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1
Taylor, John M. "Infection by Hepatitis Delta Virus." Viruses 12, no. 6 (2020): 648. http://dx.doi.org/10.3390/v12060648.
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Hepatitis delta virus (HDV) and hepatitis B virus (HBV) are blood-borne viruses that infect human hepatocytes and cause significant liver disease. Infections with HBV are more damaging when there is a coinfection with HDV. The genomes and modes of replication of these two viruses are fundamentally different, except for the fact that, in nature, HDV replication is dependent upon the envelope proteins of HBV to achieve assembly and release of infectious virus particles, ones that use the same host cell receptor. This review focuses on what has been found of the various ways, natural and experimental, by which HDV particles can be assembled and released. This knowledge has implications for the prevention and treatment of HDV infections, and maybe for an understanding of the origin of HDV.
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Gunsar, Fulya. "Delta Hepatitis." Reviews in Health Care 3, no. 4 (2012): 229. http://dx.doi.org/10.7175/rhc.26734229-241.
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Hepatitis delta virus (HDV) is a defective RNA virus that requires HBsAg for replication and transmission. It can cause acute or chronic hepatitis. Chronic infection with HDV is one of the most severe and difficult to treat forms of viral hepatitis. It has been estimated that there is a total of 15-20 million HDV carriers in the world. This review focuses on two fundamental aspects of HDV infection. On the one hand, epidemiological data are summarized, which are essential to understand the real burden of this disease. After the HBV vaccination programs in many countries all over the world, HDV infection has decreased since 1980’s but this decline has not continued further in the last decade. Therefore, HDV infection is still an important public health problem in the world. On the other hand, therapeutic options are described. Currently, interferons are the only option for the treatment of chronic hepatitis delta infection, and pegylated-interferons have shown better results than conventional interferons (IFNs). Monotherapy of nucleos(t)ide analogs have been found ineffective against the HDV infection, but adefovir and pegylated-IFN combination therapy have had some advantages for reduction of HBsAg levels. Trials with more potent nucleoside analogs and pegylated-IFN could be effective in the treatment of chronic HDV infection. New agents like prenylation inhibitors, that can affect the interactions between the large HDV antigen and HBsAg in the HDV virion, will be a hope in treatment of HDV infection.
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Gunsar, Fulya. "Delta Hepatitis." Reviews in Health Care 3, no. 4 (2012): 229–41. http://dx.doi.org/10.7175/rhc.v3i4.267.
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Hepatitis delta virus (HDV) is a defective RNA virus that requires HBsAg for replication and transmission. It can cause acute or chronic hepatitis. Chronic infection with HDV is one of the most severe and difficult to treat forms of viral hepatitis. It has been estimated that there is a total of 15-20 million HDV carriers in the world. This review focuses on two fundamental aspects of HDV infection. On the one hand, epidemiological data are summarized, which are essential to understand the real burden of this disease. After the HBV vaccination programs in many countries all over the world, HDV infection has decreased since 1980’s but this decline has not continued further in the last decade. Therefore, HDV infection is still an important public health problem in the world. On the other hand, therapeutic options are described. Currently, interferons are the only option for the treatment of chronic hepatitis delta infection, and pegylated-interferons have shown better results than conventional interferons (IFNs). Monotherapy of nucleos(t)ide analogs have been found ineffective against the HDV infection, but adefovir and pegylated-IFN combination therapy have had some advantages for reduction of HBsAg levels. Trials with more potent nucleoside analogs and pegylated-IFN could be effective in the treatment of chronic HDV infection. New agents like prenylation inhibitors, that can affect the interactions between the large HDV antigen and HBsAg in the HDV virion, will be a hope in treatment of HDV infection.
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Alves, Carolina, Cristina Branco, and Celso Cunha. "Hepatitis Delta Virus: A Peculiar Virus." Advances in Virology 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/560105.
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The hepatitis delta virus (HDV) is distributed worldwide and related to the most severe form of viral hepatitis. HDV is a satellite RNA virus dependent on hepatitis B surface antigens to assemble its envelope and thus form new virions and propagate infection. HDV has a small 1.7 Kb genome making it the smallest known human virus. This deceivingly simple virus has unique biological features and many aspects of its life cycle remain elusive. The present review endeavors to gather the available information on HDV epidemiology and clinical features as well as HDV biology.
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Gheorghe, Liana, Irma Eva Csiki, Speranta Iacob, et al. "Hepatitis Delta Virus Infection in Romania: Prevalence and Risk Factors." Journal of Gastrointestinal and Liver Diseases 24, no. 4 (2015): 413–21. http://dx.doi.org/10.15403/jgld.2014.1121.244.dtv.
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Background: Hepatitis delta virus (HDV) infection is associated with accelerated progression of fibrosis, early occurrence of hepatic decompensation and an increased risk for hepatocellular carcinoma. Epidemiological data on hepatitis delta virus (HDV) in Romania are still lacking. Aim: To assess the prevalence, virological, clinical and epidemiological features of HDV infection in Romanian patients.
 Methods: We conducted a multicenter study in 10 centers. Data on sociodemographic characteristics and potential risk factors were collected through a questionnaire. Virological markers of HBV and HDV infection, biochemical and clinical features of liver disease were evaluated.
 Results: The study population comprised 2,761 HBsAg(+) patients with a mean age of 43.8±13.8 years, out of whom 5.2% were HBeAg(+) and 55.7% were males. Liver cirrhosis was detected in 17.9% of patients, while 80.4% had chronic hepatitis. The prevalence of IgG anti-HDV(+) patients was 23.1%, out of whom 16.4% were HDV RNA positive. The highest prevalence of HDV infection was encountered in patients aged 50-59 years (28.9%) and patients aged ≥60 (24.8%) (p=0.0001). Seroprevalence of HDV was significantly higher in AgHBs(+) cirrhotics vs. noncirrhotics (43.4% vs 19.0%, p=0.0001). Risk factors for HDV infection were: occupational hazard, no HCV chronic infection, lack of anti-HBV vaccination, presence of blood transfusions, any previous surgery, frequent hospitalization or endoscopies, tattoos, body piercing, use of glass syringes, number of female sexual partners.
 Conclusions: HBsAg(+) population in Romania is characterized by a high prevalence of HBeAg(-) HBV infection as well as HDV co-infection. A cohort phenomenon for HDV prevalence is also observed similar to that of HCV/HBV monoinfections.
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Shaikh, Hafeezullah, Ahsan Mobin, Imtiaz Manzoor, and Muhammad Ashraf Ebrahim. "HEPATITIS DELTA." Professional Medical Journal 25, no. 01 (2018): 73–77. http://dx.doi.org/10.29309/tpmj/2018.25.01.541.
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Objectives: The objective of this study is to prevalence of hepatitis delta inpatients with chronic hepatitis B infection. Study Design: Cross-sectional study. Period: Oneyear starting from February 2016 to January 2017. Setting: Patients OPD and admitted to Dowuniversity hospital and Zubaida Medical Center Karachi. Methods: Hepatitis B surface antigen(HbsAg) were analyzed for the presence or absence of Hepatitis D antibody (Anti HDV). 368patients with chronic hepatitis B were included to be part of this study. Patient’s age, duration ofillness and previous treatments were recorded. HBV and HDV virus presence was confirmed byusing Polymerase chain reaction (PCR). Results: Out of 368 patients with chronic HBV infection,291 (79.07%) were males and 77 (20.92%) were females. The male to female ratio was 3.7:1.Patients were aged between 35-60 years. 251 (68.2%) were positive for anti HDV. 211 of themwere males (84%) and 40 were females (15.9%). Conclusion: We have concluded that HDVinfection is associated with higher incidence of hepatocellular carcinoma in patients. Effectiveand early treatment of HDV can reduce the frequency of patients advancing to decompensatedchronic liver disease and hepatocellular carcinoma.
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Romeo, Raffaella, Arnolfo Petruzziello, Eve Isabel Pecheur, et al. "Hepatitis delta virus and hepatocellular carcinoma: an update." Epidemiology and Infection 146, no. 13 (2018): 1612–18. http://dx.doi.org/10.1017/s0950268818001942.
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AbstractHepatitis delta virus (HDV) is a defective RNA virus that depends on the presence of hepatitis B virus (HBV) for the creation of new virions and propagation of the infection to hepatocytes. Chronic infection with HDV is usually associated with a worsening of HBV infection, leading more frequently to cirrhosis, increased risk of liver decompensation and hepatocellular carcinoma (HCC) occurrence. In spite of a progressive declining prevalence of both acute and chronic HDV infection observed over several years, mainly due to increased global health policies and mass vaccination against HBV, several European countries have more recently observed stable HDV prevalence mainly due to migrants from non-European countries. Persistent HDV replication has been widely demonstrated as associated with cirrhosis development and, as a consequence, development of liver decompensation and occurrence of HCC. Several treatment options have been attempted with poor results in terms of HDV eradication and improvement of long-term prognosis. A global effort is deemed urgent to enhance the models already existing as well as to learn more about HDV infection and correlated tumourigenesis mechanisms.
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Tserashkou, D. V., V. M. Mitsura, E. V. Voropaev, and O. V. Osipkina. "VIRAL COINFECTIONS IN PATIENTS WITH CHRONIC HEPATITIS B: THEIR PREVALENCE AND CLINICAL SIGNIFICANCE." Hepatology and Gastroenterology 4, no. 2 (2020): 171–76. http://dx.doi.org/10.25298/2616-5546-2020-4-2-171-176.
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Background. Hepatitis B virus (HBV) infection remains a global public health problem. Objective – to analyze the prevalence of viral coinfections with human immunodefciency virus (HIV), hepatitis C virus (HCV), hepatitis delta virus (HDV), TT-viruses and SENV in patients with chronic hepatitis B (CHB) and to assess their influence on liver disease severity. Material and methods. The observational cross-sectional study included 287 patients with chronic hepatitis B virus (HBV) – those with monoinfection and coinfected with HIV, HCV, HDV. Routine hematological and biochemical tests were performed, serum HBV DNA level as well as liver fbrosis stage were measured. Blood samples from 62 patients for Torque teno virus (TTV), Torque teno mini virus, Torque teno midi virus, SENV (D and H genotypes) DNAs were examined by polymerase chain reaction. Results. Among patients with CHB the prevalence of coinfection HBV + HIV is 6.6%, HBV + HCV – 6.3%, HBV + HDV – 3.8% and HBV + HDV + HCV – 1.7%. CHB patients coinfected with HIV, HCV, HDV had more pronounced biochemical differences and higher proportion of liver cirrhosis vs. HBV-monoinfected ones. The detection rate of TT viruses and their various combinations in patients with CHB is 91.9%, SENV – 66.1%. Conclusion. Coinfection with HIV, HCV, HDV in CHB patients is associated with more severe forms of chronic liver disease as compared to HBV-monoinfection. TT viruses and SENV are widespread and don’t affect the severity of liver disease in patients with CHB.
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Chou, Huei-Chi, Tsai-Yuan Hsieh, Gwo-Tarng Sheu, and Michael M. C. Lai. "Hepatitis Delta Antigen Mediates the Nuclear Import of Hepatitis Delta Virus RNA." Journal of Virology 72, no. 5 (1998): 3684–90. http://dx.doi.org/10.1128/jvi.72.5.3684-3690.1998.
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ABSTRACT Hepatitis delta virus (HDV) RNA replicates in the nuclei of virus-infected cells. The mechanism of nuclear import of HDV RNA is so far unknown. Using a fluorescein-labeled HDV RNA introduced into partially permeabilized HeLa cells, we found that HDV RNA accumulated only in the cytoplasm. However, in the presence of hepatitis delta antigen (HDAg), which is the only protein encoded by HDV RNA, the HDV RNA was translocated into the nucleus, suggesting that nuclear import of HDV RNA is mediated by HDAg. Deletion of the nuclear localization signal (NLS) or RNA-binding motifs of HDAg resulted in the failure of nuclear import of HDV RNA, indicating that both the NLS and an RNA-binding motif of HDAg are required for the RNA-transporting activity of HDAg. Surprisingly, any one of the three previously identified RNA-binding motifs was sufficient to confer the RNA-transporting activity. We have further shown that HDAg, via its NLS, interacts with karyopherin α2 in vitro, suggesting that nuclear import of the HDAg-HDV RNA complex is mediated by the karyopherin α2β heterodimer. The nuclear import of HDV RNA may be the first biological function of HDAg in the HDV life cycle.
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Gomes-Gouvêa, M. S., M. C. P. Soares, G. Bensabath, et al. "Hepatitis B virus and hepatitis delta virus genotypes in outbreaks of fulminant hepatitis (Labrea black fever) in the western Brazilian Amazon region." Journal of General Virology 90, no. 11 (2009): 2638–43. http://dx.doi.org/10.1099/vir.0.013615-0.
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The genotypes of hepatitis B (HBV) and delta (HDV) viruses circulating among fulminant hepatitis cases from the western Amazon Basin of Brazil were characterized in this study. HBV and HDV isolates were obtained from liver samples from 14 patients who developed fulminant hepatitis and died during 1978–1989. HBV DNA and HDV RNA were detected in all samples. Phylogenetic analyses of HDV sequences showed that they all clustered with previously characterized sequences of HDV genotype 3 (HDV-3). HBV genotypes F, A and D were found in 50.0, 28.6 and 21.4 % of cases, respectively. These results confirm the predominance of HDV-3 in South America and its association with the severe form of hepatitis, and the finding of the co-infection of HDV-3 with different genotypes of HBV suggests that the association between HDV-3 and HBV-F is not necessarily causally related to a more severe clinical course of infection.
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Negro, Francesco, Maurizio Baldi, Ferruccio Bonino, et al. "Chronic HDV (hepatitis delta virus) hepatitis." Journal of Hepatology 6, no. 1 (1988): 8–14. http://dx.doi.org/10.1016/s0168-8278(88)80457-4.
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Pérez-Vargas, Jimena, Rémi Pereira de Oliveira, Stéphanie Jacquet, Dominique Pontier, François-Loïc Cosset, and Natalia Freitas. "HDV-Like Viruses." Viruses 13, no. 7 (2021): 1207. http://dx.doi.org/10.3390/v13071207.
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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.
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Wille, Michelle, Hans Netter, Margaret Littlejohn, et al. "A Divergent Hepatitis D-Like Agent in Birds." Viruses 10, no. 12 (2018): 720. http://dx.doi.org/10.3390/v10120720.
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Hepatitis delta virus (HDV) is currently only found in humans and is a satellite virus that depends on hepatitis B virus (HBV) envelope proteins for assembly, release, and entry. Using meta-transcriptomics, we identified the genome of a novel HDV-like agent in ducks. Sequence analysis revealed secondary structures that were shared with HDV, including self-complementarity and ribozyme features. The predicted viral protein shares 32% amino acid similarity to the small delta antigen of HDV and comprises a divergent phylogenetic lineage. The discovery of an avian HDV-like agent has important implications for the understanding of the origins of HDV and sub-viral agents.
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Rizzetto, Mario, and Marilena Durazzo. "Hepatitis delta virus (HDV) infections." Journal of Hepatology 13 (January 1991): S116—S118. http://dx.doi.org/10.1016/0168-8278(91)90040-i.
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Besombes, Camille, Richard Njouom, Juliette Paireau, et al. "The epidemiology of hepatitis delta virus infection in Cameroon." Gut 69, no. 7 (2020): 1294–300. http://dx.doi.org/10.1136/gutjnl-2019-320027.
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ObjectiveTo investigate the distribution and risk factors of hepatitis delta virus (HDV) infection in Cameroon.DesignWe tested for hepatitis B virus (HBV) surface antigen (HBsAg) and anti-HDV antibody 14 150 samples collected during a survey whose participants were representative of the Cameroonian adult population. The samples had already been tested for hepatitis C virus and HIV antibodies.ResultsOverall, 1621/14 150 (weighted prevalence=11.9%) participants were HBsAg positive, among whom 224/1621 (10.6%) were anti-HDV positive. In 2011, the estimated numbers of HBsAg positive and HDV seropositives were 1 160 799 and 122 910 in the 15–49 years age group, respectively. There were substantial regional variations in prevalence of chronic HBV infection, but even more so for HDV (from 1% to 54%). In multivariable analysis, HDV seropositivity was independently associated with living with an HDV-seropositive person (OR=8.80; 95% CI: 3.23 to 24.0), being HIV infected (OR=2.82; 95% CI: 1.32 to 6.02) and living in the South (latitude <4°N) while having rural/outdoor work (OR=15.2; 95% CI: 8.35 to 27.6, when compared with living on latitude ≥4°N and not having rural/outdoor work).ConclusionWe found evidence for effective intra-household transmission of HDV in Cameroon. We also identified large differences in prevalence between regions, with cases concentrated in forested areas close to the Equator, as described in other tropical areas. The reasons underlying these geographical variations in HDV prevalence deserve further investigation.
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Bulut, Yasemin, Ibrahim Halil Bahcecioglu, Cem Aygun, Pinar Demirel Oner, Ibrahim Ozercan, and Kutbeddin Demirdag. "High genetic diversity of hepatitis delta virus in eastern Turkey." Journal of Infection in Developing Countries 8, no. 01 (2014): 074–78. http://dx.doi.org/10.3855/jidc.3910.
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Introduction: Hepatitis delta virus (HDV) is a serious cause of liver-related mortality in patients infected with hepatitis B virus (HBV). Determination of genotypes of HDV and phylogenetic analysis are important for better understanding the pathogenesis of the liver diseases associated with HBV infection. The aim of this study was to determine the genotype or genotypes of HDV among chronically infected patients with HBV in eastern Turkey. Methodology: A group of 113 patients infected with HBV and HDV were included in this study. The samples taken from the patients were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) and restriction enzyme cleavage. Results: According to the results of the restriction enzyme analysis, all of the RT-PCR products were determined to be HDV genotype I. Furthermore, for phylogenetic analysis and genotyping, 40 of HDV RT-PCR positive products were sequenced. Phylogenetic analysis of the sequences showed that all of the samples were infected with HDV genotype I. In addition, the results of the alignment analysis showed that the sequences of clinical samples were 82%-95% similar. Conclusion: These results indicate that high genetic diversity of the virus is possible in endemic areas such as Turkey.
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Wang, David, Joseph Pearlberg, Yu-Tsueng Liu, and Don Ganem. "Deleterious Effects of Hepatitis Delta Virus Replication on Host Cell Proliferation." Journal of Virology 75, no. 8 (2001): 3600–3604. http://dx.doi.org/10.1128/jvi.75.8.3600-3604.2001.
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ABSTRACT Hepatitis delta virus (HDV) infection and spread in vivo are dependent upon coinfection by hepatitis B virus (HBV), and dual HDV/HBV infection is frequently more severe than HBV infection alone, raising the possibility that HDV infection may be deleterious to cells. Here we have examined the effects of HDV replication on the long-term growth of cultured cells. Our results show that most cells transfected with HDV cDNA do not give rise to stable cell lines expressing viral antigens or replicative intermediates; in addition, cotransfection of HDV replicons with a plasmid vector expressing a hygromycin resistance marker results in a dose-dependent impairment of hygromycin-resistant colony formation. When cells transfected with replication-competent HDV cDNA are followed prospectively, a progressive decline in viral RNA replication and a steady decrease in the proportion of cells expressing delta antigen are observed. However, in transient transfection assays, no evidence was found to link HDV replication to apoptosis or to cell cycle arrest, nor did HDV replication confer on host cells enhanced sensitivity to inducers of apoptosis. Thus, HDV replication does not appear to be acutely cytotoxic. However, in dividing cells HDV replication is associated with a subtler growth disadvantage, leading to selection in culture for cells displaying diminished HDV expression. This effect would not be expected to cause hepatitis in vivo but might contribute to impaired liver regeneration in the setting of ongoing hepatocellular injury.
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Balmasova, I. P., R. I. Sepiashvili, T. A. Slavyanskaya, E. S. Malova, and Ya R. Sepiashvili. "COINFECTION BY HEPATITIS B AND HEPATITIS DELTA VIRUSES: MOLECULAR BIOLOGY OF PATHOGENS AND PROSPECTS OF PHARMACOTHERAPY." Journal of microbiology epidemiology immunobiology, no. 2 (April 28, 2018): 95–102. http://dx.doi.org/10.36233/0372-9311-2018-2-95-102.
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Hepatitis delta virus (HDV) is a defective virus and obligate companion of hepatitis B virus (HBV). The clinical significance of HDV and HBV coinfection is associated with more severe forms of acute or chronic viral hepatitis, a higher risk of developing liver cirrhosis and hepatocellular carcinoma compared to BGV-monoinfection. Current knowledge of the molecular biology of pathogens confirms the existence of a very complex relationship between the HBV, HDV, infected hepatocytes and cells of the immune system. Despite the fact that HBV viremia can now be controlled by using nucleoside analogues in the majority of patients, the problem of treating HDV and HBV coinfection is far from being resolved. Fundamental studies in recent years have led to significant progress in understanding the biology of HDV and provide the basis for the development and introduction into clinical practice highly effective antiviral drugs.
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Kose, Sukran, Gulfem Ece, Ayhan Gozaydin, and Melda Turken. "Study on seroprevalence of hepatitis delta in a regional hospital in western Turkey." Journal of Infection in Developing Countries 6, no. 11 (2012): 782–85. http://dx.doi.org/10.3855/jidc.1749.
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Introduction: Hepatitis delta virus (HDV) is an incomplete virus dependent on hepatitis B virus (HBV) for its multiplication. It can infect individuals with active HBV infection and cause severe liver disease. It is less prevalent than hepatitis B virus, but it causes more serious clinical pictures. In this study we investigated anti-HDV seroprevalance and epidemiological features among HBsAg seropositive outclinic patients at Izmir Tepecik Educational and Research Hospital. Methodology: Serum samples collected from outpatients at Izmir Tepecik Educational and Research Hospital between 1 September 2007 and 30 August 2009 were evaluated. Anti-HDV assay was performed by enzyme immunoassay (EIA). Patients over the age of fourteen who were referred to our hospital were taken into the study. Results: Out of 3,094 HBsAg positive patients, 79 (2.5%) had anti-HDV IgG seroprevalance. Of these 79 patients, 42 were hepatitis B carriers, 34 had chronic hepatitis B, two had liver cirrhosis, and one had hepatocellular carcinoma. Conclusion: Although superinfection and co-infection of HDV are less prevalent than hepatitis B infection, the prognosis is worse as the response to therapy is poor; therefore, patients with hepatitis B should be evaluated further for HDV infection.
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Casey, John L., and John L. Gerin. "Genotype-Specific Complementation of Hepatitis Delta Virus RNA Replication by Hepatitis Delta Antigen." Journal of Virology 72, no. 4 (1998): 2806–14. http://dx.doi.org/10.1128/jvi.72.4.2806-2814.1998.
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ABSTRACT Characterizations of genetic variations among hepatitis delta virus (HDV) isolates have focused principally on phylogenetic analysis of sequences, which vary by 30 to 40% among three genotypes and about 10 to 15% among isolates of the same genotype. The significance of the sequence differences has been unclear but could be responsible for pathogenic variations associated with the different genotypes. Studies of the mechanisms of HDV replication have been limited to cDNA clones from HDV genotype I, which is the most common. To perform a comparative analysis of HDV RNA replication in genotypes I and III, we have obtained a full-length cDNA clone from an HDV genotype III isolate. In transfected Huh-7 cells, the functional roles of the two forms of the viral protein, hepatitis delta antigen (HDAg), in HDV RNA replication are similar for both genotypes I and III; the short form is required for RNA replication, while the long form inhibits replication. For both genotypes, HDAg was able to support replication of RNAs of the same genotype that were mutated so as to be defective for HDAg production. Surprisingly, however, neither genotype I nor genotype III HDAg was able to support replication of such mutated RNAs of the other genotype. The inability of genotype III HDAg to support replication of genotype I RNA could have been due to a weak interaction between the RNA and HDAg. The clear genotype-specific activity of HDAg in supporting HDV RNA replication confirms the original categorization of HDV sequences in three genotypes and further suggests that these should be referred to as types (i.e., HDV-I and HDV-III) rather than genotypes.
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Miao, Zhijiang, Shaoshi Zhang, Xumin Ou, et al. "Estimating the Global Prevalence, Disease Progression, and Clinical Outcome of Hepatitis Delta Virus Infection." Journal of Infectious Diseases 221, no. 10 (2019): 1677–87. http://dx.doi.org/10.1093/infdis/jiz633.
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Abstract Background Hepatitis delta virus (HDV) coinfects with hepatitis B virus (HBV) causing the most severe form of viral hepatitis. However, its exact global disease burden remains largely obscure. We aim to establish the global epidemiology, infection mode-stratified disease progression, and clinical outcome of HDV infection. Methods We conducted a meta-analysis with a random-effects model and performed data synthesis. Results The pooled prevalence of HDV is 0.80% (95% confidence interval [CI], 0.63–1.00) among the general population and 13.02% (95% CI, 11.96–14.11) among HBV carriers, corresponding to 48–60 million infections globally. Among HBV patients with fulminant hepatitis, cirrhosis, or hepatocellular carcinoma, HDV prevalence is 26.75% (95% CI, 19.84–34.29), 25.77% (95% CI, 20.62–31.27), and 19.80% (95% CI, 10.97–30.45), respectively. The odds ratio (OR) of HDV infection among HBV patients with chronic liver disease compared with asymptomatic controls is 4.55 (95% CI, 3.65–5.67). Hepatitis delta virus-coinfected patients are more likely to develop cirrhosis than HBV-monoinfected patients with OR of 3.84 (95% CI, 1.79–8.24). Overall, HDV infection progresses to cirrhosis within 5 years and to hepatocellular carcinoma within 10 years, on average. Conclusions Findings suggest that HDV poses a heavy global burden with rapid progression to severe liver diseases, urging effective strategies for screening, prevention, and treatment.
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Sureau, Camille, Chantal Fournier-Wirth, and Patrick Maurel. "Role of N Glycosylation of Hepatitis B Virus Envelope Proteins in Morphogenesis and Infectivity of Hepatitis Delta Virus." Journal of Virology 77, no. 9 (2003): 5519–23. http://dx.doi.org/10.1128/jvi.77.9.5519-5523.2003.
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ABSTRACT Hepatitis delta virus (HDV) particles are coated with the large (L), middle (M), and small (S) hepatitis B virus envelope proteins. In the present study, we constructed glycosylation-defective envelope protein mutants and evaluated their capacity to assist in the maturation of infectious HDV in vitro. We observed that the removal of N-linked carbohydrates on the S, M, and L proteins was tolerated for the assembly of subviral hepatitis B virus (HBV) particles but was partially inhibitory for the formation of HDV virions. However, when assayed on primary cultures of human hepatocytes, virions coated with S, M, and L proteins lacking N-linked glycans were infectious. Furthermore, in the absence of M, HDV particles coated with nonglycosylated S and L proteins retained infectivity. These results indicate that carbohydrates on the HBV envelope proteins are not essential for the in vitro infectivity of HDV.
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Gudima, Severin, Shwu-Yuan Wu, Cheng-Ming Chiang, Gloria Moraleda, and John Taylor. "Origin of Hepatitis Delta Virus mRNA." Journal of Virology 74, no. 16 (2000): 7204–10. http://dx.doi.org/10.1128/jvi.74.16.7204-7210.2000.
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ABSTRACT Hepatitis delta virus (HDV) is unique relative to all known animal viruses, especially in terms of its ability to redirect host RNA polymerase(s) to transcribe its 1,679-nucleotide (nt) circular RNA genome. During replication there accumulates not only more molecules of the genome but also its exact complement, the antigenome. In addition, there are relatively smaller amounts of an 800-nt RNA of antigenomic polarity that is polyadenylated and considered to act as mRNA for translation of the single and essential HDV protein, the delta antigen. Characterization of this mRNA could provide insights into the in vivo mechanism of HDV RNA-directed RNA transcription and processing. Previously, we showed that the 5′ end of this RNA was located in the majority of species, at nt 1630. The present studies show that (i) at least some of this RNA, as extracted from the liver of an HDV-infected woodchuck, behaved as if it contained a 5′-cap structure; (ii) in the infected liver there were additional polyadenylated antigenomic HDV RNA species with 5′ ends located at least 202 nt and even 335 nt beyond the nt 1630 site, (iii) the 5′ end at nt 1630 was not detected in transfected cells, following DNA-directed HDV RNA transcription, in the absence of genome replication, and (iv) nevertheless, using in vitro transcription with purified human RNA polymerase II holoenzyme and genomic RNA template, we did not detect initiation of template-dependent RNA synthesis; we observed only low levels of 3′-end addition to the template. These new findings support the interpretation that the 5′ end detected at nt 1630 during HDV replication represents a specific site for the initiation of an RNA-directed RNA synthesis, which is then modified by capping.
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Vietheer, P. T. K., H. J. Netter, T. Sozzi, and A. Bartholomeusz. "Failure of the Lamivudine-Resistant rtM204I Hepatitis B Virus Mutants To Efficiently Support Hepatitis Delta Virus Secretion." Journal of Virology 79, no. 10 (2005): 6570–73. http://dx.doi.org/10.1128/jvi.79.10.6570-6573.2005.
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ABSTRACT Hepatitis delta virus (HDV) is encapsidated by the envelope proteins of hepatitis B virus (HBV). The major HBV lamivudine (LMV)-resistant mutations in the polymerase gene within the reverse transcriptase (rt) region at rtM204V or rtM204I are associated with changes in the overlapping envelope gene products, in particular, the gene encoding small envelope protein (s) at sI195M or sW196L/S/Stop. We have demonstrated that the LMV resistance mutations corresponding to sW196L/S inhibited secretion of HDV particles, while changes corresponding to sI195M did not affect secretion. Differential efficiencies of HBsAg proteins expressed by LMV-resistant HBV to support HDV secretion may have consequences for clinical prognosis as coinfected patients are treated with antiviral agents.
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Poisson, Véronique, Daniel B. Ménard, Éric Frost, and Jean-Pierre Perreault. "A Canadian Isolate of Hepatitis D (delta) Virus." Canadian Journal of Gastroenterology 14, suppl b (2000): 36B—41B. http://dx.doi.org/10.1155/2000/397947.
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HepatitisD(delta) virus (HDV) is an infectious agent that propagates in hepatocytes only in the presence of hepatitis B virus, causing fulminant or chronic hepatitis with liver cirrhosis. HDV is a 36 nm particle that includes a circular RNA genome of 1.7 kilobases with an extensive internal complementary that allows it to fold into a rod-like structure. The relationships among genotypes, sequence variability, geographical distribution and disease severity of HDV remain unknown. Consequently, in the present study, the complete nucleotide sequence of anHDVisolated from a Canadian patient was determined. The viral RNA from serum was amplified using reverse transcription coupled to polymerase chain reaction amplification. The resulting complementary DNA was cloned and sequenced. Sequence analysis revealed that this new isolate contained 1672 nucleotides corresponding to genotype 1, which has a worldwide distribution. Sequencing of four independent clones revealed 17 substitutions, corresponding to an overall sequence variability of 1%. Surprisingly, seven mutations were found in the 48-nucleotide region located between the two highly conserved self-catalytic motifs. This is the first demonstration that many substitutions are identified in this region of HDV, and prompts the present authors to define it as a hypervariable region.
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Troisi, CL, FB Hollinger, WK Hoots, et al. "A multicenter study of viral hepatitis in a United States hemophilic population." Blood 81, no. 2 (1993): 412–18. http://dx.doi.org/10.1182/blood.v81.2.412.412.
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Abstract Hemophilia A and B patients seen at nine US regional treatment centers were tested for serologic markers of hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV) during 1987 and 1988. Because human immunodeficiency virus (HIV) infection, a potentially confounding variable, was present in 53% of the group, the population was divided by HIV status for analysis purposes. In the HIV-positive group (N = 382), less than 1% had not been infected with HBV, HCV, or HDV, whereas 75% had evidence of infection with HBV and 98% with HCV. HBsAg, a marker of active HBV infection, was present in 12% of subjects; 96% of these were HCV positive. Anti-HDV was detected in 35 subjects (9.1%); all were anti-HBc positive. Ten of the 35 (29%) also were positive for IgM anti-HDV, indicating current infection. All 10 were HBsAg positive and 7 of the 9 tested were HDV RNA positive. Severe/moderate hemophilia B patients were more likely to have experienced an HBV infection and to be anti-HDV positive than were similar hemophilia A patients (22% v 8%, P < .05). In the HIV-negative group (N = 345), the subjects were younger and had less severe hemophilia than the HIV-positive patients. No evidence of HBV, HCV, or HDV infection was found in 18%, whereas 33% had experienced HBV infection and 79% were anti-HCV positive. Within this group, 4% were HBsAg positive. All 13 subjects with anti-HDV (4% of the HIV-negative group) also possessed anti-HBc. One (7.7%) was IgM anti-HDV positive and the serum from another contained HDV RNA. Both of these individuals were HBsAg positive. As in the HIV-positive group, severe/moderate hemophilia B patients were more likely to be HBV and HDV positive than were hemophilia A patients (9% v 3%, P < .05). A prevalence study of viral hepatitis in a large US hemophilic population showed that active infection with HCV is common, occurring in 89% of all study patients regardless of HIV status. Evidence of active HBV infection was found in 8%; 19% of these were actively infected with HDV. HDV was more common in hemophilia B patients after controlling for disease severity.
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Troisi, CL, FB Hollinger, WK Hoots, et al. "A multicenter study of viral hepatitis in a United States hemophilic population." Blood 81, no. 2 (1993): 412–18. http://dx.doi.org/10.1182/blood.v81.2.412.bloodjournal812412.
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Hemophilia A and B patients seen at nine US regional treatment centers were tested for serologic markers of hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV) during 1987 and 1988. Because human immunodeficiency virus (HIV) infection, a potentially confounding variable, was present in 53% of the group, the population was divided by HIV status for analysis purposes. In the HIV-positive group (N = 382), less than 1% had not been infected with HBV, HCV, or HDV, whereas 75% had evidence of infection with HBV and 98% with HCV. HBsAg, a marker of active HBV infection, was present in 12% of subjects; 96% of these were HCV positive. Anti-HDV was detected in 35 subjects (9.1%); all were anti-HBc positive. Ten of the 35 (29%) also were positive for IgM anti-HDV, indicating current infection. All 10 were HBsAg positive and 7 of the 9 tested were HDV RNA positive. Severe/moderate hemophilia B patients were more likely to have experienced an HBV infection and to be anti-HDV positive than were similar hemophilia A patients (22% v 8%, P < .05). In the HIV-negative group (N = 345), the subjects were younger and had less severe hemophilia than the HIV-positive patients. No evidence of HBV, HCV, or HDV infection was found in 18%, whereas 33% had experienced HBV infection and 79% were anti-HCV positive. Within this group, 4% were HBsAg positive. All 13 subjects with anti-HDV (4% of the HIV-negative group) also possessed anti-HBc. One (7.7%) was IgM anti-HDV positive and the serum from another contained HDV RNA. Both of these individuals were HBsAg positive. As in the HIV-positive group, severe/moderate hemophilia B patients were more likely to be HBV and HDV positive than were hemophilia A patients (9% v 3%, P < .05). A prevalence study of viral hepatitis in a large US hemophilic population showed that active infection with HCV is common, occurring in 89% of all study patients regardless of HIV status. Evidence of active HBV infection was found in 8%; 19% of these were actively infected with HDV. HDV was more common in hemophilia B patients after controlling for disease severity.
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Gudima, Severin, Yiping He, Ning Chai, et al. "Primary Human Hepatocytes Are Susceptible to Infection by Hepatitis Delta Virus Assembled with Envelope Proteins of Woodchuck Hepatitis Virus." Journal of Virology 82, no. 15 (2008): 7276–83. http://dx.doi.org/10.1128/jvi.00576-08.
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ABSTRACT Hepatitis B virus (HBV) and hepatitis delta virus (HDV) share the HBV envelope proteins. When woodchucks chronically infected with woodchuck hepatitis virus (WHV) are superinfected with HDV, they produce HDV with a WHV envelope, wHDV. Several lines of evidence are provided that wHDV infects not only cultured primary woodchuck hepatocytes (PWH) but also primary human hepatocytes (PHH). Surprisingly, HBV-enveloped HDV (hHDV) and wHDV infected PHH with comparable efficiencies; however, hHDV did not infect PWH. The basis for these host range specificities was investigated using as inhibitors peptides bearing species-specific pre-S (where S is the small envelope protein) sequences. It was found that pre-S1 contributed to the ability of wHDV to infect both PHH and PWH. In addition, the inability of hHDV to infect PWH was not overcome using a chimeric form of hHDV containing WHV S protein, again supporting the essential role of pre-S1 in infection of target cells. One interpretation of these data is that host range specificity of HDV is determined entirely by pre-S1 and that the WHV and HBV pre-S1 proteins recognize different receptors on PHH.
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Tseligka, Eirini D., Sophie Clément, and Francesco Negro. "HDV Pathogenesis: Unravelling Ariadne’s Thread." Viruses 13, no. 5 (2021): 778. http://dx.doi.org/10.3390/v13050778.
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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.
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Attiku, Keren, Joseph Bonney, Esinam Agbosu, et al. "Circulation of hepatitis delta virus and occult hepatitis B virus infection amongst HIV/HBV co-infected patients in Korle-Bu, Ghana." PLOS ONE 16, no. 1 (2021): e0244507. http://dx.doi.org/10.1371/journal.pone.0244507.
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Background Within HIV/HBV infected patients, an increase in HDV infection has been observed; there is inadequate information on HDV prevalence as well as virologic profile in Ghana. This study sought to determine the presence of HDV in HIV/HBV co-infected patients in Ghana. Methods This was a longitudinal purposive study which enrolled 113 HIV/HBV co-infected patients attending clinic at Korle-Bu Teaching Hospital (KBTH) in Accra, Ghana. After consenting, 5 mL whole blood was collected at two-time points (baseline and 4–6 months afterwards). The sera obtained were tested to confirm the presence of HIV, HBV antibodies and/or antigens, and HBV DNA. Antibodies and viral RNA were also determined for HDV. Amplified HBV DNA and HDV RNA were sequenced and phylogenetic analysis carried out with reference sequences from the GenBank to establish the genotypes. Results Of the 113 samples tested 63 (55.7%) were females and 50 (44.25%) were males with a median age of 45 years. A total of 100 (88.5%) samples had detectable HBV surface antigen (HBsAg), and 32 out of the 113 had detectable HBV DNA. Nucleotide sequences were obtained for 15 and 2 samples of HBV and HDV, respectively. Phylogenetic analysis was predominantly genotype E for the HBVs and genotype 1 for the HDVs. Of the 13 samples that were HBsAg unreactive, 4 (30.8%) had detectable HBV DNA suggesting the incidence of occult HBV infections. The percentage occurrence of HDV in this study was observed to be 3.54. Conclusion Our data suggest the presence and circulation of HDV and incidence of occult HBV infection in HIV/HBV co-infected patients in Ghana. This informs health staff and makes it imperative to look out for the presence of HDV and occult HBV in HIV/HBV co-infected patients presenting with potential risk of liver cancers and HBV transmission through haemodialysis and blood transfusions.
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RAMIA, S., M. EL-ZAATARI, A. I. SHARARA, F. RAMLAWI, and B. FARHAT. "Current prevalence of hepatitis delta virus (HDV) infection and the range of HDV genotypes in Lebanon." Epidemiology and Infection 135, no. 6 (2006): 959–62. http://dx.doi.org/10.1017/s0950268806007643.
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SUMMARYRecently the prevalence of hepatitis B virus (HBV) genotypes and the association between these genotypes and the clinical status of HBV-infected patients were recently investigated in the Lebanese population. The aim of the additional study reported here was to determine the current prevalence of hepatitis delta virus (HDV) infection and the range of HDV genotypes in this Lebanese population. Two hundred and fifty-eight HBsAg-positive patients (107 asymptomatic blood donors, 92 with chronic hepatitis, 24 with cirrhosis, 15 with hepatocellular carcinoma, 20 patients on haemodialysis) from ten medical centers in Lebanon were tested for antibody to hepatitis D virus (anti-HDV). Those testing positive were analysed further for HDV-RNA and for genotyping by reverse transcriptase–polymerase chain reaction (RT–PCR) and restriction fragment length polymorphism (RFLP). Three samples (1·2%) were anti-HDV positive and out of these, only one was HDV-RNA positive (0·6%) and was analysed as HDV genotype I. Our results point to a low endemicity of HDV in the Lebanese population which is in sharp contrast to data reported from Lebanon 20 years ago and to the situation in neighbouring Arab and non-Arab countries in the Mediterranean region. HDV genotype I seems to be the predominant genotype in Lebanon and the Middle East.
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Kuo, Yung-Bin, Mei Chao, Yi-Hsuan Lee, Chau-Ting Yeh, and Err-Cheng Chan. "New Enzyme-Linked Immunosorbent Assay for Detection of Antibodies against Hepatitis Delta Virus Using a Hepatitis Delta Antigen Derived from a Taiwanese Clone and Comparison to the Abbott Radioimmunoassay." Clinical and Vaccine Immunology 19, no. 5 (2012): 817–19. http://dx.doi.org/10.1128/cvi.05687-11.
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ABSTRACTAn anti-hepatitis delta (HD) enzyme-linked immunosorbent assay (ELISA) using a specific recombinant hepatitis delta antigen derived from a local dominant hepatitis delta virus (hepatitis D virus; HDV) strain in Taiwan has been established. The detection efficiency of this assay was comparable to that of the commercially available Abbott anti-HD radioimmunoassay (RIA) and could be useful in routine laboratory diagnoses of HDV infection.
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Williams, Virginie, Ségolène Brichler, Nadjia Radjef, et al. "Hepatitis delta virus proteins repress hepatitis B virus enhancers and activate the alpha/beta interferon-inducible MxA gene." Journal of General Virology 90, no. 11 (2009): 2759–67. http://dx.doi.org/10.1099/vir.0.011239-0.
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Co-infection and superinfection of hepatitis B virus (HBV) with hepatitis delta virus (HDV) leads to suppression of HBV replication both in patients and in animal and cellular models. The mechanisms behind this inhibition have not previously been explored fully. HBV replication is governed by four promoters and two enhancers, Enh1 and Enh2. Repression of these enhancers has been reported to be one of the main mechanisms of HBV inhibition. Moreover, in a previous study, it has been demonstrated that alpha interferon (IFN-α)-inducible MxA protein inhibits HBV replication. HDV encodes two proteins, p24 and p27. p27 was shown to activate several heterologous promoters, including HBV promoters. In an attempt to analyse the mechanisms of HBV inhibition by HDV, the question was raised whether HDV proteins could act directly by repressing HBV enhancers, and/or indirectly by activating the MxA gene. This issue was addressed in a co-transfection model in Huh-7 cells, using p24- or p27-expressing plasmids along with Enh1, Enh2, HBV and MxA promoter–luciferase constructs. Enh1 and Enh2 were strongly repressed, by 60 and 80 % and 40 and 60 %, by p24 and p27, respectively. In addition, p27 was responsible for threefold activation of the MxA promoter and potentiation of IFN-α on this promoter. MxA mRNA quantification and a virus yield reduction assay confirmed these results. In conclusion, this study shows that HDV proteins inhibit HBV replication by trans-repressing its enhancers and by trans-activating the IFN-α-inducible MxA gene.
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Chai, Ning, Ho Eun Chang, Emmanuelle Nicolas, Ziying Han, Michal Jarnik, and John Taylor. "Properties of Subviral Particles of Hepatitis B Virus." Journal of Virology 82, no. 16 (2008): 7812–17. http://dx.doi.org/10.1128/jvi.00561-08.
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ABSTRACT In the sera of patients infected with hepatitis B virus (HBV), in addition to infectious particles, there is an excess (typically 1,000- to 100,000-fold) of empty subviral particles (SVP) composed solely of HBV envelope proteins in the form of relatively smaller spheres and filaments of variable length. Hepatitis delta virus (HDV) assembly also uses the envelope proteins of HBV to produce an infectious particle. Rate-zonal sedimentation was used to study the particles released from liver cell lines that produced SVP only, HDV plus SVP, and HBV plus SVP. The SVP made in the absence of HBV or HDV were further examined by electron microscopy. They bound efficiently to heparin columns, consistent with an ability to bind cell surface glycosaminoglycans. However, unlike soluble forms of HBV envelope protein that were potent inhibitors, the SVP did not inhibit the ability of HBV and HDV to infect primary human hepatocytes.
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Gudima, Severin, Yiping He, Anja Meier, et al. "Assembly of Hepatitis Delta Virus: Particle Characterization, Including the Ability To Infect Primary Human Hepatocytes." Journal of Virology 81, no. 7 (2007): 3608–17. http://dx.doi.org/10.1128/jvi.02277-06.
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ABSTRACT Efficient assembly of hepatitis delta virus (HDV) was achieved by cotransfection of Huh7 cells with two plasmids: one to provide expression of the large, middle, and small envelope proteins of hepatitis B virus (HBV), the natural helper of HDV, and another to initiate replication of the HDV RNA genome. HDV released into the media was assayed for HDV RNA and HBV envelope proteins and characterized by rate-zonal sedimentation, immunoaffinity purification, electron microscopy, and the ability to infect primary human hepatocytes. Among the novel findings were that (i) immunostaining for delta antigen 6 days after infection with 300 genome equivalents (GE) per cell showed only 1% of cells as infected, but this was increased to 16% when 5% polyethylene glycol was present during infection; (ii) uninfected cells did not differ from infected cells in terms of albumin accumulation or the presence of E-cadherin at cell junctions; and (iii) sensitive quantitative real-time PCR assays detected HDV replication even when the multiplicity of infection was 0.2 GE/cell. In the future, this HDV assembly and infection system can be further developed to better understand the mechanisms shared by HBV and HDV for attachment and entry into host cells.
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Moraleda, Gloria, Kate Dingle, Preetha Biswas, et al. "Interactions between Hepatitis Delta Virus Proteins." Journal of Virology 74, no. 12 (2000): 5509–15. http://dx.doi.org/10.1128/jvi.74.12.5509-5515.2000.
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ABSTRACT The 195- and 214-amino-acid (aa) forms of the delta protein (δAg-S and δAg-L, respectively) of hepatitis delta virus (HDV) differ only in the 19-aa C-terminal extension unique to δAg-L. δAg-S is needed for genome replication, while δAg-L is needed for particle assembly. These proteins share a region at aa 12 to 60, which mediates protein-protein interactions essential for HDV replication. H. Zuccola et al. (Structure 6:821–830, 1998) reported a crystal structure for a peptide spanning this region which demonstrates an antiparallel coiled-coil dimer interaction with the potential to form tetramers of dimers. Our studies tested whether predictions based on this structure could be extrapolated to conditions where the peptide was replaced by full-length δAg-S or δAg-L, and when the assays were not in vitro but in vivo. Nine amino acids that are conserved between several isolates of HDV and predicted to be important in multimerization were mutated to alanine on both δAg-S and δAg-L. We found that the predicted hierarchy of importance of these nine mutations correlated to a significant extent with the observed in vivo effects on the ability of these proteins to (i) support intrans the replication of the HDV genome when expressed on δAg-S and (ii) act as dominant-negative inhibitors of replication when expressed on δAg-L. We thus infer that these biological activities of δAg depend on ordered protein-protein interactions.
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Abdukadyrova, M. A., S. M. Sharapov, and A. S. Khikmatullaeva. "HBsAg level as a predictor of disease activity in patients with chronic hepatitis B infection with delta-agent." Infekcionnye bolezni 18, no. 4 (2020): 149–52. http://dx.doi.org/10.20953/1729-9225-2020-4-149-152.
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We have conducted a pilot study to identify the association between the HBsAg level and activity of the pathological process in the liver, as well as possibility of quantitative assessment of HBsAg for monitoring chronic liver diseases caused by hepatitis B virus (HBV) and hepatitis D virus (HDV). Objective. To assess the possibility of using HBsAg levels as a predictor of disease activity and prognosis in patients with chronic HBV infection with delta-agent. Patients and methods. We analyzed serum specimens from 30 patients with HDV and HBV co-infection. Among 15 patients with chronic hepatitis B with delta-agent, there were 5 HBV DNA positive and 10 HBV DNA negative. Among patients with liver cirrhosis, HBV DNA was detected in 11 individuals, while 4 individuals had undetectable HBV DNA levels. Results. We found that mean HBsAg level in patients with chronic HBV infection and negative HBV DNA was 1.9 ± 0.56 IU/mL. Mean HBsAg level in patients with chronic HBV infection with delta-agent and positive HBV DNA was 4.3 ± 0.62 IU/mL (p < 0.05). High HBsAg levels correlated with elevated ALT in patients with chronic hepatitis B and delta-agent. Patients with liver cirrhosis caused by HDV had normal ALT levels, but elevated bilirubin concentrations regardless of HBV DNA presence and HBsAg level. Conclusion. High levels of HBsAg can be considered as a predictor of active disease in patients with chronic HBV infection with delta-agent and also a marker of transformation of chronic hepatitis B with delta-agent into liver cirrhosis. Key words: chronic hepatitis B with delta agent, liver cirrhosis, enzyme-linked immunosorbent assay, HBsAg levels, polymerase chain reaction
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TURCANU, Adela, and Suhaib TAHIR WANI. "Chronic delta hepatitis: from discovery to new treatments." One Health & Risk Management 2, no. 2 (2021): 19–26. http://dx.doi.org/10.38045/ohrm.2021.2.03.
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Introduction. Hepatitis delta virus (HDV) is a small, defective RNA virus that is related more to plant viroids than to other human pathogens. 
 Material and methods. Nearly 50 research articles from various sources were reviewed and a comprehensive analysis was done regarding various parameters concerning HDV. Articles published over a period of 30 years were selected based on their experimental and statistical relevance to HDV. This review gives a brief insight into epidemiology, genetics, clinical evolution and treatment of chronic hepatitis delta.
 Results. Chronic hepatitis delta remains a major cause of morbidity in Eastern European countries and the Mediterranean region. At the same time, there is a resurgence of HBV and HDV infection in young people (under the age of 50) in Western Europe, as a consequence of the intra-familial and sexual mode of acquisition among immigrants from Eastern Europe, the Mediterranean region and from countries of the former Soviet Union, Africa high burdened regions of Asia and South America. Prevalence among IVDU was found to be higher especially in western european countries and other regions of low HDV prevalence. Chronic delta viral hepatitis is a dynamic, progressive process. A direct cytopathic pattern of liver tissue damage was also observed, especially in the presence of HDV genotype 3. Chronic hepatitis D is reported to progress to cirrhosis and hepatocellular cancer, and this trend is greater the higher the level of HDV viremia at the time of presentation.
 Conclusions. Flaws in screening and on-time diagnosis still remain due to the insufficient research and data available. While still not classified as a carcinogen by IARC, our review ends up in support of the notion that HDV infection increases the chances and fastens the pathogenic processes leading to HCC.
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KONDILI, L. A., M. E. TOSTI, M. SZKLO, et al. "The relationships of chronic hepatitis and cirrhosis to alcohol intake, hepatitis B and C, and delta virus infection: a case-control study in Albania." Epidemiology and Infection 121, no. 2 (1998): 391–95. http://dx.doi.org/10.1017/s0950268898001216.
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The present study examined the effect of hepatitis B virus (HBV) and alcohol intake, and the role of hepatitis delta virus (HDV) and hepatitis C virus (HCV) in the aetiology of chronic liver disease in Albania. A total of 106 cases of liver cirrhosis or chronic hepatitis were compared to 195 control patients without these or other liver diseases. Adjusted odds ratios were 52·7 (95% CI 22·7–122) for HBV surface antigen, 26·9 (95% CI 4·9–147) for anti-HCV, 26·2 (95% CI 3·1–221) for anti-HDV, 2.4 (95% CI 1·3–4·4) for lifetime alcohol intake and 2·3 (95% CI 1–5·5) for duration of alcohol intake. Although not significant, an interaction was suggested between HBsAg and anti-HCV and between HBsAg and alcohol intake. Our study underlines the role of hepatitis viruses in the development of chronic liver diseases. Additionally, it suggests that heavy alcohol intake may magnify the effect of HBV on these diseases. HBV vaccination and alcohol abstention appear to be important strategies to reduce the risk of liver cirrhosis and chronic hepatitis in Albania.
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Dingle, Kate, Vadim Bichko, Harmon Zuccola, James Hogle, and John Taylor. "Initiation of Hepatitis Delta Virus Genome Replication." Journal of Virology 72, no. 6 (1998): 4783–88. http://dx.doi.org/10.1128/jvi.72.6.4783-4788.1998.
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ABSTRACT The small, 195-amino-acid form of the hepatitis delta virus (HDV) antigen (δAg-S) is essential for genome replication, i.e., for the transcription, processing, and accumulation of HDV RNAs. To better understand this requirement, we used purified recombinant δAg-S and HDV RNA synthesized in vitro to assemble high-molecular-weight ribonucleoprotein (RNP) structures. After transfection of these RNPs into human cells, we detected HDV genome replication, as assayed by Northern analysis or immunofluorescence microscopy. Our interpretation is that the input δAg-S is necessary for the RNA to undergo limited amounts of RNA-directed RNA synthesis, RNA processing, and mRNA formation, leading to de novo translation of δAg-S. It is this second source of δAg-S which then goes on to support genome replication. This assay made it possible to manipulate in vitro the composition of the RNP and then test in vivo the ability of the complex to initiate RNA-directed RNA synthesis and go on to achieve genome replication. For example, both genomic and antigenomic linear RNAs were acceptable. Substitution for δAg-S with truncated or modified forms of the δAg, and even with HIV nucleocapsid protein and polylysine, was unacceptable; the exception was a form of δAg-S with six histidines added at the C terminus. We expect that further in vitro modifications of these RNP complexes should help define the in vivo requirements for what we define as the initiation of HDV genome replication.
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Oliveira, Marcelo Siqueira de, Romeu Paulo Martins Silva, Suiane da Costa Negreiros do Valle, Elisabeth Níglio de Figueiredo, and Dayana Fram. "Chronic hepatitis B and D: prognosis according to Child-Pugh score." Revista Brasileira de Enfermagem 70, no. 5 (2017): 1048–53. http://dx.doi.org/10.1590/0034-7167-2016-0205.
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ABSTRACT Objective: compare chronic hepatitis B patients to those superinfected with hepatitis D virus, according to Child-Pugh score regarding disease severity. Method: retrospective descriptive study, performed with 59 patients followed in the ambulatory, of which 22 (37.3%) were chronically infected with hepatitis B virus (Group HBV) and 37 (62.7%) superinfected with Delta virus (Group HBV+HDV); variables of sex, age and items of Child-Pugh score were collected by consulting medical records. Results: out of the patients, 57.6% were male, with a mean age of 30.5 years. Score A, which indicates lesser severity, was found in 100% of group HBV and 78.4% of group HBV+HDV. Score B, which indicates greater severity, was found only in group HBV+HDV in 21.6% of the patients. Conclusion: by means of the Child-Pugh score, it was observed that patients with superinfection by HDV tended to present a worse prognosis.
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Botelho-Souza, Luan Felipo, Deusilene Souza Vieira, Alcione de Oliveira dos Santos, André Vinycius Cunha Pereira, and Juan Miguel Villalobos-Salcedo. "Characterization of the Genotypic Profile of Hepatitis Delta Virus: Isolation of HDV Genotype-1 in the Western Amazon Region of Brazil." Intervirology 58, no. 3 (2015): 166–71. http://dx.doi.org/10.1159/000431040.
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The hepatitis delta virus (HDV) is a hepatotropic subvirus that is dependent on the hepatitis B virus (HBV) and supplies the viral envelope containing the surface antigen of hepatitis B. Viral genetic diversity is related to the geographical origin of the isolates, and there are at least eight genotypes that are referred to as HDV-1 through HDV-8. HDV-3 is responsible for epidemics of severe and fulminant hepatitis, which are common in northeastern South America. HDV-3 is prevalent in the Brazilian Amazon and is associated with the increased aggressiveness of HDV infections. Although isolated, the characteristics of the clinical presentation of HDV-1 in the Amazon region have not yet been clearly reported. Objective: This study aims to assess the genotypic and clinical characteristics of individuals with the HDV-1 genotype in the western Amazon region. Methods: The HDV was genotyped by nested PCR-RFLP and sequencing from serum samples of 56 patients with HBV/HDV infection. The genotypes were correlated with the clinical characteristics presented by patients with HBV/HDV infection. Results: A prevalence of 92.3% for the HDV-3 genotype (n = 48) and 7.6% (n = 4) for the HDV-1 genotype was observed. Conclusion: To date, this is the most extensive clinical study of HDV-1 genotype infections in the nonindigenous population of Western Amazonia.
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Gudima, Severin, Anja Meier, Roland Dunbrack, John Taylor, and Volker Bruss. "Two Potentially Important Elements of the Hepatitis B Virus Large Envelope Protein Are Dispensable for the Infectivity of Hepatitis Delta Virus." Journal of Virology 81, no. 8 (2007): 4343–47. http://dx.doi.org/10.1128/jvi.02478-06.
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ABSTRACT Previous studies have attempted to clarify the roles of the pre-S1 and pre-S2 domains of the large envelope protein of hepatitis B virus (HBV) in attachment and entry into susceptible cells. Difficulties arise in that these domains contain regions involved in the nucleocapsid assembly of HBV and overlapping with the coding regions of the viral polymerase and RNA sequences required for reverse transcription. Such difficulties can be circumvented with hepatitis delta virus (HDV), which needs the HBV large envelope protein only for infectivity. Thus, mutated HBV envelope proteins were examined for their effects on HDV infectivity. Changing the C-terminal region of pre-S1 critical for HBV assembly allowed the envelopment of HDV and had no effect on infectivity in primary human hepatocytes. Similarly, a deletion of the 12 amino acids of a putative translocation motif (TLM) in pre-S2 had no effect. Thus, these two regions are not necessary for HDV infectivity and, by inference, are not needed for HBV attachment and entry into susceptible cells.
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Dziri, Samira, Christophe Rodriguez, Athenaïs Gerber, et al. "Variable In Vivo Hepatitis D Virus (HDV) RNA Editing Rates According to the HDV Genotype." Viruses 13, no. 8 (2021): 1572. http://dx.doi.org/10.3390/v13081572.
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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.
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Macnaughton, Thomas B., and Michael M. C. Lai. "Large Hepatitis Delta Antigen Is Not a Suppressor of Hepatitis Delta Virus RNA Synthesis once RNA Replication Is Established." Journal of Virology 76, no. 19 (2002): 9910–19. http://dx.doi.org/10.1128/jvi.76.19.9910-9919.2002.
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ABSTRACT Moderation of hepatitis delta virus (HDV) replication is a likely prerequisite in the establishment of chronic infections and is thought to be mediated by the intracellular accumulation of large hepatitis delta antigen (L-HDAg). The regulatory role of this protein was suggested from several studies showing that cotransfection of plasmid cDNAs expressing both L-HDAg and HDV RNA results in a potent inhibition of HDV RNA replication. However, since this approach differs significantly from natural HDV infections, where HDV RNA replication is initiated from an RNA template, and L-HDAg appears only late in the replication cycle, it remains unclear whether L-HDAg can modulate HDV RNA replication in the natural HDV replication cycle. In this study, we investigated the effect of L-HDAg, produced as a result of the natural HDV RNA editing event, on HDV RNA replication. The results showed that following cDNA-free HDV RNA transfection, a steady-state level of RNA was established at 3 to 4 days posttransfection. The same level of HDV RNA was reached when a mutant HDV genome unable to make L-HDAg was used, suggesting that L-HDAg did not play a role. The rates of HDV RNA synthesis, as measured by metabolic labeling experiments, were identical at 4 and 8 days posttransfection and in the wild type and the L-HDAg-deficient mutant. We further examined the effect of overexpression of L-HDAg at various stages of the HDV replication cycle, showing that HDV RNA synthesis was resistant to L-HDAg when it was overexpressed 3 days after HDV RNA replication had initiated. Finally, we showed that, contrary to conventional thinking, L-HDAg alone, at a certain molar ratio with HDV RNA, can initiate HDV RNA replication. Thus, L-HDAg does not inherently inhibit HDV RNA synthesis. Taken together, these results indicated that L-HDAg affects neither the rate of HDV RNA synthesis nor the final steady-state level of HDV RNA and that L-HDAg is unlikely to act as an inhibitor of HDV RNA replication in the natural HDV replication cycle.
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Ouedraogo, Henri G., Seni Kouanda, Sara Goodman, et al. "Hepatitis B, C and Delta Viruses’ Infections and Correlate Factors Among Female Sex Workers in Burkina Faso, West-Africa." Open Virology Journal 13, no. 1 (2019): 9–17. http://dx.doi.org/10.2174/1874357901913010009.
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Background:Female Sex Workers (FSW) have increased vulnerability to viral hepatitis B, C and D transmission. Our study aimed to assess the seroprevalence of hepatitis B, C and D viruses and their associated factors among FSW in Ouagadougou, Burkina Faso.Methods:This is a cross-sectional study among FSW at least 18 years old in Ouagadougou, Burkina Faso. Data were collected from February 2013 to May 2013 using Respondent-Driven Sampling (RDS). Hepatitis B, C, and D tests were performed on FSW storage serums using fourth generation ELISA kits. Survey-weighted bivariate and multivariate logistic regression analyses were performed using Stata version 14 to identify factors associated with viral hepatitis infections.Results:Population-weighted prevalence of viral hepatitis infections in FSW was respectively 18.2% (95%CI: 14.4-22.9) for Hepatitis B Virus (HBV), 10.6% (95%CI: 07.5-14.8) for Hepatitis C Virus (HCV) and 1.5% (95Cl: 0.2-10.3) for Hepatitis D Virus (HDV). Factors independently associated with HCV include positive HIV status, inconsistent condom use during the last 12 months, condom reuse with clients, sex with clients in the street, bars or public gardens. No sociodemographic or behavioral factors were independently associated with HBV infection.Conclusion:The prevalence of HBV and HCV was high among FSW and the prevalence of HDV was relatively low in this group in Burkina Faso. These findings suggest urgent and comprehensive prevention of these viruses through education for safer sex and behaviors, and immunization against HBV for FSW.
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Brindle, R. J., R. P. Eglin, A. J. Parsons, A. V. S. Hill, and J. B. Selkon. "HTLV-1, HIV-1, hepatitis B and hepatitis delta in the Pacific and South-East Asia: a serological survey." Epidemiology and Infection 100, no. 1 (1988): 153–56. http://dx.doi.org/10.1017/s095026880006564x.
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SUMMARYBlood samples from 13 locations in the Pacific and South-East Asia were tested for evidence of infection with human T-cell lymphotropic virus type-1 (HTLV-1), human immunodeficiency virus (HIV-1), hepatitis B virus (HBV) and hepatitis delta virus (HDV). No samples were positive for antibody to HIV-1. Antibodies to HTLV-1 were found in samples from five locations, the maximum prevalence being 19%, in Vanuatu. Serological markers of HBV infection were found in all locations, the maximal prevalence being 88%, in Majuro, Micronesia. Antibodies to HDV in HBsAg positive sera were found in six locations with a maximum prevalence of 81% in Kiribati.
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Casey, John, Paul J. Cote, Illia A. Toshkov, et al. "Clevudine Inhibits Hepatitis Delta Virus Viremia: a Pilot Study of Chronically Infected Woodchucks." Antimicrobial Agents and Chemotherapy 49, no. 10 (2005): 4396–99. http://dx.doi.org/10.1128/aac.49.10.4396-4399.2005.
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ABSTRACT In a small controlled study, clevudine, a potent inhibitor of hepadnaviruses, including hepatitis B virus and woodchuck hepatitis virus, suppressed hepatitis delta virus (HDV) viremia in chronically infected woodchucks. Suppression was correlated with the marked reduction of woodchuck hepatitis virus surface antigen in individual animals, consistent with the concept that repression of surface antigen expression may be a useful antiviral strategy for HDV.
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Defenbaugh, Dawn A., Matthew Johnson, Renxiang Chen, Ying Yi Zheng, and John L. Casey. "Hepatitis Delta Antigen Requires a Minimum Length of the Hepatitis Delta Virus Unbranched Rod RNA Structure for Binding." Journal of Virology 83, no. 9 (2009): 4548–56. http://dx.doi.org/10.1128/jvi.02467-08.
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ABSTRACT Hepatitis delta virus (HDV) is a subviral pathogen that increases the severity of liver disease caused by hepatitis B virus. Both the small circular RNA genome and its complement, the antigenome, form a characteristic unbranched rod structure in which approximately 70% of the nucleotides are base paired. These RNAs are associated with the sole virally encoded protein, hepatitis delta antigen (HDAg), in infected cells; however, the nature of the ribonucleoprotein complexes (RNPs) is not well understood. Previous analyses of binding in vitro using native, bacterially expressed HDAg have been hampered by a lack of specificity for HDV RNA. Here, we show that removal of the C-terminal 35 amino acids of HDAg yields a native, bacterially expressed protein, HDAg-160, that specifically binds HDV unbranched rod RNA with high affinity. In an electrophoretic mobility shift assay, this protein produced a discrete, micrococcal nuclease-resistant complex with an ∼400-nucleotide (nt) segment of HDV unbranched rod RNA. Binding occurred with several segments of HDV RNA, although with various affinities and efficiencies. Analysis of the effects of deleting segments of the unbranched rod indicated that binding did not require one or two specific binding sites within these RNA segments. Rather, a minimum-length HDV RNA unbranched rod approximately 311 nt was essential for RNP formation. The results are consistent with a model in which HDAg binds HDV unbranched rod RNA as multimers of fixed size rather than as individual subunits.
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Hoan, Nghiem Xuan, Mirjam Hoechel, Alexandru Tomazatos, et al. "Predominance of HBV Genotype B and HDV Genotype 1 in Vietnamese Patients with Chronic Hepatitis." Viruses 13, no. 2 (2021): 346. http://dx.doi.org/10.3390/v13020346.
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Hepatitis delta virus (HDV) coinfection will additionally aggravate the hepatitis B virus (HBV) burden in the coming decades, with an increase in HBV-related liver diseases. Between 2018 and 2019, a total of 205 HBV patients clinically characterized as chronic hepatitis B (CHB; n = 115), liver cirrhosis (LC; n = 21), and hepatocellular carcinoma (HCC; n = 69) were recruited. HBV surface antigen (HBsAg), antibodies against surface antigens (anti-HBs), and core antigens (anti-HBc) were determined by ELISA. The presence of hepatitis B viral DNA and hepatitis delta RNA was determined. Distinct HBV and HDV genotypes were phylogenetically reconstructed and vaccine escape mutations in the “a” determinant region of HBV were elucidated. All HBV patients were HbsAg positive, with 99% (n = 204) and 7% (n = 15) of them being positive for anti-HBc and anti-HBs, respectively. Anti-HBs positivity was higher among HCC (15%; n = 9) compared to CHB patients. The HBV-B genotype was predominant (65%; n = 134), followed by HBV-C (31%; n = 64), HBV-D, and HBV-G (3%; n = 7). HCC was observed frequently among young individuals with HBV-C genotypes. A low frequency (2%; n = 4) of vaccine escape mutations was observed. HBV-HDV coinfection was observed in 16% (n = 33) of patients with the predominant occurrence of the HDV-1 genotype. A significant association of genotypes with alanine aminotransferase (ALT) and aspartate aminotransferase (AST) enzyme levels was observed in HBV monoinfections. The prevalence of the HDV-1 genotype is high in Vietnam. No correlation was observed between HDV-HBV coinfections and disease progression when compared to HBV monoinfections.