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A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (24 December 2021) | Viewed by 53100

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Prof. Dr. Stephan Urban

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Department of Infectious Diseases, Molecular Virology (Translational Virology), Heidelberg University, 69120 Heidelberg, Germany
Interests: hepatitis B and hepatitis D virus–host interactions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since its discovery in 1977, the human Hepatitis Delta Virus (HDV) has occupied a unique position among all known animal viruses. HDV is the smallest known circular single-stranded animal RNA virus, causes the most severe form of viral hepatitis, and depends on its helper, the human Hepatitis B virus (HBV), to provide the envelope proteins for dissemination and hepatocyte-specific entry. However, HDV replication proceeds differently from HBV replication and resembles in many respects the host-dependent rolling circle amplification of RNA genomes used by plant viroids. Although at least 15–25 million people worldwide are affected, the public’s recognition of the global medical problems caused by HDV remains poor. In recent years, basic and clinical research on Hepatitis D Virus has led to: (i) the discovery of the HBV/HDV receptor, which led to the development of novel cell culture systems for studying HDV replication, HBV dependency, and virus–host interactions in more detail and under more authentic conditions; (ii) new insights into the innate and adaptive immune reactions induced by HDV, which have helped us to understand host control and its failure; and (iii) the discovery of HDV-like agents in other species without an apparent association with HBV-like helper viruses, which changed our view on the co-evolution of these novel Delta-like agents with their hosts. Finally, the identification of novel drugs that specifically interfere with different steps in the HDV replication process led to the approval of the entry inhibitor Hepcludex in 2020 as the first specific drug against chronic HDV infection.

This Special Issue will address topics related to HDV epidemiology, HDV prevention, the molecular biology of HDV and HDV-like agents, animal models of HDV, novel insights into HDV–host interaction, HDV persistence, innate and adaptive immune responses, the pathogenesis of infection, translational HDV research, and novel combinatorial approaches to clinically managing chronic HDV infections.

Prof. Dr. Stefan Urban
Guest Editor

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Keywords

hepatitis D virus (HDV)
HDV-like agents
HDV epidemiology
HDV persistence
in vitro and in vivo models of HDV/hepatitis B virus (HBV) coinfection
HDV pathogenesis
current and future treatment of chronic hepatitis D (CHD)

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Published Papers (14 papers)

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Editorial

Jump to: Research, Review, Other

6 pages, 213 KiB

Open AccessEditorial

Forty-Five Years after the Discovery of the Hepatitis D Virus: Where Do We Stand?

by Mario Rizzetto and Tommaso Stroffolini

Viruses 2021, 13(4), 555; https://doi.org/10.3390/v13040555 - 26 Mar 2021

Cited by 5 | Viewed by 2037

Abstract

The discovery of the Australia Antigen in the mid-1960s led, in a few years, to the identification of the virus of Hepatitis B [...] Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

Research

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13 pages, 1488 KiB

Open AccessArticle

Inspecting the Ribozyme Region of Hepatitis Delta Virus Genotype 1: Conservation and Variability

by Beatriz Pacin-Ruiz, María Francesca Cortese, David Tabernero, Sara Sopena, Josep Gregori, Selene García-García, Rosario Casillas, Adrián Najarro, Unai Aldama, Adriana Palom, Ariadna Rando-Segura, Anna Galán, Marta Vila, Mar Riveiro-Barciela, Josep Quer, Gloria González-Aseguinolaza, María Buti and Francisco Rodríguez-Frías

Viruses 2022, 14(2), 215; https://doi.org/10.3390/v14020215 - 22 Jan 2022

Cited by 5 | Viewed by 3634

Abstract

The hepatitis delta virus (HDV) genome has an autocatalytic region called the ribozyme, which is essential for viral replication. The aim of this study was to use next-generation sequencing (NGS) to analyze the ribozyme quasispecies (QS) in order to study its evolution and identify highly conserved regions potentially suitable for a gene-silencing strategy. HDV RNA was extracted from 2 longitudinal samples of chronic HDV patients and the ribozyme (nucleotide, nt 688–771) was analyzed using NGS. QS conservation, variability and genetic distance were analyzed. Mutations were identified by aligning sequences with their specific genotype consensus. The main relevant mutations were tested in vitro. The ribozyme was conserved overall, with a hyper-conserved region between nt 715–745. No difference in QS was observed over time. The most variable region was between nt 739–769. Thirteen mutations were observed, with three showing a higher frequency: T23C, T69C and C64 deletion. This last strongly reduced HDV replication by more than 1 log in vitro. HDV Ribozyme QS was generally highly conserved and was maintained during follow-up. The most conserved portion may be a valuable target for a gene-silencing strategy. The presence of the C64 deletion may strongly impair viral replication, as it is a potential mechanism of viral persistence. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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10 pages, 1838 KiB

Open AccessArticle

A Rapid Point-of-Care Test for the Serodiagnosis of Hepatitis Delta Virus Infection

by Florian A. Lempp, Imme Roggenbach, Shirin Nkongolo, Volkan Sakin, Franziska Schlund, Paul Schnitzler, Heiner Wedemeyer, Frédéric Le Gal, Emmanuel Gordien, Cihan Yurdaydin and Stephan Urban

Viruses 2021, 13(12), 2371; https://doi.org/10.3390/v13122371 - 26 Nov 2021

Cited by 20 | Viewed by 3505

Abstract

Hepatitis Delta virus (HDV) is a satellite of the Hepatitis B virus (HBV) and causes severe liver disease. The estimated prevalence of 15–20 million infected people worldwide may be underestimated as international diagnostic guidelines are not routinely followed. Possible reasons for this include the limited awareness among healthcare providers, the requirement for costly equipment and specialized training, and a lack of access to reliable tests in regions with poor medical infrastructure. In this study, we developed an HDV rapid test for the detection of antibodies against the hepatitis delta antigen (anti-HDV) in serum and plasma. The test is based on a novel recombinant large hepatitis delta antigen that can detect anti-HDV in a concentration-dependent manner with pan-genotypic activity across all known HDV genotypes. We evaluated the performance of this test on a cohort of 474 patient samples and found that it has a sensitivity of 94.6% (314/332) and a specificity of 100% (142/142) when compared to a diagnostic gold-standard ELISA. It also works robustly for a broad range of anti-HDV titers. We anticipate this novel HDV rapid test to be an important tool for epidemiological studies and clinical diagnostics, especially in regions that currently lack access to reliable HDV testing. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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15 pages, 2110 KiB

Open AccessArticle

HDV Seroprevalence in HBsAg-Positive Patients in China Occurs in Hotspots and Is Not Associated with HCV Mono-Infection

by Imme Roggenbach, Xiumei Chi, Florian A. Lempp, Bingqian Qu, Lisa Walter, Ruihong Wu, Xiuzhu Gao, Paul Schnitzler, Yanhua Ding, Stephan Urban and Junqi Niu

Viruses 2021, 13(9), 1799; https://doi.org/10.3390/v13091799 - 10 Sep 2021

Cited by 26 | Viewed by 2984

Abstract

HDV infection causes severe liver disease, the global health burden of which may be underestimated due to limited epidemiological data. HDV depends on HBV for infection, but recent studies indicated that dissemination can also be supported by other helper viruses such as HCV. We used a rapid point-of-care test and an ELISA to retrospectively test for antibodies against the Hepatitis Delta antigen (anti-HDV-Ab) in 4103 HBsAg-positive and 1661 HBsAg-negative, anti-HCV-positive sera from China and Germany. We found that the HDV seroprevalence in HBsAg-positive patients in China is limited to geographic hotspots (Inner Mongolia: 35/251, 13.9%; Xinjiang: 7/180, 3.9%) and high-risk intravenous drug users (HBV mono-infected: 23/247, 9.3%; HBV-HCV co-infected: 34/107, 31.8%), while none of the 2634 HBsAg carriers from other metropolitan regions were anti-HDV-Ab-positive. In Germany, we recorded an HDV seroprevalence of 5.3% in a university hospital environment. In a cohort of HBsAg-negative, anti-HCV-positive patients that were not exposed to HBV before (anti-HBc-negative), HDV was not associated with HCV mono-infection (Chinese high-risk cohort: 0/365, 0.0%; German mixed cohort: 0/263, 0.0%). However, 21/1033 (2.0%) high-risk HCV patients in China with markers of a previously cleared HBV infection (anti-HBc-positive) were positive for anti-HDV-Ab, with two of them being positive for both HDV and HCV RNA but negative for HBV DNA. The absence of anti-HDV-Ab in HCV mono-infected patients shows that HCV cannot promote HDV transmission in humans. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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15 pages, 10849 KiB

Open AccessArticle

Variable In Vivo Hepatitis D Virus (HDV) RNA Editing Rates According to the HDV Genotype

by Samira Dziri, Christophe Rodriguez, Athenaïs Gerber, Ségolène Brichler, Chakib Alloui, Dominique Roulot, Paul Dény, Jean Michel Pawlotsky, Emmanuel Gordien and Frédéric Le Gal

Viruses 2021, 13(8), 1572; https://doi.org/10.3390/v13081572 - 9 Aug 2021

Cited by 11 | Viewed by 2885

Abstract

Human hepatitis delta virus (HDV) is a small defective RNA satellite virus that requires hepatitis B virus (HBV) envelope proteins to form its own virions. The HDV genome possesses a single coding open reading frame (ORF), located on a replicative intermediate, the antigenome, encoding the small (s) and the large (L) isoforms of the delta antigen (s-HDAg and L-HDAg). The latter is produced following an editing process, changing the amber/stop codon on the s-HDAg-ORF into a tryptophan codon, allowing L-HDAg synthesis by the addition of 19 (or 20) C-terminal amino acids. The two delta proteins play different roles in the viral cell cycle: s-HDAg activates genome replication, while L-HDAg blocks replication and favors virion morphogenesis and propagation. L-HDAg has also been involved in HDV pathogenicity. Understanding the kinetics of viral editing rates in vivo is key to unravel the biology of the virus and understand its spread and natural history. We developed and validated a new assay based on next-generation sequencing and aimed at quantifying HDV RNA editing in plasma. We analyzed plasma samples from 219 patients infected with different HDV genotypes and showed that HDV editing capacity strongly depends on the genotype of the strain. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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19 pages, 4958 KiB

Open AccessArticle

AAV-HDV: An Attractive Platform for the In Vivo Study of HDV Biology and the Mechanism of Disease Pathogenesis

by Sheila Maestro, Nahia Gómez-Echarte, Gracián Camps, Carla Usai, Lester Suárez, África Vales, Cristina Olagüe, Rafael Aldabe and Gloria González-Aseguinolaza

Viruses 2021, 13(5), 788; https://doi.org/10.3390/v13050788 - 28 Apr 2021

Cited by 7 | Viewed by 3190

Abstract

Hepatitis delta virus (HDV) infection causes the most severe form of viral hepatitis, but little is known about the molecular mechanisms involved. We have recently developed an HDV mouse model based on the delivery of HDV replication-competent genomes using adeno-associated vectors (AAV), which developed a liver pathology very similar to the human disease and allowed us to perform mechanistic studies. We have generated different AAV-HDV mutants to eliminate the expression of HDV antigens (HDAgs), and we have characterized them both in vitro and in vivo. We confirmed that S-HDAg is essential for HDV replication and cannot be replaced by L-HDAg or host cellular proteins, and that L-HDAg is essential to produce the HDV infectious particle and inhibits its replication. We have also found that lack of L-HDAg resulted in the increase of S-HDAg expression levels and the exacerbation of liver damage, which was associated with an increment in liver inflammation but did not require T cells. Interestingly, early expression of L-HDAg significantly ameliorated the liver damage induced by the mutant expressing only S-HDAg. In summary, the use of AAV-HDV represents a very attractive platform to interrogate in vivo the role of viral components in the HDV life cycle and to better understand the mechanism of HDV-induced liver pathology. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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Review

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10 pages, 672 KiB

Open AccessReview

Combination of Novel Therapies for HDV

by Menashe Elazar and Jeffrey S. Glenn

Viruses 2022, 14(2), 268; https://doi.org/10.3390/v14020268 - 28 Jan 2022

Cited by 9 | Viewed by 3539

Abstract

Treatment options for HDV have been limited to interferon alfa-based therapies with its poor efficacy to side effects ratio. Several novel therapies have now advanced into the clinic. As they each have a different mechanism of action, there is the potential for combination therapy. Here we review how studying the HDV life cycle has led to the development of these novel therapies, the key developments leading to, and the details of, the first combination study of novel anti-HDV therapies, and suggest what additional combinations of novel therapies can be anticipated as we enter this exciting new area of HDV treatments. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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22 pages, 2284 KiB

Open AccessReview

Adaptive Immune Responses, Immune Escape and Immune-Mediated Pathogenesis during HDV Infection

by Valerie Oberhardt, Maike Hofmann, Robert Thimme and Christoph Neumann-Haefelin

Viruses 2022, 14(2), 198; https://doi.org/10.3390/v14020198 - 20 Jan 2022

Cited by 12 | Viewed by 4528

Abstract

The hepatitis delta virus (HDV) is the smallest known human virus, yet it causes great harm to patients co-infected with hepatitis B virus (HBV). As a satellite virus of HBV, HDV requires the surface antigen of HBV (HBsAg) for sufficient viral packaging and spread. The special circumstance of co-infection, albeit only one partner depends on the other, raises many virological, immunological, and pathophysiological questions. In the last years, breakthroughs were made in understanding the adaptive immune response, in particular, virus-specific CD4+ and CD8+ T cells, in self-limited versus persistent HBV/HDV co-infection. Indeed, the mechanisms of CD8+ T cell failure in persistent HBV/HDV co-infection include viral escape and T cell exhaustion, and mimic those in other persistent human viral infections, such as hepatitis C virus (HCV), human immunodeficiency virus (HIV), and HBV mono-infection. However, compared to these larger viruses, the small HDV has perfectly adapted to evade recognition by CD8+ T cells restricted by common human leukocyte antigen (HLA) class I alleles. Furthermore, accelerated progression towards liver cirrhosis in persistent HBV/HDV co-infection was attributed to an increased immune-mediated pathology, either caused by innate pathways initiated by the interferon (IFN) system or triggered by misguided and dysfunctional T cells. These new insights into HDV-specific adaptive immunity will be discussed in this review and put into context with known well-described aspects in HBV, HCV, and HIV infections. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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10 pages, 264 KiB

Open AccessReview

Cell Culture Models for the Study of Hepatitis D Virus Entry and Infection

by Margaux J. Heuschkel, Thomas F. Baumert and Eloi R. Verrier

Viruses 2021, 13(8), 1532; https://doi.org/10.3390/v13081532 - 3 Aug 2021

Cited by 8 | Viewed by 2937

Abstract

Chronic hepatitis D is one of the most severe and aggressive forms of chronic viral hepatitis with a high risk of developing hepatocellular carcinoma (HCC). It results from the co-infection of the liver with the hepatitis B virus (HBV) and its satellite, the hepatitis D virus (HDV). Although current therapies can control HBV infection, no treatment that efficiently eliminates HDV is available and novel therapeutic strategies are needed. Although the HDV cycle is well described, the lack of simple experimental models has restricted the study of host–virus interactions, even if they represent relevant therapeutic targets. In the last few years, the discovery of the sodium taurocholate co-transporting polypeptide (NTCP) as a key cellular entry factor for HBV and HDV has allowed the development of new cell culture models susceptible to HBV and HDV infection. In this review, we summarize the main in vitro model systems used for the study of HDV entry and infection, discuss their benefits and limitations and highlight perspectives for future developments. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

15 pages, 1078 KiB

Open AccessReview

HDV-Like Viruses

by Jimena Pérez-Vargas, Rémi Pereira de Oliveira, Stéphanie Jacquet, Dominique Pontier, François-Loïc Cosset and Natalia Freitas

Viruses 2021, 13(7), 1207; https://doi.org/10.3390/v13071207 - 23 Jun 2021

Cited by 24 | Viewed by 4120

Abstract

Hepatitis delta virus (HDV) is a defective human virus that lacks the ability to produce its own envelope proteins and is thus dependent on the presence of a helper virus, which provides its surface proteins to produce infectious particles. Hepatitis B virus (HBV) was so far thought to be the only helper virus described to be associated with HDV. However, recent studies showed that divergent HDV-like viruses could be detected in fishes, birds, amphibians, and invertebrates, without evidence of any HBV-like agent supporting infection. Another recent study demonstrated that HDV can be transmitted and propagated in experimental infections ex vivo and in vivo by different enveloped viruses unrelated to HBV, including hepatitis C virus (HCV) and flaviviruses such as Dengue and West Nile virus. All this new evidence, in addition to the identification of novel virus species within a large range of hosts in absence of HBV, suggests that deltaviruses may take advantage of a large spectrum of helper viruses and raises questions about HDV origins and evolution. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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13 pages, 452 KiB

Open AccessReview

Hepatitis D Virus and Hepatocellular Carcinoma

by Patrizia Farci, Grazia Anna Niro, Fausto Zamboni and Giacomo Diaz

Viruses 2021, 13(5), 830; https://doi.org/10.3390/v13050830 - 4 May 2021

Cited by 33 | Viewed by 3895

Abstract

Hepatitis D virus (HDV) is a small, defective RNA virus that depends on hepatitis B virus (HBV) for virion assembly and transmission. It replicates within the nucleus of hepatocytes and interacts with several cellular proteins. Chronic hepatitis D is a severe and progressive disease, leading to cirrhosis in up to 80% of cases. A high proportion of patients die of liver decompensation or hepatocellular carcinoma (HCC), but the lack of large prospective studies has made it difficult to precisely define the rate of these long-term complications. In particular, the question of whether HDV is an oncogenic virus has been a matter of debate. Studies conducted over the past decade provided evidence that HDV is associated with a significantly higher risk of developing HCC compared to HBV monoinfection. However, the mechanisms whereby HDV promotes liver cancer remain elusive. Recent data have demonstrated that the molecular profile of HCC-HDV is unique and distinct from that of HBV-HCC, with an enrichment of upregulated genes involved in cell-cycle/DNA replication, and DNA damage and repair, which point to genome instability as an important mechanism of HDV hepatocarcinogenesis. These data suggest that HBV and HDV promote carcinogenesis by distinct molecular mechanisms despite the obligatory dependence of HDV on HBV. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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22 pages, 2710 KiB

Open AccessReview

HDV Pathogenesis: Unravelling Ariadne’s Thread

by Eirini D. Tseligka, Sophie Clément and Francesco Negro

Viruses 2021, 13(5), 778; https://doi.org/10.3390/v13050778 - 28 Apr 2021

Cited by 19 | Viewed by 7982

Abstract

Hepatitis Delta virus (HDV) lies in between satellite viruses and viroids, as its unique molecular characteristics and life cycle cannot categorize it according to the standard taxonomy norms for viruses. Being a satellite virus of hepatitis B virus (HBV), HDV requires HBV envelope glycoproteins for its infection cycle and its transmission. HDV pathogenesis varies and depends on the mode of HDV and HBV infection; a simultaneous HDV and HBV infection will lead to an acute hepatitis that will resolve spontaneously in the majority of patients, whereas an HDV super-infection of a chronic HBV carrier will mainly result in the establishment of a chronic HDV infection that may progress towards cirrhosis, liver decompensation, and hepatocellular carcinoma (HCC). With this review, we aim to unravel Ariadne’s thread into the labyrinth of acute and chronic HDV infection pathogenesis and will provide insights into the complexity of this exciting topic by detailing the different players and mechanisms that shape the clinical outcome. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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15 pages, 1302 KiB

Open AccessReview

In Vivo Models of HDV Infection: Is Humanizing NTCP Enough?

by Katja Giersch and Maura Dandri

Viruses 2021, 13(4), 588; https://doi.org/10.3390/v13040588 - 31 Mar 2021

Cited by 8 | Viewed by 3274

Abstract

The discovery of sodium taurocholate co-transporting polypeptide (NTCP) as a hepatitis B (HBV) and delta virus (HDV) entry receptor has encouraged the development of new animal models of infection. This review provides an overview of the different in vivo models that are currently available to study HDV either in the absence or presence of HBV. By presenting new advances and remaining drawbacks, we will discuss human host factors which, in addition to NTCP, need to be investigated or identified to enable a persistent HDV infection in murine hepatocytes. Detailed knowledge on species-specific factors involved in HDV persistence also shall contribute to the development of therapeutic strategies. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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Other

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9 pages, 1263 KiB

Open AccessBrief Report

Inhibitory Effect of IL-1β on HBV and HDV Replication and HBs Antigen-Dependent Modulation of Its Secretion by Macrophages

by Marion Delphin, Suzanne Faure-Dupuy, Nathalie Isorce, Michel Rivoire, Anna Salvetti, David Durantel and Julie Lucifora

Viruses 2022, 14(1), 65; https://doi.org/10.3390/v14010065 - 30 Dec 2021

Cited by 7 | Viewed by 2074

Abstract

Co-infection with the hepatitis B virus and hepatitis delta virus (HDV) leads to the most aggressive form of viral hepatitis. Using in vitro infection models, we confirmed that IL-1β, a crucial innate immune molecule for pathogen control, was very potent against HBV from different genotypes. Additionally, we demonstrated for the first time a strong and rapid antiviral effect induced by very low doses of IL-1β against HDV. In parallel, using co-culture assays, we demonstrated that monocytes exposed to HBV, and in particular to HBsAg, during differentiation into pro-inflammatory macrophages secreted less IL-1β. Altogether, our data emphasize the importance of developing combined antiviral strategies that would, for instance, reduce the secretion of HBsAg and stimulate the immune system to produce endogenous IL-1β efficient against both HBV and HDV. Full article

(This article belongs to the Special Issue Hepatitis Delta Virus)

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