RNA in total RNA from PBMC seems to depend on the HCV concentration in serum. Contamination or passive adsorption by circulating virus could be the reason for detection of HCV-RNA in PBMCpreparations of chronically infected patients. | Volker Meier Sabine Mihm Perdita Wietzke-Braun Guliano Ramadori | 2001 | World Journal of Gastroenterology2001，7，2： | 29 |
| 2 | Hepatitis C virus infection of human hepatoma cell line 7721 in vitro显示文摘AIM To establish a cell culture system with long-term replication of hepatitis C virus in vitro.``METHODS Human hepatoma cell line 7721 was tested for its susceptibility to HCV by incubating with a serum from a patient with chronic hepatitis C. Cells and supernatant were harvested at various phases during the culturing periods The presence of HCV RNA, the expression of HCV antigens in cells and/or supernatant were examined by RT-PCR, in situ hybridization and immunohistochemistry respectively.``RESULTS The intracellular HCV RNA was first detected on d 2 after infection and then could be intermittently detected in both cells and supernatant over a period of at least three months. The expression of HCV NS3, CP10antigens could be observed in cells. The fresh cells could be infected by supematant from cultured infected cells and the transmission of viral genome from HCV-infected 7721 cells to PBMCs was also observed.``CONCLUSION The hepatoma line 7721 is not only susceptible to HCV but also supports its long-term replication in vitro. | Zhi-Qiang Song~1 Fei Hao~1 Feng Min~2 Qiao-Yu Ma~2 Guo-Dong Liu~2 Department of Dermatology~1Department of Infectious Diseases~2,Southwest Hospital,Third Military Medical University,Chongqing 400038,China | 2001 | World Journal of Gastroenterology2001，7，5： | 26 |
| 3 | Hepatitis B virus and micro RNAs:Complex interactions affecting hepatitis B virus replication and hepatitis B virusassociated diseases显示文摘Chronic infection with the hepatitis B virus(HBV) is the leading risk factor for the development of hepatocellular carcinoma(HCC). With nearly 750000 deaths yearly, hepatocellular carcinoma is the second highest cause of cancer-related death in the world. Unfortunately, the molecular mechanisms that contribute to the development of HBV-associated HCC remain incompletely understood. Recently, micro RNAs(mi RNAs), a family of small non-coding RNAs that play a role primarily in post-transcriptional gene regulation, have been recognized as important regulators of cellular homeostasis, and altered regulation of mi RNA expression has been suggested to play a significant role in virus-associated diseases and the development of many cancers. With this in mind, many groups have begun to investigate the relationship between mi RNAs and HBV replication and HBV-associated disease. Multiple findings suggest that some mi RNAs, such as mi R-122, and mi R-125 and mi R-199 family members, are playing a role in HBV replication and HBV-associated disease, including the development of HBV-associated HCC. In this review, we discuss the current state of our understanding of the relationship between HBV and mi RNAs, including how HBV affects cellular mi RNAs, how these mi RNAs impact HBV replication, and the relationship between HBV-mediated mi RNA regulation and HCC development. We also address the impact of challenges in studying HBV, such as the lack of an effective model system for infectivity and a reliance on transformed cell lines, on our understanding of the relationship between HBV and mi RNAs, and proposepotential applications of mi RNA-related techniques that could enhance our understanding of the role mi RNAs play in HBV replication and HBV-associated disease, ultimately leading to new therapeutic options and improved patient outcomes. | Jason Lamontagne Laura F Steel Michael J Bouchard | 2015 | World Journal of Gastroenterology2015，21，24： | 17 |
| 4 | Na^+/K^+-ATPase β1 subunit interacts with M2 proteins of influenza A and B viruses and affects the virus replication显示文摘Interplay between the host and influenza virus has a pivotal role for the outcome of infection.The matrix proteins M2/BM2 from influenza (A and B) viruses are small type III integral membrane proteins with a single transmembrane domain,a short amino-terminal ectodomain and a long carboxy-terminal cytoplasmic domain.They function as proton channels,mainly forming a membrane-spanning pore through the transmembrane domain tetramer,and are essential for virus assembly and release of the viral genetic materials in the endosomal fusion process.However,little is known about the host factors which interact with M2/BM2 proteins and the functions of the long cytoplasmic domain are currently unknown.Starting with yeast two-hybrid screening and applying a series of experiments we identified that the β1 subunit of the host Na+/K+-ATPase β1 subunit (ATP1B1) interacts with the cytoplasmic domain of both the M2 and BM2 proteins.A stable ATP1B1 knockdown MDCK cell line was established and we showed that the ATP1B1 knockdown suppressed influenza virus A/WSN/33 replication,implying that the interaction is crucial for influenza virus replication in the host cell.We propose that influenza virus M2/BM2 cytoplasmic domain has an important role in the virus-host interplay and facilitates virus replication. | GAO George Fu | 2010 | Science China(Life Sciences)2010，53，9： | 10 |
| 5 | Hepatitis B virus pathogenesis: Fresh insights into hepatitis B virus RNA显示文摘Hepatitis B virus(HBV) is still a worldwide health concern. While divergent factors are involved in its pathogenesis, it is now clear that HBV RNAs, principally templates for viral proteins and viral DNAs, have diverse biological functions involved in HBV pathogenesis. These functions include viral replication, hepatic fibrosis and hepatocarcinogenesis. Depending on the sequence similarities, HBV RNAs may act as sponges for host mi RNAs and may deregulate mi RNA functions, possibly leading to pathological consequences. Some parts of the HBV RNA molecule may function as viralderived mi RNA, which regulates viral replication. HBV DNA can integrate into the host genomic DNA and produce novel viral-host fusion RNA, which may have pathological functions. To date, elimination of HBVderived covalently closed circular DNA has not been achieved. However, RNA transcription silencing may be an alternative practical approach to treat HBVinduced pathogenesis. A full understanding of HBV RNA transcription and the biological functions of HBV RNA may open a new avenue for the development of novel HBV therapeutics. | Kazuma Sekiba Motoyuki Otsuka Motoko Ohno Mari Yamagami Takahiro Kishikawa Tatsunori Suzuki Rei Ishibashi Takahiro Seimiya Eri Tanaka Kazuhiko Koike | 2018 | World Journal of Gastroenterology2018，24，21： | 10 |
| 6 | Autophagy and microRNA in hepatitis B virus-relatedhepatocellular carcinoma显示文摘Approximately 350 million people worldwide are chronically infected by hepatitis B virus(HBV).HBV causes severe liver diseases including cirrhosis and hepatocellular carcinoma(HCC).In about 25%of affected patients,HBV infection proceeds to HCC.Therefore,the mechanisms by which HBV affects the host cell to promote viral replication and its pathogenesis have been the subject of intensive research efforts.Emerging evidence indicates that both autophagy and micro RNAs(mi RNAs)are involved in HBV replication and HBV-related hepatocarcinogenesis.In this review,we summarize how HBV induces autophagy,the role of autophagy in HBV infection,and HBV-related tumorigenesis.We further discuss the emerging roles of mi RNAs in HBV infection and how HBV affects mi RNAs biogenesis.The accumulating knowledge pertaining to autophagy and mi RNAs in HBV replication and its pathogenesis may lead to the development of novel strategies against HBV infection and HBV-related HCC tumorigenesis. | Shan-Ying Wu Sheng-Hui Lan Hsiao-Sheng Liu | 2016 | World Journal of Gastroenterology2016，22，1： | 8 |
| 7 | Identification and characterization of a novel bipartite nuclear localization signal in the hepatitis B virus polymerase显示文摘AIM:To characterize the nuclear import of hepatitis B virus(HBV)polymerase(P)and its relevance for the viral life cycle.METHODS:Sequence analysis was performed to predict functional motives within P.Phosphorylation of P was analyzed by in vitro phosphorylation.Phosphorylation site and nuclear localization signal(NLS)were destroyed by site directed mutagenesis.Functionality of the identified NLS was analyzed by confocal fluorescence microscopy and characterizing the karyopherin binding.Relevance of the structural motives for viral life cycle was studied by infection of primary Tupaia hepatocytes with HBV.RESULTS:We identified by sequence alignment and functional experiments a conserved bipartite NLS containing a casein kinaseⅡ(CKⅡ)phosphorylation site located within the terminal protein domain(TP)of the HBV polymerase.Inhibition of CKⅡimpairs the functionality of this NLS and thereby prevents the nuclear import of the polymerase.Binding of the import factor karyopherin-α2 to the polymerase depends on its CKⅡ-mediated phosphorylation of the bipartite NLS.In HBV-infected primary Tupaia hepatocytes CKⅡinhibition in the early phase(post entry phase)of the infection process prevents the establishment of the infection.CONCLUSION:Based on these data it is suggested that during HBV infection the final import of the genome complex into the nucleus is mediated by a novel bipartite NLS localized in the TP domain of HBV polymerase. | Joachim Lupberger Stephanie Schaedler Alexander Peiran Eberhard Hildt | 2013 | World Journal of Gastroenterology2013，19，44： | 8 |
| 8 | Nuclear domain 10 of the viral aspect显示文摘Nuclear domain 10(ND10) are spherical bodies distributed throughout the nucleoplasm and measuring around 0.2-1.0 μm. First observed under an electron microscope, they were originally described as dense bodies found in the nucleus. They are known by a number of other names, including Promyelocytic Leukemia bodies(PML bodies), Kremer bodies, and PML oncogenic domains. ND10 are frequently associated with Cajal bodies and cleavage bodies. It has been suggested that they play a role in regulating gene transcription. ND10 were originally characterized using human autoantisera, which recognizes Speckled Protein of 100 kD a, from patients with primary biliary cirrhosis. At the immunohistochemical level, ND10 appear as nuclear punctate structures, with 10 indicating the approximate number of dots per nucleus observed. ND10 do not colocalize with kinetochores, centromeres, sites of mR NA processing, or chromosomes. Resistance of ND10 antigens to nuclease digestion and salt extraction suggest that ND10 are associated with the nuclear matrix.They are often identified by immunofluorescent assay using specific antibodies against PML, Death domainassociated protein, nuclear dot protein(NDP55), and so on. The role of ND10 has long been the subject of investigation, with the specific connection of ND10 and viral infection having been a particular focus for almost 20 years. This review summarizes the relationship of ND10 and viral infection. Some future study directions are also discussed. | Yisel A Rivera-Molina Francisco Puerta Martínez Qiyi Tang | 2013 | World Journal of Virology2013，2，3： | 7 |
| 9 | Roles of hepatocyte nuclear factors in hepatitis B virus infection显示文摘Approximately 350 million people are estimated to be persistently infected with hepatitis B virus(HBV) worldwide. HBV maintains persistent infection by employing covalently closed circular DNA(ccc DNA), a template for all HBV RNAs. Chronic hepatitis B(CHB) patients are currently treated with nucleos(t)ide analogs such as lamivudine, adefovir, entecavir, and tenofovir. However, these treatments rarely cure CHB because they are unable to inhibit ccc DNA transcription and inhibit only a late stage in the HBV life cycle(the reverse transcription step in the nucleocapsid). Therefore, an understanding of the factors regulating ccc DNA transcription is required to stop this process. Among numerous factors, hepatocyte nuclear factors(HNFs) play the most important roles in ccc DNA transcription, especially in the generation of viral genomic RNA, a template for HBV replication. Therefore, proper control of HNF function could lead to the inhibition of HBV replication. In this review, we summarize and discuss the current understanding of the roles of HNFs in the HBV life cycle and the upstream factors that regulate HNFs. This knowledge will enable the identification of new therapeutic targets to cure CHB. | Doo Hyun Kim Hong Seok Kang Kyun-Hwan Kim | 2016 | World Journal of Gastroenterology2016，22，31： | 6 |
| 10 | Life cycle and pathogenesis of hepatitis D virus:A review显示文摘Hepatitis D virus(HDV) is a defective RNA virus which requires the help of hepatitis B virus(HBV) virus for its replication and assembly of new virions. HDV genome contains only one actively transcribed open reading frame which encodes for two isoforms of hepatitis delta antigen. Post-translational modifications of small and large delta antigens(S-HDAg and L-HDAg) involving phosphorylation and isoprenylation respectively con- fer these antigens their specific properties. S-HDAg is required for the initiation of the viral genome replica- tion, whereas L-HDAg serves as a principal inhibitor of replication and is essential for the assembly of new virion particles. Immune mediation has usually been implicated in HDV-associated liver damage. The patho- genesis of HDV mainly involves interferon-α signaling inhibition, HDV-specific T-lymphocyte activation and cytokine responses, and tumor necrosis factor-alpha and nuclear factor kappa B signaling. Due to limited protein coding capacity, HDV makes use of host cel- lular proteins to accomplish their life cycle processes, including transcription, replication, post-transcriptional and translational modifications. This intimate host- pathogen interaction significantly alters cell proteome and is associated with an augmented expression of pro-inflammatory, growth and anti-apoptotic factorswhich explains severe necroinflammation and increased cell survival and an early progression to hepatocellular carcinoma in HDV patients. The understanding of the process of viral replication, HBV-HDV interactions, and etio-pathogenesis of the severe course of HDV infection is helpful in identifying the potential therapeutic targets in the virus life cycle for the prophylaxis and treatment of HDV infection and complications. | Zaigham Abbas Rafia Afzal | 2013 | World Journal of Hepatology2013，5，12： | 6 |
| 11 | MicroRNA-135a Modulates Hepatitis C Virus Genome Replication through Downregulation of Host Antiviral Factors显示文摘Cellular microRNAs(miRNAs) have been shown to modulate HCV infection via directly acting on the viral genome or indirectly through targeting the virus-associated host factors. Recently we generated a comprehensive map of HCV–miRNA interactions through genome-wide miRNA functional screens and transcriptomics analyses. Many previously unappreciated cellular miRNAs were identified to be involved in HCV infection, including miR-135a, a human cancerrelated miRNA. In the present study, we investigated the role of miR-135a in regulating HCV life cycle and showed that it preferentially enhances viral genome replication. Bioinformatics-based integrative analyses and subsequent functional assays revealed three antiviral host factors, including receptor interacting serine/threonine kinase 2(RIPK2), myeloid differentiation primary response 88(MYD88), and C-X-C motif chemokine ligand 12(CXCL12), as bona fide targets of miR-135a. These genes have been shown to inhibit HCV infection at the RNA replication stage. Our data demonstrated that repression of key host restriction factors mediated the proviral effect of miR-135a on HCV propagation. In addition,miR-135a hepatic abundance is upregulated by HCV infection in both cultured hepatocytes and human liver, likely mediating a more favorable environment for viral replication and possibly contributing to HCV-induced liver malignancy.These results provide novel insights into HCV–host interactions and unveil molecular pathways linking miRNA biology to HCV pathogenesis. | Catherine Sodroski Brianna Lowey Laura Hertz T.Jake Liang Qisheng Li | 2019 | Virologica Sinica2019，34，2： | 5 |
| 12 | Architecture and biogenesis of plus-strand RNA virus replication factories显示文摘Plus-strand RNA virus replication occurs in tight association with cytoplasmic host cell membranes. Both, viral and cellular factors cooperatively generate distinct organelle-like structures, designated viral replication factories. This compartmentalization allows coordination of the different steps of the viral replication cycle, highly efficient genome replication and protection of the viral RNA from cellular defense mechanisms. Electron tomography studies conducted during the last couple of years revealed the three dimensional structure of numerous plus-strand RNA virus replication compartments and highlight morphological analogies between different virus families. Based on the morphology of virusinduced membrane rearrangements, we propose two separate subclasses: the invaginated vesicle/spherule type and the double membrane vesicle type. This review discusses common themes and distinct differences in the architecture of plus-strand RNA virus-induced membrane alterations and summarizes recent progress that has been made in understanding the complex interplay between viral and co-opted cellular factors in biogenesis and maintenance of plus-strand RNA virus replication factories. | David Paul Ralf Bartenschlager | 2013 | World Journal of Virology2013，2，2： | 4 |
| 13 | Qualitative, quantitative and structural analysis of non-coding regions of classical swine fever virus genome显示文摘Classical swine fever virus (CSFV) is the pathogen of the swine fever. Understanding of the replication and expression of its genome is the basis for research of the pathogenicity for CSFV and development of antiviral drug. The noncoding regions (NCRs) of CSFV are the main regulatory regions for replication and expression. Qualitative, quantitative and structural analysis of 3’ NCRs and 5’ NCRs was done in order to locate the regulatory region in the NCRs and to character the NCRs. The sites, conserved sequences and structural elements related to the initiation of replication and expression were extracted from 17 3’ NCRs and 56 5’ NCRs. Those cis-elements may be initial recognition sites for replication, binding sites for transcription factors of host cell and interacting sites for initiation of protein synthesis, based on which a mechanism for the replication and expression of CSFV was brought forth. This research offers the direction for further experiment and lays down a basis for the research on | XIAO Ming ZHU Zhizhan ZHANG Chuyu | 2001 | Chinese Science Bulletin2001，46，15： | 3 |
| 14 | Hepatitis delta virus: A fascinating and neglected pathogen显示文摘Hepatitis delta virus(HDV) is the etiologic agent of the most severe form of virus hepatitis in humans. Sharing some structural and functional properties with plant viroids, the HDV RNA contains a single open reading frame coding for the only virus protein, the Delta antigen. A number of unique features, including ribozyme activity, RNA editing, rolling-circle RNA replication, and redirection for a RNA template of host DNA-dependent RNA polymerase Ⅱ, make this small pathogen an excellent model to study virus-cell interactions and RNA biology. Treatment options for chronic hepatitis Delta are scarce and ineffective. The disease burden is perhaps largely underestimated making the search for new, specific drugs, targets, and treatment strategies an important public health challenge. In this review we address the main features of virus structure, replication, and interaction with the host. Virus pathogenicity and current treatment options are discussed in the light of recent developments. | Celso Cunha Jo?o Paulo Tavanez Severin Gudima | 2015 | World Journal of Virology2015，4，4： | 3 |
| 15 | Host restriction factors for hepatitis C virus显示文摘Host-hepatitis C virus(HCV) interactions have both informed fundamental concepts of viral replication and pathogenesis and provided novel insights into host cell biology. These findings are illustrated by the recent discovery of host-encoded factors that restrict HCV infection. In this review, we briefly discuss these restriction factors in different steps of HCV infection. In each case, we discuss how these restriction factors were identified, the mechanisms by which they inhibit HCV infection and their potential contribution to viral pathogenesis. | li-ya zhou lei-liang zhang | 2016 | World Journal of Gastroenterology2016，22，4： | 2 |
| 16 | Hepatitis c virus markers in infection by hepatitis c virus: In the era of directly acting antivirals显示文摘About 130-170 million people are infected with the hepatitis C virus(HCV) worldwide and more than 350000 people die each year of HCV-related liver diseases. The combination of pegylated interferon(Peg-IFN) and ribavirin(RBV) was recommended as the treatment of choice for chronic hepatitis C for nearly a decade. In 2011 the directly acting antivirals(DAA) HCV NS3/4A protease inhibitors,telaprevir and boceprevir,were approved to treat HCV-genotype-1 infection,each in triple combination with Peg-IFN and RBV. These treatments allowed higher rates of SVR than the double Peg-IFN + RBV,but the low tolerability and high pill burden of these triple regimes were responsible for reduced adherence and early treatment discontinuation. The second and third wave DAAs introduced in 2013-2014 enhanced the efficacy and tolerability of anti-HCV treatment. Consequently,the traditional indicators for disease management and predictors of treatment response should be revised in light of these new therapeutic options. This review article will focus on the use of the markers of HCV infection and replication,of laboratory and instrumental data to define the stage of the disease and of predictors,if any,of response to therapy in the DAA era. The article is addressed particularly to physicians who have patients with hepatitis C in care in their everyday clinical practice. | Nicola Coppola Mariantonietta Pisaturo Rosa Zampino Margherita Macera Caterina Sagnelli Evangelista Sagnelli | 2015 | World Journal of Gastroenterology2015，21，38： | 2 |
| 17 | Oxymatrine Inhibits Bocavirus MVC Replication, Reduces Viral Gene Expression and Decreases Apoptosis Induced by Viral Infection显示文摘Oxymatrine(OMT), as the main active component of Sophoraflavescens, exhibits a variety of pharmacological properties,including anti-oxidative, anti-inflammatory, anti-tumor, and anti-viral activities, and currently is extensively employed to treat viral hepatitis; however, its effects on parvovirus infection have yet to be reported. In the present study, we investigated the effects of OMT on cell viability, virus DNA replication, viral gene expression, cell cycle, and apoptosis in Walter Reed canine cells/3873 D infected with minute virus of canines(MVC). OMT, at concentrations below 4 mmol/L(no cellular toxicity), was found to inhibit MVC DNA replication and reduce viral gene expression at both mRNA and protein levels, which was associated with the inhibition of cell cycle S-phase arrest in early-stage of MVC infection.Furthermore, OMT significantly increased cell viability, decreased MVC-infected cell apoptosis, and reduced the expression of activated caspase 3. Our results suggest that OMT has potential application in combating parvovirus infection. | Yanqin Ding Na Li Jinhan Sun Linran Zhang Jianhui Guo Xueqi Hao Yuning Sun | 2019 | Virologica Sinica2019，34，1： | 2 |
| 18 | Post-translational modifications of hepatitis C viral proteins and their biological significance显示文摘Replication of hepatitis C virus(HCV)depends on the interaction of viral proteins with various host cellular proteins and signalling pathways.Similar to cellular proteins,post-translational modifications(PTMs)of HCV proteins are essential for proper protein function and regulation,thus,directly affecting viral life cycle and the generation of infectious virus particles.Cleavage of the HCV polyprotein by cellular and viral proteases into more than 10 proteins represents an early protein modification step after translation of the HCV positivestranded RNA genome.The key modifications include the regulated intramembranous proteolytic cleavage of core protein,disulfide bond formation of core,glycosylation of HCV envelope proteins E1 and E2,methylation of nonstructural protein 3(NS3),biotinylation of NS4A,ubiquitination of NS5B and phosphorylation of core and NS5B.Other modifications like ubiquitination of core and palmitoylation of core and NS4B proteins have been reported as well.For some modifications such as phosphorylation of NS3 and NS5A and acetylation of NS3,we have limited understanding of their effects on HCV replication and pathogenesis while the impact of other modifications is far from clear.In this review,we summarize the available information on PTMs of HCV proteins and discuss their relevance to HCV replication and pathogenesis. | Jana Hundt Zhubing Li Qiang Liu | 2013 | World Journal of Gastroenterology2013，19，47： | 2 |
| 19 | Porcine Parvovirus Inducing Autophagy to Benefit Its Replication显示文摘Porcine parvovirus(PPV) is one of the major causes of reproductive failure in pigs, which poses a great threat to the pig breeding industry and results in tremendous economic losses worldwide. Autophagy is the biological process of cell self-defense and self-protection. Despite many viruses can cause cell autophagy, when they enter cell or copied, the relationship between autophagy and PPV infection has not been reported. In this study, impact of autophagy after swine testicular(ST) cells infected by PPV was studied. Autophagy was demonstrated by the effective replication of PPV through transmission electron microscopy, immunofluorescence and western blot analysis. Moreover, autophagy was confirmed to benefit PPV replication by real-time fluorescence quantitative PCR and determination of median tissue culture infective dose(TCID_(50)). For the first time, the complex interaction between PPV infection and autophagy was explored in this study. It indicated that PPV could induce autophagy in ST cells, which in turn facilitated its own replication, which might be one of the mechanisms of the virus infection. These findings could facilitate the study of the pathogenesis of PPV infection and provide new insight into the development of effective therapeutic strategies. | Zhang Yue Li Xiao-xue Zhong Ming Chen Hui-jie Huang Xiao-dan Bai Yun-yun Cong Ying-ying Zhang Rui-li Li Guang-xing | 2018 | Journal of Northeast Agricultural University(English Edition)2018，25，4： | 2 |
| 20 | Histone Deacetylase 3 Inhibitor Suppresses Hepatitis C Virus Replication by Regulating Apo-A1 and LEAP-1 Expression显示文摘Histone deacetylase (HDAC) inhibitors show clinical promise for the treatment of cancers, including hepatocellular carcinoma (HCC). In this study, we investigated the effect of HDAC inhibitor treatment on hepatitis C virus (HCV)replication in Huh7 human liver cells and in a mouse model of HCV infection. Viral replication was markedly suppressed by the HDAC3 inhibitor at concentrations below 1 mmol/L, with no cellular toxicity. This was accompanied by upregulation of liver-expressed antimicrobial peptide 1 (LEAP-1) and downregulation of apolipoprotein-A1 (Apo-A1), as determined by microarray and quantitative RT-PCR analyses. Moreover, HDAC3 was found to modulate the binding of CCAAT-enhancer-binding protein a (C/EBPa), hypoxia-inducible factor 1 a (HIF1 a), and signal transducer and activator of transcription 3 (STAT3) to the LEAP-1 promoter. HDAC3 inhibitor treatment also blocked HCV replication in a mouse model of HCV infection. These results indicate that epigenetic therapy with HDAC3 inhibitor may be a potential treatment for diseases associated with HCV infection such as HCC. | Yuan Zhou Qian Wang Qi Yang Jielin Tang Chonghui Xu Dongwei Gai Xinwen Chen Jizheng Chen | 2018 | Virologica Sinica2018，33，5： | 2 |
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