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Viruses
Special Issues
Cellular Factors in HBV and HDV Replication and Pathogenesis
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Cellular Factors in HBV and HDV Replication and Pathogenesis

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 6961

Special Issue Editors

Dr. Bingqian Qu

E-Mail Website
Guest Editor
Department of Veterinary Medicine, Paul Ehrlich Institute, 63225 Langen, Germany
Interests: SARS-CoV-2; variant of concern; vaccine evaluation
Special Issues, Collections and Topics in MDPI journals
Dr. Chunkyu Ko

E-Mail Website
Guest Editor
Infectious Diseases Therapeutic Research Center, Korea Research Institute of Chemical Technology (KRICT), Daejeon 34114, Korea
Interests: hepatitis B virus; SARS-CoV-2; antivirals

Special Issue Information

Dear Colleagues,

The World Health Organization has called for the elimination of viral hepatitis by 2030, aiming at a 65% reduction in mortality and a 90% reduction in incidence compared to the baseline in 2015. Viral hepatitis, in most cases, is caused by five hepatitis viruses A, B, C, D and E, but only hepatitis B/D and C viruses lead to chronicity. Since hepatitis C virus can be cured with the treatment of direct-acting antivirals, a particular focus on hepatitis B virus (HBV) and hepatitis D virus (HDV) affecting 296 million (in 2019) and 15-20 million people, respectively, is necessary.

Replication of both viruses requires obligatory cellular factors in the host machinery. Cellular factors that have been identified play cooperative and restrictive roles in HBV replication. However, those in the steps of e.g., nuclear import of nucleocapsids, formation and transcription of covalently closed circular DNA, are largely uncharacterized. HDV is a defective RNA virus with a viroid-like RNA genome for replication. It also requires compulsory HBV envelope proteins in the same cell for virion assembly. Both HBV and HDV share some factors in their replication and pathogenesis, but each of them hijacks a number of virus-specific factors.

Ten years since the discovery of the functional HBV and HDV receptor NTCP, this is an exciting opportunity to further promote HBV and HDV research. This Special Issue aims to update recent advances in (I) novel cellular factors (e.g., proteins, RNA), (II) the new role of previously reported factors in HBV and HDV replication and pathogenesis, and (III) host determinants allowing better in vitro and in vivo infection models.

Dr. Bingqian Qu
Dr. Chunkyu Ko
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. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • hepatitis B virus
  • hepatitis D virus
  • chronic hepatitis
  • hepatocellular carcinoma
  • host dependency factor
  • host restriction factor
  • HBV/HDV research model

Published Papers (3 papers)

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Review

34 pages, 6236 KiB  
Review
Cellular Factors Involved in the Hepatitis D Virus Life Cycle
by Keerthihan Thiyagarajah, Michael Basic and Eberhard Hildt
Viruses 2023, 15(8), 1687; https://doi.org/10.3390/v15081687 - 03 Aug 2023
Viewed by 2676
Abstract
Hepatitis D virus (HDV) is a defective RNA virus with a negative-strand RNA genome encompassing less than 1700 nucleotides. The HDV genome encodes only for one protein, the hepatitis delta antigen (HDAg), which exists in two forms acting as nucleoproteins. HDV depends on [...] Read more.
Hepatitis D virus (HDV) is a defective RNA virus with a negative-strand RNA genome encompassing less than 1700 nucleotides. The HDV genome encodes only for one protein, the hepatitis delta antigen (HDAg), which exists in two forms acting as nucleoproteins. HDV depends on the envelope proteins of the hepatitis B virus as a helper virus for packaging its ribonucleoprotein complex (RNP). HDV is considered the causative agent for the most severe form of viral hepatitis leading to liver fibrosis/cirrhosis and hepatocellular carcinoma. Many steps of the life cycle of HDV are still enigmatic. This review gives an overview of the complete life cycle of HDV and identifies gaps in knowledge. The focus is on the description of cellular factors being involved in the life cycle of HDV and the deregulation of cellular pathways by HDV with respect to their relevance for viral replication, morphogenesis and HDV-associated pathogenesis. Moreover, recent progress in antiviral strategies targeting cellular structures is summarized in this article. Full article
(This article belongs to the Special Issue Cellular Factors in HBV and HDV Replication and Pathogenesis)
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11 pages, 273 KiB  
Review
The Role of Antiviral Prophylaxis in Preventing HBV and HDV Recurrence in the Setting of Liver Transplantation
by Sara Battistella, Alberto Zanetto, Martina Gambato, Giacomo Germani, Marco Senzolo, Patrizia Burra and Francesco Paolo Russo
Viruses 2023, 15(5), 1037; https://doi.org/10.3390/v15051037 - 23 Apr 2023
Cited by 1 | Viewed by 2032
Abstract
Hepatitis B virus (HBV) is a prevalent underlying disease, leading to liver transplantation (LT) for both decompensated cirrhosis and hepatocellular carcinoma (HCC). The hepatitis delta virus (HDV) affects approximately 5–10% of HBsAg carriers, accelerating the progression of liver injury and HCC. The initial [...] Read more.
Hepatitis B virus (HBV) is a prevalent underlying disease, leading to liver transplantation (LT) for both decompensated cirrhosis and hepatocellular carcinoma (HCC). The hepatitis delta virus (HDV) affects approximately 5–10% of HBsAg carriers, accelerating the progression of liver injury and HCC. The initial introduction of HBV immunoglobulins (HBIG), and then of nucleos(t)ide analogues (NUCs), considerably improved the survival of HBV/HDV patients post-transplantation, as they helped prevent re-infection of the graft and recurrence of liver disease. Combination therapy with HBIG and NUCs is the primary post-transplant prophylaxis strategy in patients transplanted for HBV- and HDV-related liver disease. However, monotherapy with high-barrier NUCs, such as entecavir and tenofovir, is safe and also effective in some individuals who are at low risk of HBV reactivation. To address the problems of organ shortage, last-generation NUCs have facilitated the use of anti-HBc and HBsAg-positive grafts to meet the ever-increasing demand for grafts. Full article
(This article belongs to the Special Issue Cellular Factors in HBV and HDV Replication and Pathogenesis)
12 pages, 944 KiB  
Review
PPIases Par14/Par17 Affect HBV Replication in Multiple Ways
by Kyongmin Kim
Viruses 2023, 15(2), 457; https://doi.org/10.3390/v15020457 - 06 Feb 2023
Cited by 2 | Viewed by 1262
Abstract
Human parvulin 14 (Par14) and parvulin 17 (Par17) are peptidyl-prolyl cis/trans isomerases that upregulate hepatitis B virus (HBV) replication by binding to the conserved 133Arg-Pro134 (RP) motif of HBc and core particles, and 19RP20-28RP29 motifs [...] Read more.
Human parvulin 14 (Par14) and parvulin 17 (Par17) are peptidyl-prolyl cis/trans isomerases that upregulate hepatitis B virus (HBV) replication by binding to the conserved 133Arg-Pro134 (RP) motif of HBc and core particles, and 19RP20-28RP29 motifs of HBx. In the absence of HBx, Par14/Par17 have no effect on HBV replication. Interaction with Par14/Par17 enhances the stability of HBx, core particles, and HBc. Par14/Par17 binds outside and inside core particles and is involved in HBc dimer–dimer interaction to facilitate core particle assembly. Although HBc RP motif is important for HBV replication, R133 residue is solely important for its interaction with Par14/Par17. Interaction of Par14 and Par17 with HBx involves two substrate-binding residues, Glu46/Asp74 (E46/D74) and E71/D99, respectively, and promotes HBx translocation to the nucleus and mitochondria. In the presence of HBx, Par14/Par17 are efficiently recruited to cccDNA and promote transcriptional activation via specific DNA-binding residues Ser19/44 (S19/44). S19 and E46/D74 of Par14, and S44 and E71/D99 of Par17, are also involved in the recruitment of HBc onto cccDNA. Par14/Par17 upregulate HBV replication via various effects that are mediated in part through the HBx–Par14/Par17–cccDNA complex and triple HBc, Par14/Par17, and cccDNA interactions in the nucleus, as well as via core particle-Par14/Par17 interactions in the cytoplasm. Full article
(This article belongs to the Special Issue Cellular Factors in HBV and HDV Replication and Pathogenesis)
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