Review article: emerging insights into the immunopathology, clinical and therapeutic aspects of hepatitis delta virus
Summary Background Hepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect naïve subjects simultaneously with HBV (co‐infection), or chronically infect HBV carriers (super‐infection). An estimated 12...
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| Published in | Alimentary pharmacology & therapeutics Vol. 55; no. 8; pp. 978 - 993 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Wiley Subscription Services, Inc
01.04.2022
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Summary
Background
Hepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect naïve subjects simultaneously with HBV (co‐infection), or chronically infect HBV carriers (super‐infection). An estimated 12 million people are infected by HDV worldwide.
Aims
To summarise the most relevant aspects of the molecular biology of HDV, and to discuss the latest understanding of the induced pathology, interactions with the immune system, as well as both approved and investigational treatment options.
Methods
References for this review were identified through searches of PubMed with the terms “HDV” “viral hepatitis” “co‐infection” and “super‐infection,” published between 1980 and October 2021
Results
The limited access to the HDV‐infected liver has hampered the investigation of the intrahepatic compartment and our understanding of the mechanisms of HDV pathogenesis. In the absence of standardised and sensitive diagnostic tools, HDV is often underdiagnosed and owing to its strong dependence on host cellular factors, the development of direct antiviral agents has been challenging. New therapeutic agents targeting different steps of the viral cycle have recently been investigated, among which bulevirtide (which was conditionally approved by EMA in July 2020) and lonafarnib; both drugs having received orphan drug designation from both the EMA and FDA.
Conclusions
The HBV cure programme potentially offers a unique opportunity to enhance HDV treatment strategies. In addition, a more comprehensive analysis of the intrahepatic compartment is mandated to better understand any liver‐confined interaction of HDV with the host immune system.
The diagrams show the time‐course of the most common outcomes of (A) HBV‐HDV co‐infection and (B) HDV super‐infection of an HBV carrier. Biochemical and serological parameters are indicated. |
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| AbstractList | The diagrams show the time‐course of the most common outcomes of (A) HBV‐HDV co‐infection and (B) HDV super‐infection of an HBV carrier. Biochemical and serological parameters are indicated. BackgroundHepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect naïve subjects simultaneously with HBV (co‐infection), or chronically infect HBV carriers (super‐infection). An estimated 12 million people are infected by HDV worldwide.AimsTo summarise the most relevant aspects of the molecular biology of HDV, and to discuss the latest understanding of the induced pathology, interactions with the immune system, as well as both approved and investigational treatment options.MethodsReferences for this review were identified through searches of PubMed with the terms “HDV” “viral hepatitis” “co‐infection” and “super‐infection,” published between 1980 and October 2021ResultsThe limited access to the HDV‐infected liver has hampered the investigation of the intrahepatic compartment and our understanding of the mechanisms of HDV pathogenesis. In the absence of standardised and sensitive diagnostic tools, HDV is often underdiagnosed and owing to its strong dependence on host cellular factors, the development of direct antiviral agents has been challenging. New therapeutic agents targeting different steps of the viral cycle have recently been investigated, among which bulevirtide (which was conditionally approved by EMA in July 2020) and lonafarnib; both drugs having received orphan drug designation from both the EMA and FDA.ConclusionsThe HBV cure programme potentially offers a unique opportunity to enhance HDV treatment strategies. In addition, a more comprehensive analysis of the intrahepatic compartment is mandated to better understand any liver‐confined interaction of HDV with the host immune system. Summary Background Hepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect naïve subjects simultaneously with HBV (co‐infection), or chronically infect HBV carriers (super‐infection). An estimated 12 million people are infected by HDV worldwide. Aims To summarise the most relevant aspects of the molecular biology of HDV, and to discuss the latest understanding of the induced pathology, interactions with the immune system, as well as both approved and investigational treatment options. Methods References for this review were identified through searches of PubMed with the terms “HDV” “viral hepatitis” “co‐infection” and “super‐infection,” published between 1980 and October 2021 Results The limited access to the HDV‐infected liver has hampered the investigation of the intrahepatic compartment and our understanding of the mechanisms of HDV pathogenesis. In the absence of standardised and sensitive diagnostic tools, HDV is often underdiagnosed and owing to its strong dependence on host cellular factors, the development of direct antiviral agents has been challenging. New therapeutic agents targeting different steps of the viral cycle have recently been investigated, among which bulevirtide (which was conditionally approved by EMA in July 2020) and lonafarnib; both drugs having received orphan drug designation from both the EMA and FDA. Conclusions The HBV cure programme potentially offers a unique opportunity to enhance HDV treatment strategies. In addition, a more comprehensive analysis of the intrahepatic compartment is mandated to better understand any liver‐confined interaction of HDV with the host immune system. The diagrams show the time‐course of the most common outcomes of (A) HBV‐HDV co‐infection and (B) HDV super‐infection of an HBV carrier. Biochemical and serological parameters are indicated. Hepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect naïve subjects simultaneously with HBV (co-infection), or chronically infect HBV carriers (super-infection). An estimated 12 million people are infected by HDV worldwide. To summarise the most relevant aspects of the molecular biology of HDV, and to discuss the latest understanding of the induced pathology, interactions with the immune system, as well as both approved and investigational treatment options. References for this review were identified through searches of PubMed with the terms "HDV" "viral hepatitis" "co-infection" and "super-infection," published between 1980 and October 2021 RESULTS: The limited access to the HDV-infected liver has hampered the investigation of the intrahepatic compartment and our understanding of the mechanisms of HDV pathogenesis. In the absence of standardised and sensitive diagnostic tools, HDV is often underdiagnosed and owing to its strong dependence on host cellular factors, the development of direct antiviral agents has been challenging. New therapeutic agents targeting different steps of the viral cycle have recently been investigated, among which bulevirtide (which was conditionally approved by EMA in July 2020) and lonafarnib; both drugs having received orphan drug designation from both the EMA and FDA. The HBV cure programme potentially offers a unique opportunity to enhance HDV treatment strategies. In addition, a more comprehensive analysis of the intrahepatic compartment is mandated to better understand any liver-confined interaction of HDV with the host immune system. Hepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect naïve subjects simultaneously with HBV (co-infection), or chronically infect HBV carriers (super-infection). An estimated 12 million people are infected by HDV worldwide.BACKGROUNDHepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect naïve subjects simultaneously with HBV (co-infection), or chronically infect HBV carriers (super-infection). An estimated 12 million people are infected by HDV worldwide.To summarise the most relevant aspects of the molecular biology of HDV, and to discuss the latest understanding of the induced pathology, interactions with the immune system, as well as both approved and investigational treatment options.AIMSTo summarise the most relevant aspects of the molecular biology of HDV, and to discuss the latest understanding of the induced pathology, interactions with the immune system, as well as both approved and investigational treatment options.References for this review were identified through searches of PubMed with the terms "HDV" "viral hepatitis" "co-infection" and "super-infection," published between 1980 and October 2021 RESULTS: The limited access to the HDV-infected liver has hampered the investigation of the intrahepatic compartment and our understanding of the mechanisms of HDV pathogenesis. In the absence of standardised and sensitive diagnostic tools, HDV is often underdiagnosed and owing to its strong dependence on host cellular factors, the development of direct antiviral agents has been challenging. New therapeutic agents targeting different steps of the viral cycle have recently been investigated, among which bulevirtide (which was conditionally approved by EMA in July 2020) and lonafarnib; both drugs having received orphan drug designation from both the EMA and FDA.METHODSReferences for this review were identified through searches of PubMed with the terms "HDV" "viral hepatitis" "co-infection" and "super-infection," published between 1980 and October 2021 RESULTS: The limited access to the HDV-infected liver has hampered the investigation of the intrahepatic compartment and our understanding of the mechanisms of HDV pathogenesis. In the absence of standardised and sensitive diagnostic tools, HDV is often underdiagnosed and owing to its strong dependence on host cellular factors, the development of direct antiviral agents has been challenging. New therapeutic agents targeting different steps of the viral cycle have recently been investigated, among which bulevirtide (which was conditionally approved by EMA in July 2020) and lonafarnib; both drugs having received orphan drug designation from both the EMA and FDA.The HBV cure programme potentially offers a unique opportunity to enhance HDV treatment strategies. In addition, a more comprehensive analysis of the intrahepatic compartment is mandated to better understand any liver-confined interaction of HDV with the host immune system.CONCLUSIONSThe HBV cure programme potentially offers a unique opportunity to enhance HDV treatment strategies. In addition, a more comprehensive analysis of the intrahepatic compartment is mandated to better understand any liver-confined interaction of HDV with the host immune system. |
| Author | Gill, Upkar S. Riddell, Anna C. Kennedy, Patrick T. Asselah, Tarik Usai, Carla |
| AuthorAffiliation | 2 The Royal London Hospital Barts Health NHS Trust London UK 6 Present address: Unitat mixta d’Investigació IRTA‐UAB en Sanitat Animal Centre de Recerca en Sanitat Animal (CReSA) Campus de la Universitat Autònoma de Barcelona (UAB) Bellaterra 08193 Spain 1 Centre for Immunobiology, Blizard Institute, Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK 4 Centre de recherche sur l'inflammation, Inserm U1149 Université́ de Paris Paris France 5 Department of Hepatology, AP‐HP Hôpital Beaujon Clichy France 3 Division of Infection, Virology Department Barts Health NHS Trust London UK |
| AuthorAffiliation_xml | – name: 3 Division of Infection, Virology Department Barts Health NHS Trust London UK – name: 2 The Royal London Hospital Barts Health NHS Trust London UK – name: 1 Centre for Immunobiology, Blizard Institute, Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK – name: 4 Centre de recherche sur l'inflammation, Inserm U1149 Université́ de Paris Paris France – name: 6 Present address: Unitat mixta d’Investigació IRTA‐UAB en Sanitat Animal Centre de Recerca en Sanitat Animal (CReSA) Campus de la Universitat Autònoma de Barcelona (UAB) Bellaterra 08193 Spain – name: 5 Department of Hepatology, AP‐HP Hôpital Beaujon Clichy France |
| Author_xml | – sequence: 1 givenname: Carla orcidid: 0000-0002-6373-2765 surname: Usai fullname: Usai, Carla organization: Queen Mary University of London – sequence: 2 givenname: Upkar S. orcidid: 0000-0001-6146-9708 surname: Gill fullname: Gill, Upkar S. organization: Barts Health NHS Trust – sequence: 3 givenname: Anna C. surname: Riddell fullname: Riddell, Anna C. organization: Barts Health NHS Trust – sequence: 4 givenname: Tarik surname: Asselah fullname: Asselah, Tarik organization: Hôpital Beaujon – sequence: 5 givenname: Patrick T. orcidid: 0000-0001-9201-0094 surname: Kennedy fullname: Kennedy, Patrick T. email: p.kennedy@qmul.ac.uk organization: Barts Health NHS Trust |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35292991$$D View this record in MEDLINE/PubMed |
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| References | 2019; 91 2015; 424 1991; 13 1983; 3 2019; 10 2002; 99 2021; 161 2021; 74 2021; 73 2019; 164 1986; 83 2019; 26 2014; 19 2018; 38 2010; 30 2019; 156 2011; 364 2005; 79 2006; 50 2019; 5 2000; 113 2017; 66 2015; 123 1989; 9 2017; 67 2016; 10 2019; 105 2021; 142 2014; 40 2012; 32 2018; 25 2016; 11 2001; 276 2016; 6 2021; 54 2015; 62 2015; 64 1977; 18 1992; 256 2018; 92 2011; 85 2019; 219 2020; 158 2001; 33 2017; 145 2018; 10 2005; 12 2014; 146 2004; 126 2017; 2 1986; 255 2021; 28 2007; 142 2017; 45 2014; 63 2014; 60 1996; 105 2020; 3 2014; 4 2014; 209 2016; 90 1995; 69 2019; 68 2007; 132 1980; 77 2004; 78 2014; 9 2021; 41 2016; 88 2004; 85 2015; 15 1998; 28 2019; 71 2021; 5 2015; 3 2006; 12 2017; 25 2006; 13 1986; 58 2015; 11 2011; 31 2018; 67 2011; 39 2017; 214 2017; 215 2009; 137 2003; 77 2018; 68 2007; 357 2021; 13 1990; 64 1986; 323 1997; 71 2012; 1 2020; 73 2020 2017; 12 2016; 65 2019 2016; 64 2017 1988; 62 2007; 46 e_1_2_8_26_1 e_1_2_8_49_1 e_1_2_8_68_1 e_1_2_8_5_1 e_1_2_8_9_1 e_1_2_8_117_1 e_1_2_8_22_1 e_1_2_8_45_1 e_1_2_8_64_1 e_1_2_8_87_1 e_1_2_8_113_1 e_1_2_8_41_1 e_1_2_8_60_1 e_1_2_8_83_1 e_1_2_8_19_1 e_1_2_8_15_1 e_1_2_8_38_1 e_1_2_8_57_1 (e_1_2_8_88_1) 2019 e_1_2_8_91_1 e_1_2_8_95_1 e_1_2_8_99_1 (e_1_2_8_102_1) 2020 e_1_2_8_105_1 e_1_2_8_11_1 e_1_2_8_34_1 e_1_2_8_53_1 e_1_2_8_76_1 e_1_2_8_101_1 e_1_2_8_30_1 e_1_2_8_72_1 e_1_2_8_25_1 Shamur MM (e_1_2_8_109_1) 2017; 66 e_1_2_8_48_1 e_1_2_8_2_1 e_1_2_8_110_1 e_1_2_8_6_1 e_1_2_8_21_1 e_1_2_8_67_1 e_1_2_8_44_1 e_1_2_8_86_1 e_1_2_8_118_1 e_1_2_8_63_1 e_1_2_8_40_1 e_1_2_8_82_1 e_1_2_8_114_1 e_1_2_8_18_1 e_1_2_8_14_1 e_1_2_8_37_1 e_1_2_8_79_1 e_1_2_8_94_1 e_1_2_8_90_1 e_1_2_8_98_1 e_1_2_8_10_1 e_1_2_8_56_1 e_1_2_8_106_1 e_1_2_8_33_1 e_1_2_8_75_1 e_1_2_8_52_1 e_1_2_8_71_1 e_1_2_8_28_1 e_1_2_8_24_1 e_1_2_8_47_1 e_1_2_8_3_1 e_1_2_8_81_1 e_1_2_8_111_1 e_1_2_8_7_1 e_1_2_8_20_1 e_1_2_8_43_1 e_1_2_8_66_1 e_1_2_8_89_1 e_1_2_8_119_1 e_1_2_8_62_1 e_1_2_8_85_1 e_1_2_8_115_1 e_1_2_8_17_1 e_1_2_8_13_1 e_1_2_8_36_1 e_1_2_8_59_1 e_1_2_8_70_1 e_1_2_8_97_1 e_1_2_8_32_1 e_1_2_8_55_1 e_1_2_8_78_1 e_1_2_8_107_1 e_1_2_8_51_1 e_1_2_8_74_1 e_1_2_8_103_1 e_1_2_8_93_1 e_1_2_8_46_1 e_1_2_8_27_1 e_1_2_8_69_1 e_1_2_8_80_1 e_1_2_8_4_1 e_1_2_8_8_1 e_1_2_8_42_1 e_1_2_8_116_1 e_1_2_8_23_1 e_1_2_8_65_1 e_1_2_8_84_1 e_1_2_8_112_1 e_1_2_8_61_1 e_1_2_8_39_1 e_1_2_8_35_1 e_1_2_8_16_1 e_1_2_8_58_1 e_1_2_8_92_1 e_1_2_8_96_1 e_1_2_8_100_1 World Health Organization (e_1_2_8_29_1) 2017 e_1_2_8_31_1 e_1_2_8_77_1 e_1_2_8_12_1 e_1_2_8_54_1 e_1_2_8_108_1 e_1_2_8_73_1 e_1_2_8_50_1 e_1_2_8_104_1 |
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Hepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that... Hepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either infect... BackgroundHepatitis delta virus (HDV), which causes the most severe form of viral hepatitis, is an obligated hepatitis B (HBV) satellite virus that can either... The diagrams show the time‐course of the most common outcomes of (A) HBV‐HDV co‐infection and (B) HDV super‐infection of an HBV carrier. Biochemical and... |
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| SubjectTerms | Antiviral agents Antiviral Agents - therapeutic use Coinfection - drug therapy fine‐needle aspiration HDV Hepatitis B Hepatitis Delta Virus Humans Immune system Immunosuppressive agents Infections intrahepatic compartment Lipopeptides Liver Review viral hepatitis Viruses |
| Title | Review article: emerging insights into the immunopathology, clinical and therapeutic aspects of hepatitis delta virus |
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