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Hepatitis C Virus – Molecular Biology, Disease and Treatment (Section 1) 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 4571

Special Issue Editor


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Guest Editor
Institute of Biochemistry, Medical Faculty, Justus-Liebig-University, Friedrichstrasse 24, 35392 Giessen, Germany
Interests: translation; replication; miR-122; cellular gene regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Hepatitis C Virus (HCV) preferentially replicates in the human liver and frequently causes chronic infection, often leading to cirrhosis and liver cancer. HCV is an enveloped virus classified in the genus Hepacivirus in the family Flaviviridae and has a single-stranded RNA genome of positive orientation. Both hepatocyte surface receptors and the liver-specific microRNA-122 contribute to HCV hepatotropism, and the HCV life cycle is closely linked to the lipid metabolism of hepatocytes. The HCV RNA genome is translated by virtue of an internal ribosome entry site. After a pilot round of genome translation, replication factories called “membranous webs” are formed in the cytoplasm, which are the sites of genome replication. During RNA genome synthesis, the error-prone viral replicase provides a high mutation rate in the genome, allowing the virus to easily escape from host immune responses and treatment. Moreover, viral proteins interfere with the immune response in order to establish an ongoing chronic infection “under the radar” of the host, a strategy to ensure its spread among host individuals not aware of the infection, even at the time of effective anti-viral treatment. While such treatment does not protect against repeated infection, vaccines are under development.

In this Special Issue, we would like to provide comprehensive overviews over important aspects of the molecular events in the HCV life cycle, disease development and the current state of HCV treatment.

Potential topics include, without being limited to, the following:

  • Introduction to Hepatitis C Virus
  • HCV phylogeny and molecular evolution
  • Cell culture model systems used in HCV research
  • Animal model systems used in HCV research
  • HCV model systems
  • HCV protein structure
  • Entry receptors and events
  • Regulation of HCV translation
  • The structure of viral replication complexes
  • Molecular biology of viral RNA replication, cis-signals and protein factors
  • Long-range RNA-RNA interactions and switches in the viral life cycle
  • Functions of the liver-specific microRNA-122 in the HCV replication cycle
  • Non-coding RNAs in HCV replication (including lncRNAs)
  • cis-Determinants of viral RNA encapsidation during assembly
  • Virus assembly and release, lipid metabolism
  • Innate immune responses to HCV infection and viral counter-measures
  • Adaptive immune response and viral escape
  • Pathogenesis, cirrhosis and Hepatocellular Carcinoma (HCC)
  • Clinical HCV treatment: state of the art, problems and perspectives
  • Vaccine development

Accepted original research articles will be published in the joint Special Issue in IJMS (https://www.mdpi.com/journal/ijms/special_issues/Hepatitis_C_Virus_Section_2).

Prof. Dr. Michael Niepmann
Guest Editor

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

  • entry receptors
  • HCV genome model systems
  • cell culture systems
  • animal models
  • translation
  • replication
  • lipid metabolism
  • assembly
  • immune response
  • Hepatocellular Carcinoma (HCC)
  • Direct-acting antivirals (DAAs)
  • treatment
  • escape mutants

Published Papers (2 papers)

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Research

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20 pages, 3942 KiB  
Article
Longitudinal Assessment of Multiple Immunological and Inflammatory Parameters during Successful DAA Therapy in HCV Monoinfected and HIV/HCV Coinfected Subjects
by Paola Zuccalà, Tiziana Latronico, Raffaella Marocco, Stefano Savinelli, Serena Vita, Fabio Mengoni, Tiziana Tieghi, Cosmo Borgo, Blerta Kertusha, Anna Carraro, Gabriella D’Ettorre, Vincenzo Vullo, Claudio Maria Mastroianni, Grazia Maria Liuzzi and Miriam Lichtner
Int. J. Mol. Sci. 2022, 23(19), 11936; https://doi.org/10.3390/ijms231911936 - 8 Oct 2022
Cited by 4 | Viewed by 1791
Abstract
In the direct-acting antiviral (DAA) era, it is important to understand the immunological changes after HCV eradication in HCV monoinfected (mHCV) and in HIV/HCV coinfected (HIV/HCV) patients. In this study, we analyzed sub-populations of monocytes, dendritic cells (DCs), T-lymphocytes and inflammatory biomarkers following [...] Read more.
In the direct-acting antiviral (DAA) era, it is important to understand the immunological changes after HCV eradication in HCV monoinfected (mHCV) and in HIV/HCV coinfected (HIV/HCV) patients. In this study, we analyzed sub-populations of monocytes, dendritic cells (DCs), T-lymphocytes and inflammatory biomarkers following initiation of DAA in 15 mHCV and 16 HIV/HCV patients on effective antiretroviral therapy at baseline and after sustained virological response at 12 weeks (SVR12). Fifteen age- and sex-matched healthy donors (HD) were enrolled as a control group. Activated CD4+ and CD8+ T-lymphocytes, mDCs, pDCs, MDC8 and classical, non-classical and intermediate monocytes were detected using flow cytometry. IP-10, sCD163 and sCD14 were assessed by ELISA while matrix metalloproteinase-2 (MMP-2) was measured by zymography. At baseline, increased levels of IP-10, sCD163 and MMP-2 were found in both HIV/HCV and mHCV patients compared to HD, whereas sCD14 increased only in HIV/HCV patients. After therapy, IP-10, sCD163 and sCD14 decreased, whereas MMP-2 persistently elevated. At baseline, activated CD8+ T-cells were high in HIV/HCV and mHCV patients compared to HD, with a decrease at SVR12 only in HIV/HCV patients. Activated CD4+ T-cells were higher in HIV/HCV patients without modification after DAAs therapy. These results suggest complex interactions between both viruses and the immune system, which are only partially reversed by DAA treatment. Full article
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Review

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17 pages, 897 KiB  
Review
Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences
by Zakaria Boulahtouf, Alessia Virzì, Thomas F. Baumert, Eloi R. Verrier and Joachim Lupberger
Int. J. Mol. Sci. 2022, 23(5), 2787; https://doi.org/10.3390/ijms23052787 - 3 Mar 2022
Cited by 4 | Viewed by 2350
Abstract
Chronic viral hepatitis is a main cause of liver disease and hepatocellular carcinoma. There are striking similarities in the pathological impact of hepatitis B, C, and D, although these diseases are caused by very different viruses. Paired with the conventional study of protein–host [...] Read more.
Chronic viral hepatitis is a main cause of liver disease and hepatocellular carcinoma. There are striking similarities in the pathological impact of hepatitis B, C, and D, although these diseases are caused by very different viruses. Paired with the conventional study of protein–host interactions, the rapid technological development of -omics and bioinformatics has allowed highlighting the important role of signaling networks in viral pathogenesis. In this review, we provide an integrated look on the three major viruses associated with chronic viral hepatitis in patients, summarizing similarities and differences in virus-induced cellular signaling relevant to the viral life cycles and liver disease progression. Full article
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