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Hepatitis Virus Infection and Molecular Research 2018
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Hepatitis Virus Infection and Molecular Research 2018

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 September 2018) | Viewed by 41482

Special Issue Editors

Dr. Tatsuo Kanda

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
Interests: viral hepatitis; hepatocellular carcinoma, innate immunity; unfolded protein response
Special Issues, Collections and Topics in MDPI journals
Assist. Prof. Kazushige Nirei

E-Mail
Guest Editor
Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
Interests: viral hepatitis; hepatocellular carcinoma; fatty liver; alcoholic liver diseases

Special Issue Information

Dear Colleagues,

Welcome to this Special Issue, “Hepatitis Virus Infection and Molecular Research 2018”, of the International Journal of Molecular Sciences. Recently, interferon-free treatment against hepatitis C virus (HCV) has been available, and its efficacy is higher, with less adverse events and a shorter duration. although there are several problems, such as the occurrence of hepatocellular carcinoma (HCC) after sustained virological response (SVR), reactivation of hepatitis B virus (HBV) and drug-resistance-associated substitutions (RASs). New cancer immune therapies, such as the blockers of immune checkpoints, also have effective efficacies and cause liver injuries. This Special Issue will present the recent findings related to viral hepatitis, other liver diseases and liver-related gastrointestinal diseases. Original research and review articles on all topics in this area are invited. We also have great interest of molecular research, such as resistance-mutation and host responses. It is our greatest pleasure to invite research scientists and clinicians from all relevant fields to submit their articles for this Special Issue. Please accept my special thanks for choosing to publish in the International Journal of Molecular Sciences. We are looking forward to your submissions for this highly-important Special Issue.

Assoc. Prof. Tatsuo Kanda
Assist. Prof. Kazushige Nirei
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • viral hepatitis
  • DAA
  • NASH
  • drug-induced liver injury
  • HCC
  • cirrhosis

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Related Special Issues

Published Papers (6 papers)

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Research

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13 pages, 4024 KiB  
Article
Cytokine-Modulated Natural Killer Cells Differentially Regulate the Activity of the Hepatitis C Virus
by Yoo Jin Cho, Hwan Hee Lee, Hyojeung Kang and Hyosun Cho
Int. J. Mol. Sci. 2018, 19(9), 2771; https://doi.org/10.3390/ijms19092771 - 14 Sep 2018
Cited by 4 | Viewed by 3827
Abstract
HCV genotype 2a strain JFH-1 replicates and produces viral particles efficiently in human hepatocellular carcinoma (huh) 7.5 cells, which provide a stable in vitro cell infection system for the hepatitis C virus (HCVcc system). Natural killer (NK) cells are large lymphoid cells that [...] Read more.
HCV genotype 2a strain JFH-1 replicates and produces viral particles efficiently in human hepatocellular carcinoma (huh) 7.5 cells, which provide a stable in vitro cell infection system for the hepatitis C virus (HCVcc system). Natural killer (NK) cells are large lymphoid cells that recognize and kill virus-infected cells. In this study, we investigated the interaction between NK cells and the HCVcc system. IL-10 is a typical immune regulatory cytokine that is produced mostly by NK cells and macrophages. IL-21 is one of the main cytokines that stimulate the activation of NK cells. First, we used anti-IL-10 to neutralize IL-10 in a coculture of NK cells and HCVcc. Anti-IL-10 treatment increased the maturation of NK cells by enhancing the frequency of the CD56+dim population in NK-92 cells. However, with anti-IL-10 treatment of NK cells in coculture with J6/JFH-1-huh 7.5 cells, there was a significant decrease in the expression of STAT1 and STAT5 proteins in NK-92 cells and an increase in the HCV Core and NS3 proteins. In addition, rIL-21 treatment increased the frequency of the CD56+dim population in NK-92 cells, Also, there was a dramatic increase in the expression of STAT1 and STAT5 proteins in rIL-21 pre-stimulated NK cells and a decrease in the expression of HCV Core protein in coculture with J6/JFH-1-huh 7.5 cells. In summary, we found that the functional activation of NK cells can be modulated by anti-IL-10 or rIL-21, which controls the expression of HCV proteins as well as HCV RNA replication. Full article
(This article belongs to the Special Issue Hepatitis Virus Infection and Molecular Research 2018)
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16 pages, 2796 KiB  
Article
Serum miRNAs Predicting Sustained HBs Antigen Reduction 48 Weeks after Pegylated Interferon Therapy in HBe Antigen-Negative Patients
by Koji Fujita, Shima Mimura, Hisakazu Iwama, Mai Nakahara, Kyoko Oura, Tomoko Tadokoro, Takako Nomura, Joji Tani, Hirohito Yoneyama, Asahiro Morishita, Makoto Oryu, Takashi Himoto, Hironori Nishitsuji, Kunitada Shimotohno, Masao Omata and Tsutomu Masaki
Int. J. Mol. Sci. 2018, 19(7), 1940; https://doi.org/10.3390/ijms19071940 - 2 Jul 2018
Cited by 9 | Viewed by 4168
Abstract
The therapeutic goal for hepatitis B virus (HBV) infection is HBs antigen (HBsAg) seroclearance, which is achieved through 48-week pegylated interferon (Peg-IFN) therapy. This study aimed to identify predictive biomarkers for sustained HBsAg reduction by analyzing serum microRNAs. Twenty-two consecutive chronic HBV infection [...] Read more.
The therapeutic goal for hepatitis B virus (HBV) infection is HBs antigen (HBsAg) seroclearance, which is achieved through 48-week pegylated interferon (Peg-IFN) therapy. This study aimed to identify predictive biomarkers for sustained HBsAg reduction by analyzing serum microRNAs. Twenty-two consecutive chronic HBV infection patients negative for HBe antigen (HBeAg) with HBV-DNA levels <5 log copies/mL, alanine aminotransferase (ALT) <100 U/L, and compensated liver functions, were enrolled. The patients were subcutaneously injected with Peg-IFNα-2a weekly for 48 weeks (treatment period), followed by the 48-week observation period. HBsAg 1-log drop relative to baseline levels recorded at the end of the observation period was considered effective. Sera were obtained at weeks 0 and 24 during the treatment period analyzed for microRNAs. The microRNA (miRNA) antiviral activity was evaluated in vitro using Huh7/sodium taurocholate cotransporting polypeptide (NTCP) cells. As a result, six patients achieved the HBsAg 1-log drop after the observation periods. Comparison of serum microRNA levels demonstrated that high miR-6126 levels at week 24 predicted HBsAg 1-log drop. Furthermore, miR-6126 reduced HBsAg in culture medium supernatants and intracellular HBV-DNA quantities in Huh7/NTCP cells. In conclusion, high serum miR-6126 levels during Peg-IFN therapy predicted the HBsAg 1-log drop 48 weeks after the completion of therapy. In vitro assays revealed that miR-6126 was able to suppress HBsAg production and HBV replication. Full article
(This article belongs to the Special Issue Hepatitis Virus Infection and Molecular Research 2018)
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Review

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18 pages, 584 KiB  
Review
Exosomes and Hepatocellular Carcinoma: From Bench to Bedside
by Reina Sasaki, Tatsuo Kanda, Osamu Yokosuka, Naoya Kato, Shunichi Matsuoka and Mitsuhiko Moriyama
Int. J. Mol. Sci. 2019, 20(6), 1406; https://doi.org/10.3390/ijms20061406 - 20 Mar 2019
Cited by 98 | Viewed by 9996
Abstract
As hepatocellular carcinoma (HCC) usually occurs in the background of cirrhosis, which is an end-stage form of liver diseases, treatment options for advanced HCC are limited, due to poor liver function. The exosome is a nanometer-sized membrane vesicle structure that originates from the [...] Read more.
As hepatocellular carcinoma (HCC) usually occurs in the background of cirrhosis, which is an end-stage form of liver diseases, treatment options for advanced HCC are limited, due to poor liver function. The exosome is a nanometer-sized membrane vesicle structure that originates from the endosome. Exosome-mediated transfer of proteins, DNAs and various forms of RNA, such as microRNA (miRNA), long noncoding RNA (lncRNA) and messenger RNA (mRNA), contributes to the development of HCC. Exosomes mediate communication between both HCC and non-HCC cells involved in tumor-associated cells, and several molecules are implicated in exosome biogenesis. Exosomes may be potential diagnostic biomarkers for early-stage HCC. Exosomal proteins, miRNAs and lncRNAs could provide new biomarker information for HCC. Exosomes are also potential targets for the treatment of HCC. Notably, further efforts are required in this field. We reviewed recent literature and demonstrated how useful exosomes are for diagnosing patients with HCC, treating patients with HCC and predicting the prognosis of HCC patients. Full article
(This article belongs to the Special Issue Hepatitis Virus Infection and Molecular Research 2018)
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16 pages, 659 KiB  
Review
Molecular Mechanisms Involved in HCC Recurrence after Direct-Acting Antiviral Therapy
by Rosanna Villani, Gianluigi Vendemiale and Gaetano Serviddio
Int. J. Mol. Sci. 2019, 20(1), 49; https://doi.org/10.3390/ijms20010049 - 22 Dec 2018
Cited by 42 | Viewed by 5382
Abstract
Chronic hepatitis C is associated with a high risk of developing hepatocellular carcinoma (HCC) because of a direct effect of the Hepatitis C Virus (HCV) proteins and an indirect oncogenic effect of chronic inflammation and impaired immune response. The treatment of chronic hepatitis [...] Read more.
Chronic hepatitis C is associated with a high risk of developing hepatocellular carcinoma (HCC) because of a direct effect of the Hepatitis C Virus (HCV) proteins and an indirect oncogenic effect of chronic inflammation and impaired immune response. The treatment of chronic hepatitis C markedly reduces all-cause mortality; in fact, interferon-based treatment has shown a reduction of HCC incidence of more than 70%. The recent introduction of the highly effective direct-acting antivirals (DAAs) has completely changed the scenario of chronic hepatitis C (CHC) with rates of HCV cure over 90%. However, an unexpectedly high incidence of HCC recurrence was observed in patients after DAA treatment (27% versus 0.4–2% in patients who received interferon treatment). The mechanism that underlies the high rate of tumor relapse is currently unknown and is one of the main issues in hepatology. We reviewed the possible mechanisms involved in HCC recurrence after DAA treatment. Full article
(This article belongs to the Special Issue Hepatitis Virus Infection and Molecular Research 2018)
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62 pages, 1311 KiB  
Review
The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions
by Po-Yuan Ke
Int. J. Mol. Sci. 2018, 19(12), 3940; https://doi.org/10.3390/ijms19123940 - 7 Dec 2018
Cited by 48 | Viewed by 8051
Abstract
Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis. Flavivirus infections underlie multiple human diseases and thus exert an immense burden on public health worldwide. Mounting evidence [...] Read more.
Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis. Flavivirus infections underlie multiple human diseases and thus exert an immense burden on public health worldwide. Mounting evidence indicates that host autophagy is subverted to modulate the life cycles of flaviviruses, such as hepatitis C virus, dengue virus, Japanese encephalitis virus, West Nile virus and Zika virus. The diverse interplay between autophagy and flavivirus infection not only regulates viral growth in host cells but also counteracts host stress responses induced by viral infection. In this review, we summarize the current knowledge on the role of autophagy in the flavivirus life cycle. We also discuss the impacts of virus-induced autophagy on the pathogeneses of flavivirus-associated diseases and the potential use of autophagy as a therapeutic target for curing flavivirus infections and related human diseases. Full article
(This article belongs to the Special Issue Hepatitis Virus Infection and Molecular Research 2018)
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Graphical abstract

12 pages, 1899 KiB  
Review
Wnt/β-Catenin Signaling as a Potential Target for the Treatment of Liver Cirrhosis Using Antifibrotic Drugs
by Koji Nishikawa, Yosuke Osawa and Kiminori Kimura
Int. J. Mol. Sci. 2018, 19(10), 3103; https://doi.org/10.3390/ijms19103103 - 10 Oct 2018
Cited by 96 | Viewed by 9298
Abstract
Cirrhosis is a form of liver fibrosis resulting from chronic hepatitis and caused by various liver diseases, including viral hepatitis, alcoholic liver damage, nonalcoholic steatohepatitis, and autoimmune liver disease. Cirrhosis leads to various complications, resulting in poor prognoses; therefore, it is important to [...] Read more.
Cirrhosis is a form of liver fibrosis resulting from chronic hepatitis and caused by various liver diseases, including viral hepatitis, alcoholic liver damage, nonalcoholic steatohepatitis, and autoimmune liver disease. Cirrhosis leads to various complications, resulting in poor prognoses; therefore, it is important to develop novel antifibrotic therapies to counter liver cirrhosis. Wnt/β-catenin signaling is associated with the development of tissue fibrosis, making it a major therapeutic target for treating liver fibrosis. In this review, we present recent insights into the correlation between Wnt/β-catenin signaling and liver fibrosis and discuss the antifibrotic effects of the cAMP-response element binding protein/β-catenin inhibitor PRI-724. Full article
(This article belongs to the Special Issue Hepatitis Virus Infection and Molecular Research 2018)
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