Academic literature on the topic 'HDV (Hepatitis delta virus)'

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Journal articles on the topic "HDV (Hepatitis delta virus)"

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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