Relevant bibliographies by topics / Hepatitis E virus (HEV)

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Academic literature on the topic 'Hepatitis E virus (HEV)'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 June 2025

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Journal articles on the topic "Hepatitis E virus (HEV)"

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Makiala-Mandanda, Sheila, Frédéric Le Gal, Nadine Ngwaka-Matsung, et al. "High Prevalence and Diversity of Hepatitis Viruses in Suspected Cases of Yellow Fever in the Democratic Republic of Congo." Journal of Clinical Microbiology 55, no. 5 (2017): 1299–312. http://dx.doi.org/10.1128/jcm.01847-16.

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ABSTRACTThe majority of patients with acute febrile jaundice (>95%) identified through a yellow fever surveillance program in the Democratic Republic of Congo (DRC) test negative for antibodies against yellow fever virus. However, no etiological investigation has ever been carried out on these patients. Here, we tested for hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV) viruses, all of which can cause acute febrile jaundice, in patients included in the yellow fever surveillance program in the DRC. On a total of 498 serum samples collected from suspected cases of yellow fever from January 2003 to January 2012, enzyme-linked immunosorbent assay (ELISA) techniques were used to screen for antibodies against HAV (IgM) and HEV (IgM) and for antigens and antibodies against HBV (HBsAg and anti-hepatitis B core protein [HBc] IgM, respectively), HCV, and HDV. Viral loads and genotypes were determined for HBV and HVD. Viral hepatitis serological markers were diagnosed in 218 (43.7%) patients. The seroprevalences were 16.7% for HAV, 24.6% for HBV, 2.3% for HCV, and 10.4% for HEV, and 26.1% of HBV-positive patients were also infected with HDV. Median viral loads were 4.19 × 105IU/ml for HBV (range, 769 to 9.82 × 109IU/ml) and 1.4 × 106IU/ml for HDV (range, 3.1 × 102to 2.9 × 108IU/ml). Genotypes A, E, and D of HBV and genotype 1 of HDV were detected. These high hepatitis prevalence rates highlight the necessity to include screening for hepatitis viruses in the yellow fever surveillance program in the DRC.
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Takahashi, Masaharu, Tsutomu Nishizawa, Yuhko Gotanda, et al. "High Prevalence of Antibodies to Hepatitis A and E Viruses and Viremia of Hepatitis B, C, and D Viruses among Apparently Healthy Populations in Mongolia." Clinical Diagnostic Laboratory Immunology 11, no. 2 (2004): 392–98. http://dx.doi.org/10.1128/cdli.11.2.392-398.2004.

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ABSTRACT The prevalence of infection with hepatitis A virus (HAV), HBV, HCV, HDV, and HEV was evaluated in 249 apparently healthy individuals, including 122 inhabitants in Ulaanbaatar, the capital city of Mongolia, and 127 age- and sex-matched members of nomadic tribes who lived around the capital city. Overall, hepatitis B surface antigen (HBsAg) was detected in 24 subjects (10%), of whom 22 (92%) had detectable HBV DNA. Surprisingly, HDV RNA was detectable in 20 (83%) of the 24 HBsAg-positive subjects. HCV-associated antibodies were detected in 41 (16%) and HCV RNA was detected in 36 (14%) subjects, none of whom was coinfected with HBV, indicating that HBV/HCV carriers account for one-fourth of this population. Antibodies to HAV and HEV were detected in 249 (100%) and 28 (11%) subjects, respectively. Of 22 HBV DNA-positive subjects, genotype D was detected in 21 subjects and genotype F was detected in 1 subject. All 20 HDV isolates recovered from HDV RNA-positive subjects segregated into genotype I, but these differed by 2.1 to 11.4% from each other in the 522- to 526-nucleotide sequence. Of 36 HCV RNA-positive samples, 35 (97%) were genotype 1b and 1 was genotype 2a. Reflecting an extremely high prevalence of hepatitis virus infections, there were no appreciable differences in the prevalence of hepatitis virus markers between the two studied populations with distinct living place and lifestyle. A nationwide epidemiological survey of hepatitis viruses should be conducted in an effort to prevent de novo infection with hepatitis viruses in Mongolia.
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Ilchenko, L. Yu, I. A. Morozov, T. V. Kozhanova, N. V. Soboleva, L. I. Melnikova, and I. V. Kruglova. "The Frequency of Hepatitis Virus Infection Markers Among Highly Qualified Sportsmen." Russian Archives of Internal Medicine 10, no. 4 (2020): 305–13. http://dx.doi.org/10.20514/2226-6704-2020-10-4-305-313.

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Study Objective is to evaluate prevalence of hepatitis A, B, C, E, and TT virus infection markers in highly qualified sportsmen. Study Design: multicenter open single-site clinical study.Materials and Methods: 100 blood serum samples of sportsmen (game, complex coordination, technical, etc.) were studied. Biological material (blood serum) was obtained from 54 men and 46 women aged 16 to 45 years during an in-depth medical examination. All sportsmen filled out a questionnaire, including demographic data, description of the sport, information about infection risk factors, information about the presence of acute viral hepatitis and vaccination. Anti-HAV IgG, HBsAg, anti-HBcore, anti-HCV, anti-HEV IgG, anti-HEV IgM were determined in the blood serum by enzyme immunoassay; using polymerase chain reaction — DNA Anelloviridae (TTV, TTMDV, TTMV). Study Results: Anti-HAV IgG was detected in 57/66 (86,4%) sportsmen, women (91,2%) predominated, among them a third were engaged in synchronized swimming. 7/57 (12,3%) of the examined had indications of vaccination against hepatitis A. The frequency of anti-HEV IgG did not exceed 3% (2/66). anti-HEV IgM were not detected in any case. Also, none of the examined sportsmen in the blood serum was not determined HBsAg. However, anti-HBcore (marker of latent HBV infection) was detected in 13% (13/100) of the samples. The detection rate of anti-HCV was low, combined with the presence of anti-HBcore was 2% (2/100). In addition, DNA TTV, TTMDV and TTMV, respectively, were found in serum samples from 66/100 (86%), 79/100 (79%), 71/100 of sportsmen. Conclusion: The high frequency of hepatitis virus markers was found (HAV — 74,1%, TTV/TTMDV /TTMV — 71-86%), HBV — 13%, HEV — 3%, HCV — 2%). All patients denied a history of acute viral hepatitis. Vaccination against hepatitis A and B is a modern strategy that prevents infection and the development of acute viral hepatitis. Its mandatory holding should become part of the targeted preparation of sportsmen to achieve the highest sports results.
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Vasickova, P., I. Psikal, P. Kralik, F. Widen, Z. Hubalek, and I. Pavlik. "Hepatitis E virus: a review." Veterinární Medicína 52, No. 9 (2008): 365–84. http://dx.doi.org/10.17221/1999-vetmed.

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The hepatitis E virus (HEV), the causative agent of hepatitis E, is a non-enveloped RNA virus. The HEV genome is formed by a non-segmented positive-sense RNA chain. The 3´end of the chain is polyadenylated and the 5´end is structurally characterised by the so called “capping”. According to currently accepted taxonomy, HEV is classified in the genus <i>Hepevirus</i>, the only member of the Hepeviridae family. HE is usually transmitted via the faecal-oral route due to the fact that drinking water or water for industrial purposes is contaminated due to poor sanitation. This spread of HEV has been reported in developing countries of Asia, Africa, South and Central America. However, cases in countries with the sporadic occurrence of HEV have been associated with travelling to countries with an increased risk of infection (developing countries in Asia, Africa and America). HEV infections have subsequently been described in people who have not travelled to endemic countries. Further studies of the HEV suggested other routes of transmission and a zoonotic potential of the virus (pigs and deer as the potential source of human infection).
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Chu, Chia-Ming, Chau-Ting Yeh, and Yun-Fan Liaw. "Viral Superinfection in Previously Unrecognized Chronic Carriers of Hepatitis B Virus with Superimposed Acute Fulminant versus Nonfulminant Hepatitis." Journal of Clinical Microbiology 37, no. 1 (1999): 235–37. http://dx.doi.org/10.1128/jcm.37.1.235-237.1999.

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The role of viral superinfection in hepatitis B surface antigen carriers with superimposed fulminant (n = 60) versus nonfulminant (n = 90) acute hepatitis was studied. The frequency of hepatitis A virus (HAV) (0 versus 2.2%), HCV (18.3 versus 21.1%), HDV (15.0 versus 7.8%), and HEV (1.7 versus 4.4%) infection showed no significant difference, while simultaneous HCV and HDV infection was significantly more prevalent in the former (8.3 versus 0%). Only 3.6% of fulminant cases and 3.3% of nonfulminant controls were HGV RNA positive.
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Pinho, João R. R., Paolo M. De A. Zanotto, João L. P. Ferreira, et al. "High Prevalence of GB Virus C in Brazil and Molecular Evidence for Intrafamilial Transmission." Journal of Clinical Microbiology 37, no. 5 (1999): 1634–37. http://dx.doi.org/10.1128/jcm.37.5.1634-1637.1999.

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The prevalence of GB virus C (GBV-C) in candidate Brazilian blood donors with normal and elevated alanine aminotransferase levels was found to be 5.2% (5 of 95) and 6.5% (5 of 76), respectively. Among Brazilian patients, GBV-C was found in 9.5% (13 of 137) of cases of hepatitis not caused by hepatitis A virus (HAV), HBV, HCV, HDV, or HEV (non-A-E hepatitis) and in 18.2% (8 of 44) of individuals infected with HCV. Molecular characterization of GBV-C by partial sequencing of the NS3 region showed clustering between members of a single family, implying intrafamilial transmission. In conclusion, these results together suggest that contagion mechanisms which facilitate intrafamilial transmission of GBV-C may partially explain the high prevalence of viremic carriers worldwide.
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Horvatits, Thomas, Julian Schulze zur Wiesch, Susanne Polywka, et al. "Significance of Anti-Nuclear Antibodies and Cryoglobulins in Patients with Acute and Chronic HEV Infection." Pathogens 9, no. 9 (2020): 755. http://dx.doi.org/10.3390/pathogens9090755.

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Background: Hepatitis E virus (HEV) has been associated with immunological phenomena. Their clinical significance, however, still needs to be clarified, that is, whether cryoglobulins or autoantibodies impact overt disease in HEV-infected individuals. To better understand, we analyzed these different immune phenomena in three cohorts, each representing different types of HEV infection. Methods: The cohorts included: (i) immunocompetent patients with acute hepatitis E, (ii) immunosuppressed patients with chronic hepatitis E, and (iii) individuals with asymptomatic HEV infection. Together, they consisted of 57 individuals and were studied retrospectively for the presence of anti-nuclear antibodies (ANAs), cryoglobulins, and serum total IgG. They were then compared with a control cohort of 17 untreated patients with chronic hepatitis B virus (HBV) infection or hepatitis C virus (HCV) infection. Results: Thirteen (23%) were immunocompetent patients with acute hepatitis E (median alanine aminotransferase (ALT) = 872 U/L), 15 (26%) were immunosuppressed patients with chronic hepatitis E (median ALT = 137 U/L), and 29 (51%) were blood donors with asymptomatic HEV infection (median ALT = 35 U/L). Overall, 24% tested positive for elevated ANA titers of >1:160, and 11% presented with a specific ANA pattern. ANA detection was not associated with the type of HEV infection, IgG levels, sex, or age. All individuals tested negative for anti-mitochondrial antibodies, anti-neutrophil cytoplasmic antibodies, liver-kidney microsomal antibodies, anti-myeloperoxidase-, and anti-proteinase-3 antibodies. Five patients (9%) tested positive for cryoglobulins. Notably, cryoglobulinemia was present in overt hepatitis E (Groups (i) and (ii); one acute and four chronic HEV infections), but was not present in any of the asymptomatic blood donors (p = 0.02). The frequency of cryoglobulins and elevated ANAs did not differ significantly between HEV and HBV/HCV patients. Conclusion: In line with findings on HBV and HCV infections, we frequently observed detection of ANAs (24%) and cryoglobulins (9%) in association with HEV infections. The presence of cryoglobulins was limited to patients with overt hepatitis E. We add to the findings on the immune phenomena of hepatitis E.
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Rawat, Sarita, P. S. Gill, Tanuj Gupta, Praveen Malhotra, and Aparna Parmar. "Prevalence of hepatitis A virus and hepatitis E virus in the patients presenting with acute viral hepatitis in Rohtak, Haryana, India." International Journal of Research in Medical Sciences 7, no. 5 (2019): 1792. http://dx.doi.org/10.18203/2320-6012.ijrms20191678.

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Background: Hepatitis A virus (HAV) and hepatitis E virus (HEV) cause acute hepatitis in humans and are transmitted mainly through the fecal-oral route. They pose major health problems in developing countries. This study was done to determine prevalence of HAV and HEV in patients presenting with AVH and the co-infection of HAV and HEV in these patients.Methods: The study was conducted in the virology research and diagnostic laboratory, PGIMS Rohtak during the study period of August 2017-December 2018. The study population included sera of individuals from all age group who were suspected of acute viral hepatitis (AVH). All the sera were screened for IgM antibody to HEV and HAV using IgM capture ELISA.Results: HEV IgM ELISA test was performed in 307 patients (mean age 34 years;), with an overall seroprevalence rate of 138(44.9%). HAV antibodies were detected in 109 subjects, with a median age of 9.5 years the seroprevalence of HAV was 34 (31.1%). HEV seropositivity was highest in the age group 20-30 years. Mean age was 34 years whereas the interquartile range was from 14-71 years. HAV infection was positive mainly in the age group <10 years. With interquartile range from 6-16 years. Out of total 34 patients positive for HAV infection males were 20 (58.8%), whereas females were 14(41.1%). HEV IgM was positive in 138 patients, out of which male were 96 (69.56%) and females were 42 (30.43%). HEV IgM was positive in 138 patients, out of which male were 96 (69.56%) and females were 42 (30.43%). HAV and HEV seen to be prevalent all with highest predominance seen towards the end of monsoons (August and September) and beginning of winters.Conclusions: The present study also points toward HEV being the prime etiological agent for outbreaks of acute hepatitis in the studied region of Haryana (Rohtak), India. A comparatively lower HAV prevalence may be the consequence of an overall declining trend due to improved living standards and environmental hygiene.
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Chandra, Nidhi S., Durbadal Ojha, Sanjoy Chatterjee, and Debprasad Chattopadhyay. "Prevalence of hepatitis E virus infection in West Bengal, India: a hospital-based study." Journal of Medical Microbiology 63, no. 7 (2014): 975–80. http://dx.doi.org/10.1099/jmm.0.072249-0.

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India is an endemic zone for hepatitis E virus (HEV), which is associated with both epidemic and sporadic infections. In West Bengal, only two hepatitis E outbreaks have been studied to date. However, sporadic cases of HEV infection also occur during inter-epidemic periods. The aim of this hospital-based study was to detect the prevalence of HEV infection in patients with acute sporadic hepatitis in West Bengal, India. Blood samples and clinical information were collected from 285 patients of both sexes and different ages with acute viral hepatitis (AVH) at Calcutta Medical College, Kolkata, a tertiary-care centre. Samples were tested for hepatitis B virus (HBV) surface antigen, anti-hepatitis C virus antibodies, anti-hepatitis A virus IgM and anti-HEV antibodies (IgM and IgG) by ELISA. Only those patients with AVH who were in their first week of illness and negative for all hepatotropic viral antibodies were tested for HEV RNA by reverse transcriptase nested PCR. HEV was identified as the most common cause of AVH (41.8 % of patients), followed by HBV (21.4 %), hepatitis A virus (17.2 %) and hepatitis C virus (4.6 %). Co-infections with more than one virus were found in 22 patients, with HBV–HEV the most common co-infection (3.8 %). Only 14.7 % of patients had no viral marker. To the best of our knowledge, this is the first documented epidemiological study of acute sporadic hepatitis with HEV in the state of West Bengal, India, indicating that this state is an endemic zone for HEV infection.
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Sarker, Nihar Ranjan, Santosh Kumar Saha, Dilip Kumar Ghosh, Alpana Adhikary, Alamin Mridha, and Md Razibul Alam. "Seropositivity of hepatitis viral markers in icteric children." Bangladesh Medical Journal 43, no. 1 (2014): 26–29. http://dx.doi.org/10.3329/bmj.v43i1.21373.

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Viral hepatitis is a major public health problem in the world affecting millions of children every year despite the availability of vaccines, prophylactic measures and improved sanitation. The prevalence of infection varies from country to country and within countries, having a close association with behavioral, environmental, host factors. This study was an attempt to evaluate the sero-prevalence rate of various viral hepatitis markers of 50 icteric children who attended pediatric outpatient department of Shaheed Suhrawardy Medical College Hospital from January 2010 to December 2010. All the patients were screened for HAV, HEV, HBV, HCV. Anti HAV IgM were positive in in 65.22 %, Anti HEV IgM in 34.78 % and HBsAg in 4% of icteric children. None of the icteric children were positive for hepatitis C virus. Most of the icteric children presented with fever, anorexia and nausea /vomiting. This study shows high rate of HAV and HEV infection among icteric children DOI: http://dx.doi.org/10.3329/bmj.v43i1.21373 Bangladesh Med J. 2014 January; 43 (1): 26-29
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Dissertations / Theses on the topic "Hepatitis E virus (HEV)"

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Huang, Fang-Fang. "Molecular Characterization of Animal Strains of Hepatitis E Virus (HEV): Avian HEV and Swine HEV." Diss., Virginia Tech, 2004. http://hdl.handle.net/10919/29893.

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Hepatitis E virus (HEV), the causative agent of hepatitis E, is an important public health concern in many developing countries. It mainly infects young adults and has a mortality of up to 25% in pregnant women. Although hepatitis E is only sporadic in industrialized countries including the United States, a relative high seroprevalence rate has been reported in healthy individuals. Evidence suggests that there exist animal reservoirs for HEV and HEV transmission is zoonotic. Animal strains of HEV, swine HEV and avian HEV have been identified from a pig and a chicken, respectively, in the United States. Studies showed that swine HEV and avian HEV are genetically and antigenically related to human HEV, and that pigs and chickens are useful animal models to study HEV replication, pathogenesis and cross-species infection. The objectives of this dissertation were to genetically characterize both avian HEV and swine HEV, to determine their serological and molecular epidemiology in the United States, to assess the ability of avian HEV cross-species infection in non-human primates, to determine the full-length genomic sequence and genome organization, and to construct an infectious cDNA clone of avian HEV. The prevalence of swine HEV infections in US swine herds and the heterogeneity of swine HEV isolates from different geographic regions of the United States were determined. We found that 35% pigs and 54% swine herds were positive for swine HEV RNA. Partial capsid gene region of twenty-seven US swine HEV isolates was sequenced and was showed to share 88%-100% nucleotide sequence identity to each other and 89-98% identity with the prototype US swine HEV, but only <79% identity with Taiwanese swine HEV isolates and most known human strains of HEV worldwide. All US swine HEV isolates belong to the same genotype 3 with the prototype US swine HEV and the two US strains of human HEV. Similarly, the prevalence of avian HEV infections in US chicken flocks and the heterogeneity of avian HEV isolates were also determined. Helicase gene region of eleven field isolates of avian HEV from chickens with hepatitis-splenomegaly (HS) syndrome was sequenced and was found to share 78-100% nucleotide sequence identities with each other, 79-88% identities with the prototype avian HEV, 76-80% identities with Australian chicken big liver and spleen disease virus (BLSV), and 56-61% identities with other known strains of mammalian HEV. A relative high prevalence of anti-avian HEV antibodies was found in apparently healthy chicken flocks in 5 states. Like swine HEV, the seropositivity of avian HEV in adult chickens was higher than that in young chickens. To genetically characterize the avian HEV genome, we determined the full-length genomic sequence of avian HEV, which is 6,654 bp in length excluding the poly (A) tail, and 600 bp shorter than that of mammalian HEVs. Avian HEV has similar genomic organization with human and swine HEVs, but shared only about 50% nucleotide sequence identity with mammalian HEVs in the complete genome. Significant genetic variations such as deletions and insertions, particularly in the ORF1 of avian HEV, were observed, but motifs in the putative functional domains of the ORF1 were relatively conserved between avian HEV and mammalian HEVs. Phylogenetic analyses based on the full-length genomic sequence revealed that avian HEV represents a branch distinct from human and swine HEVs. Since swine HEV infects non-human primates and possibly humans, the ability of avian HEV cross-species infection in non-human primates was also assessed. However, unlike swine HEV, avian HEV failed to infect two rhesus monkeys under experimental conditions. With the availability of the complete genome sequence of avian HEV, we constructed three full-length cDNA clones of avian HEV and tested their infectivity by in vitro transfection of the LMH chicken liver cells and by in vivo intrahepatic inoculation of specific-pathogen-free (SPF) chickens. The results showed that all 3 cDNA clones of avian HEV were infectious both in vitro and in vivo, as the capped RNA transcripts from each of the clones were replication-competent in transfected LMH cells and developed active infection in inoculated SPF chickens. In summary, avian HEV and swine HEV infections are enzootic in chicken flocks and in swine herds in the United States, respectively. Like human HEV, swine HEV and avian HEV isolates from different geographic regions are also genetically heterogenic. Complete genomic sequence analyses showed that avian HEV is related to, but distinct from, human and swine HEVs. Unlike swine HEV, avian HEV is probably not transmissible to non-human primates. Infectious cDNA clones of avian HEV have been successfully constructed. The availability of the infectious clones for a chicken strain of HEV now affords us an opportunity to study the mechanisms of HEV replication, pathogenesis and cross-species infection.
Ph. D.
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Yadav, Kush Kumar. "Genotype 1 hepatitis E virus (HEV) ORF4 protein enhances genotype 3 HEV replication." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1574781581580768.

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Ferreira, Ariana Carolina. "Pesquisa de marcadores sorológicos e moleculares da infecção pelo Vírus da Hepatite E (HEV) em indivíduos portadores do Vírus da Imunodeficiência Humana (HIV)." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-30062016-115114/.

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A infecção pelo HEV é reconhecida como um considerável problema de saúde pública em diversas regiões do mundo. Embora caracterizada como uma infecção benigna com um curso evolutivo autolimitado, recentes estudos têm mostrado sua evolução para cronicidade em indivíduos imunocomprometidos. Além disso, tem sido verificado que nesses indivíduos a infecção crônica pelo HEV pode evoluir para fibrose hepática progressiva, culminando com o desenvolvimento de cirrose. Não existem dados acerca da prevalência da infecção pelo HEV em pacientes infectados pelo HIV no Brasil, onde a circulação deste vírus tem sido demonstrada em diversos grupos de indivíduos imunocompetentes e, até mesmo, em alguns animais provenientes de diferentes regiões do país. Com base nisso, este trabalho teve como objetivo estimar a prevalência de marcadores sorológicos e moleculares da infecção pelo HEV, bem como a padronização de uma PCR em tempo real para a detecção e quantificação da carga viral do HEV na população de soropositivos da cidade de São Paulo. Foram incluídos neste estudo soro e plasma de pacientes infectados pelo HIV (n=354), que foram divididos em grupos de acordo com a presença ou ausência de coinfecção pelos vírus das hepatites B (HBV) e C (HCV). Essas amostras foram coletadas entre 2007 e 2013. Anticorpos anti-HEV IgM e IgG foram pesquisados pela técnica de ELISA (RecomWell HEV IgM/ IgG - MIKROGEN®), e, em alguns casos, confirmados por Immunoblotting (RecomLine HEV IgM/ IgG - MIKROGEN®). Todas as amostras foram submetidas à pesquisa de HEV RNA através da PCR em tempo real padronizada. Cerca de 72% dos indivíduos avaliados pertenciam ao sexo masculino. A média de idade entre a população analisada foi de 48,4 anos. Os anticorpos anti-HEV IgM e IgG foram encontrados em 1,4% e 10,7% dos indivíduos dessa população, respectivamente. Apenas dois pacientes apresentaram positividade simultânea para anti-HEV IgM e IgG. Não houve diferença estatisticamente relevante quanto à presença de marcadores sorológicos nos grupos de estudo. Além disso, foi detectado o HEV RNA em 10,7% das amostras analisadas, entre as quais, seis apresentaram simultaneamente algum marcador sorológico (5 anti-HEV IgG e 1 IgM). A presença deste marcador foi predominante no grupo de pacientes com coinfecção pelo HCV. Através deste trabalho pôde-se constatar, portanto, que o HEV é circulante entre a população de infectados pelo HIV em São Paulo, e que o seguimento desses pacientes se faz necessário dado a possibilidade de progressão para infecção crônica e cirrose
HEV infection is recognized as a significant public health problem in different world regions. Although initially characterized as a benign infection with selflimited course, recent studies have showing its evolution to chronicity in immunocompromised individuals. Furthermore, in these individuals the chronic infection can develop progressive liver fibrosis leading to cirrhosis. There are no data regarding prevalence of HEV infections in HIV- infected patients in Brazil, where the circulation of this virus has been demonstrated in different individuals groups and in some animals from different regions of the country. Based on this, this study aimed to assess the prevalence of serological and molecular makers of HEV infection and the standardization of real-time PCR for the detection and quantification of HEV viral load in HIV-infected individuals in São Paulo. Serum and plasma samples of HIV-infected patients (n=354), collected between 2007 and 2013, were included and organized in groups of co-infection (HIV/ HBV, HIV/HCV and HIV/ HBV/ HCV) and HIV mono-infection. Antibodies anti-HEV IgM and IgG were detected by ELISA (RecomWell HEV IgM/ IgG - MIKROGEN®), and in some cases confirmed by immunoblotting (RecomLine HEV IgM/ IgG - MIKROGEN®). All samples were submitted to research HEV RNA by real-time PCR. About 72% of the patients were male. The mean age of this population was 48.4 years. The anti-HEV IgM and IgG antibodies were found in 1.4% and 10.7%, respectively. Only two patients presented simultaneous anti-HEV IgM and anti- HEV IgG. There was no statistically significant difference in the presence of serological makers among the HIV infection groups. In addition, HEV RNA was detected in 10.7% of samples and six of these samples presented simultaneously a serological maker (5 anti-HEV IgG and 1 IgM). The presence of this maker was more frequent in the co-infection HIV/ HCV group. Through this work, we observed that HEV is circulating among the HIV-infected population in São Paulo, and the monitoring these patients is necessary because of the possibility progression to chronic infection and cirrhosis
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Billam, Padma. "Mechanism of Pathogenesis and Replication of an Avian Strain of the Hepatitis E Virus in a Chicken Model." Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/27382.

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Hepatitis E is an acute, enterically transmitted disease of public health importance. The mechanism of pathogenesis of HEV is poorly understood due to the lack of an in vitro cell culture system and an ideal animal model system. With the discovery of avian HEV and its association with a hepatic disease (Hepatitis-Splenomegaly syndrome), chickens provide an excellent small homologous animal model system to study this important virus. The objectives of this dissertation were to utilize chickens as a model system to study the pathogenesis and replication of avian HEV under the natural route of infection, to identify potential extrahepatic replication sites, to determine and analyze the complete genomic sequence of the avirulent strain of avian HEV, and to study the compartive pathogenesis of the two isolates of avian HEV, the prototype pathogenic and avirulent strains of avian HEV. We attempted to experimentally infect specific-pathogen-free (SPF) adult chickens by the natural fecal-oral route in order to systematically study HEV pathogenesis and replication and to characterize the clinical course and pathological lesions associated with avian HEV infection. Sixty-week-old, specific-pathogen-free (SPF) chickens were inoculated with 5 x104.5 50% chicken infectious dose of avian HEV by oronasal route and IV route. All oronasally- and IV- inoculated chickens had seroconverted to avian HEV antibodies and fecal virus shedding was detected variably from 1 to 20 DPI in the IV group, and from 10 to 56 DPI in the oronasal group. Avian HEV RNA was detected in serum, bile, and liver samples earlier during the course of infection in IV-inoculated chickens than in oronasally-inoculated ones. Gross liver lesions including subcapsular hemorrhages and enlargement of right intermediate lobe and microscopic hepatic lesions in the liver characterized by lymphocytic periphlebitis and phlebitis were observed in inoculated chickens. This is the first report of experimental HEV infection via its natural route in a homologous animal model system. Very little is known about HEV pathogenesis and it has been hypothesized that HEV replicates in tissues other than liver. The replicating negative-strand viral RNA was detected by negative-strand-specific RT-PCR in liver, serum, colon, cecum, jejunum, ileum, duodenum and cecal tonsils,but not in other non-GIT tissues. Immunohistochemistry using an avian HEV capsid protein-specific anti-peptide antibody revealed positive signal in liver and GIT tissues including colon, jejunum, ileum, cecum, cecal tonsils and pancreas. The detection of avian HEV capsid antigen and replicative negative-strand viral RNA in the GIT tissues indicates that HEV replicates in the GI tract following infection by fecal-oral route. The complete genomic sequence of an avirulent strain of avian HEV was determined using primer walking strategy. The full-length genome of the avirulent strain is 6649 nts in length and has a nucleotide sequence identity of 90.1% with the prototype pathogenic strain. Numerous non-silent mutations were observed in ORF1, the region coding for the nonstructural proteins. Six unique non-silent mutations were identified in the capsid-encoding ORF2 region and the ORF3 had four non-silent mutations. Phylogenetic analysis based on full-length genomic sequence revealed that the avirulent strain is clustered together with the pathogenic avian HEV and represents a branch distinct from mammalian HEVs. In order to study the comparative pathogenesis between the pathogenic and avirulent strains of avian HEV, an infectious stock of the avirulent avian HEV was generated and infectivity titer was determined to be 5 x 102.5 CID50 per ml by experimentally infecting young SPF chickens. Six-week-old SPF chickens were inoculated with one of two strains of avian hepatitis E viruses, pathogenic avian HEV recovered from a chicken with HS syndrome and avirulent avian HEV isolated from a healthy chicken to study comparative pathogenesis. Most of the chickens seroconverted by 3 wpi in both pathogenic avian HEV and avirulent avian HEV groups. Avian HEV RNA was detected in feces and serum of the chickens from both the inoculated group from 1 wpi. Microscopic liver lesions included lymphocytic periphlebitis and phlebitis the overall hepatic lesion mean score was higher for the pathogenic avian HEV group compared to the avirulent avian HEV and control groups, suggestive of attenuation In summary, SPF chickens were experimentally infected with avian HEV by natural route to study the systematic pathogenesis and replication. Non-liver replication sites of avian HEV were also identified in a chicken model. The complete genomic sequence of an apparently avirulent strain of avian hepatitis E virus was determined and the comparative pathogenesis of avian hepatitis E virus isolates from a chicken with HS syndrome and from a healthy chicken was also studied by experimental infections in young SPF chickens. The results from this dissertation research have important implications for the understanding of HEV pathogenesis.
Ph. D.
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Sun, Zhifeng. "Cross-Species Infection and Characterization of Avian Hepatitis E Virus." Diss., Virginia Tech, 2005. http://hdl.handle.net/10919/26049.

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As novel or variant strains of HEV continue to evolve rapidly both in humans and other animals, it is important to develop a rapid pre-sequencing screening method to select field isolates for further molecular characterization. Two heteroduplex mobility assays (HMA) were developed to genetically differentiate field strains of swine HEV and avian HEV from known reference strains. It was shown that the HMA profiles generally correlate well with nucleotide sequence identities and with phylogenetic clustering between field strains and the reference swine HEV or avian HEV strains. Therefore, by using different HEV isolates as references, the HMA developed in this study can be used as a pre-sequencing screening tool to identify variant HEV isolates for further molecular epidemiological studies. Our previous study showed that avian HEV antibody is prevalent in apparently healthy chickens. A prospective study was conducted on a known seropositive but healthy chicken farm. Avian HEV was identified from the healthy chicken flock. Avian HEV isolates recovered from the healthy chicken share 70-97% nucleotide sequence identities with those isolates which cause hepatitis-splenomegaly (HS) syndrome based on partial helicase and capsid gene regions. Recovery of identical viruses from the experimentally inoculated chickens in the subsequent transmission study further confirmed our field results. The capsid gene of avian HEV isolates from chickens with HS syndrome were also characterized and found to be heterogeneic, with 76-100% nucleotide sequence identities to each other. The study indicates that avian HEV is enzootic in chicken flocks and spread subclinically among chicken populations, and that the virus is heterogeneic. As HEV can not be propagated in vitro, in order to further characterize avian HEV, an infectious viral stock with a known infectious titer must be generated. Bile and feces collected from specific-pathogen-free (SPF) chickens experimentally infected with avian HEV were used to prepare an avian HEV infectious stock. The infectivity titer of this infectious stock was determined, by intravenously inoculating one-week old SPF chickens, to be 5 x 104.5 50% chicken infectious doses (CID₅₀) per ml. Seroconversion, viremia as well as fecal virus shedding were observed in the inoculated chickens. Contact control chickens also became infected via direct contact with inoculated ones. Avian HEV infection in chickens was found to be dose-dependent. To determine if avian HEV can infect across species, one-week old SPF turkeys were intravenously inoculated each with 104.5(CID₅₀) of avian HEV. The inoculated turkeys seroconverted to avian HEV antibodies at 4-8 weeks postinoculation (WPI). Viremia was detected at 2-6 WPI, and fecal virus shedding at 4-7 WPI in inoculated turkeys. This is the first demonstration of cross-species infection by avian HEV. Little is known regarding the characteristics of the small ORF3 protein largely due to the lack of a cell culture system for HEV. To characterize the small protein, the ORF3 proteins of avian HEV and swine HEV were expressed in Escherchia coli, and purified by BugBuster His-Bind Purification System. Western blot analysis showed that avian HEV ORF3 protein is unique and does not share common antigenic epitopes with those of swine HEV and human HEV. However, swine HEV (genotype 3) and human HEV (genotype 1) ORF3 proteins cross-react with each other antigenically. To determine if the ORF3 protein is a virion protein, infectious stocks of avian HEV and swine HEV were first generated in SPF chickens and pigs, respectively. Virions were subsequently purified by sucrose density gradient centrifugation and virion proteins were characterized by SDS-PAGE and Western blot analysis. Two major forms of ORF2 proteins of avian HEV were identified: a 56 kDa and an 80 kDa proteins. Multiple immunoreactive forms of ORF2 proteins of swine HEV were also observed: 40 kDa, 53 kDa, 56 kDa and 72 kDa. However, the ORF3 protein was not detected from the native virions of avian HEV or swine HEV. These findings provide direct evidence that ORF2 indeed encodes a structural protein of HEV, whereas ORF3 does not. To search for other potential animal reservoirs for HEV, the prevalence of IgG anti-HEV antibody was determined in field mice caught in chicken farms to assess the possibility of mice as a potential reservoir for HEV infection in chickens. Three different recombinant HEV antigens derived from avian HEV, swine HEV, and human HEV were used in the ELISA assays. The anti-HEV seropositive rates in wild field mice (Mus musculus), depending upon the antigen used, are 15/76 (20%), 39/74 (53%), and 43/74 (58%), respectively. HEV RNA was also detected from 29 fecal and/or serum samples of mice. The HEV sequences recovered from field mice shared 72-100% nucleotide sequence identities with each other, 73-99% sequence identities with avian HEV isolates, and 51-60% sequence identities with representative strains of swine and human HEVs. However, attempts to experimentally infect laboratory mice (Mus musculus) with the PCR-positive fecal materials recovered from the wild field mice were unsuccessful. We also attempted to experimentally infect 10 Wistar rats each with avian HEV, swine HEV, and an US-2 strain of human HEV, respectively. However, the inoculated rats did not become infected as evidenced by the lack of viremia, virus shedding in feces or seroconversion. These data suggest that mice caught in chicken farms are infected by a HEV-like virus, but additional work is needed to determine the origin of the mouse virus as well as the potential role of rodents in HEV transmission. In summary, we developed two HMAs which are useful for differentiation and identification of variant strains of swine and avian HEVs. We genetically identified and characterized an avian HEV strain from apparently healthy chickens in seropositive flocks. We showed that avian HEV can cross species barriers and infect turkeys. Our data indicated that avian and swine HEV ORF2 genes encode structural proteins, whereas ORF3 genes do not. Evidence in this study also showed that HEV or HEV-like agent exists in field mice on a chicken farm.
Ph. D.
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Sanford, Brenton Joel. "Cross-protection and Potential Animal Reservoir of the Hepatitis E Virus." Diss., Virginia Tech, 2012. http://hdl.handle.net/10919/77133.

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HEV is an important public health concern due largely to water-borne outbreak. Recent research confirms individual cases of zoonotic transmission due to human exposure to contaminated animal meats. At least four recognized and two putative genotypes of mammalian HEV have been reported: genotypes 1 and 2 are restricted to humans whereas genotypes 3 and 4 are zoonotic. In addition to humans, strains of HEV have been genetically identified from pigs, chickens, rats, mongoose, deer, rabbits and fish. The current experimental vaccines are all based on a single strain of HEV, even though multiple genotypes of HEV are co-circulating in some countries and thus an individual may be exposed to more than one genotype. Therefore, it is important to know if prior infection with a genotype 3 swine HEV will confer protective immunity against subsequent exposure to genotypes 3 and 4 human and swine HEV. In the first study, specific-pathogen-free pigs were divided into 4 groups of 6 each. Pigs in the three treatment groups were each inoculated with a genotype 3 swine HEV, and 12 weeks later, challenged with the same genotype 3 swine HEV, a genotype 3 human HEV, and a genotype 4 human HEV, respectively. Sera from all pigs were tested for HEV RNA and IgG anti-HEV, and fecal samples were also tested for HEV RNA each week. The pigs inoculated with swine HEV became infected as evidenced by fecal virus shedding and viremia, and the majority of pigs also developed IgG anti-HEV prior to challenge at 12 weeks post-inoculation. After challenge, viremia and fecal virus shedding of challenge viruses were not detected, suggesting that prior infection with a genotype 3 swine HEV prevented pigs from developing viremia and fecal virus shedding after challenge with homologous and heterologous genotypes 3 and 4 HEV, respectively. Immunogenic epitopes are located within the open reading frame 2 (ORF 2) capsid protein and recombinant ORF 2 antigens are capable of preventing HEV infection in non-human primates and chickens. In the second study we expressed and purified N-truncated ORF 2 antigens based on swine, rat, and avian HEV strains. Thirty pigs were randomly divided into groups of 6 pigs each and initially vaccinated with 200µg swine ORF 2 antigen, rat ORF 2 antigen, avian ORF 2 antigen, or PBS buffer (positive and negative control groups) and booster with the same vaccine 2 weeks later. At 4 wks, after confirming seroconversion to IgG anti-HEV antibody with ELISA, all groups except the negative control were challenged with swine genotype 3 HEV (administered intravenously). The protective and cross-protective abilities of these antigens were determined following swine genotype 3 challenge by evaluating both serum and fecal samples for HEV RNA using nested RT-PCR and IgG anti-HEV using ELISA. The results from these two studies have important implications for future development of an effective HEV vaccine. As a part of our ongoing efforts to search for potential animal reservoirs for HEV, we tested goats from Virginia for evidence of HEV infection and showed that 16% (13/80) of goat sera from Virginia herds were positive for IgG anti-HEV. Importantly, we demonstrated that selected goat sera were capable of neutralizing HEV in cell culture. Subsequently, in an attempt to genetically identify the HEV-related agent from goats, we conducted a prospective study in a closed goat herd with known anti-HEV seropositivity and monitored a total of 11 kids from the time of birth until 14 weeks of age for evidence of HEV infection. Seroconversion to IgG anti-HEV was detected in 7 out of the 11 kids, although repeated attempts to detect HEV RNA by a broad-spectrum nested RT-PCR from the fecal and serum samples of the goats that had seroconverted were unsuccessful. In addition, we also attempted to experimentally infect laboratory goats with three well-characterized mammalian strains of HEV but with no success. The results indicate that a HEV-related agent is circulating and maintained in the goat population in Virginia and that the goat HEV is likely genetically very divergent from the known HEV strains.
Ph. D.
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Feagins, Alicia R. "Foodborne Transmission and Molecular Mechanism of Cross-species Infection of Hepatitis E Virus (HEV)." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/77266.

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Hepatitis E virus (HEV), the causative agent of hepatitis E, is an emerging virus of global distribution. At least four distinct genotypes of HEV exist worldwide: genotype 1 and 2 HEV strains are responsible for waterborne epidemics; genotype 3 and 4 HEV strains are responsible for sporadic occurrences of acute hepatitis E. Genotype 3 and 4 HEVs are zoonotic and have a more expanded host range than genotypes 1 and 2 which are restricted to humans. Genotype 3 and 4 HEV isolates obtained from animal tissues are genetically very similar, or identical in some cases, to human HEV recovered from hepatitis E patients. The objectives of this dissertation research were to assess the zoonotic foodborne transmission of HEV and elucidate the viral determinants of HEV host range. To determine the risk of HEV foodborne transmission, 127 packages of commercial pig liver were tested for HEV RNA. Eleven percent of them were positive for HEV RNA and the contaminating virus remained infectious. We also demonstrated that medium-to-rare cooking condition (56°C) does not completely inactivate HEV, although frying and boiling of the contaminated livers inactivated the virus. To reduce the risk of foodborne HEV transmission, commercial pig livers must be thoroughly cooked for consumption. To determine the host range of genotype 4 HEVs, pigs were inoculated with a genotype 4 human HEV. All pigs developed an active HEV infection indicating that genotype 4 human HEVs can cross species barriers and infect pigs. To identify viral determinant(s) of species tropism, ORF2 alone or in combination with its adjacent 5′ junction region (JR) and 3′ non-coding region (NCR), were swapped between genotypes 1 and 4, 3 and 4, and 1 and 3 to produce 5 chimeric viruses. Chimeric viruses containing ORF2 or JR+ORF2+3' NCR from genotype 4 human HEV in the backbone of genotype 3 swine HEV were viable in vitro and infectious in vivo. Chimeric viruses containing the JR+ORF2+3'NCR of genotypes 3 or 4 HEV in the backbone of genotype 1 human HEV were viable in vitro but non-infectious in pigs, suggesting that ORF1 may also be important for host range.
Ph. D.
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Guo, Hailong. "Antigenic epitope composition and protectivity of avian hepatitis E virus (avian HEV) ORF2 protein and vertical transmission of avian HEV." [Ames, Iowa : Iowa State University], 2006.

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Williams, Peter John. "Hepatitis E virus in South Africa : seroprevalence of anti-HEV IgG in swine and detection of the virus in swine faecal specimens and domestic sewage samples." Diss., University of Pretoria, 2004. http://hdl.handle.net/2263/28441.

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Asante, Mark. "Hepatitis E-virus (HEV) comparative evaluation of IgG antibody assays in a low-endemicity setting /." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=970784708.

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Books on the topic "Hepatitis E virus (HEV)"

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Mathet, Verónica L. Genetic diversity & variability of hepatitis B virus (HBV). Nova Science Publishers, 2008.

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Mathet, Verónica L. Genetic diversity & variability of hepatitis B virus (HBV). Nova Science Publishers, 2009.

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United States. Occupational Safety and Health Administration. Enforcement procedures for occupational exposure to Hepatitis B Virus (HBV) and Human Immunodeficiency Virus (HIV). U.S. Dept. of Labor, Assistant Secretary for Occupational Safety and Health, 1988.

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Administration, United States Occupational Safety and Health. Enforcement procedures for occupational exposure to hepatitis B virus (HBV) and human immunodeficiency virus (HIV). U.S. Dept. of Labor, Assistant Secretary for Occupational Safety and Health, 1990.

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United States. Occupational Safety and Health Administration. Enforcement procedures for occupational exposure to hepatitis B virus (HBV) and human immunodeficiency virus (HIV). U.S. Dept. of Labor, Assistant Secretary for Occupational Safety and Health, 1990.

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Honig, Robert E. A review of public and private programs that test for the human immunodeficiency virus (HIV) and the hepatitis B virus (HBV): And issues related to vaccination programs for bloodborne diseases. Dept. of Labor, 1989.

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Lindh, Gudrun. Chronic hepatitis B: Impact of hepatitis D virus superinfection and the hepatitis B e-system on histological outcome, and correlation of the hepatitis B e-system to HBV-DNA in serum. Distributed by the Almqvist & Wiksell Periodical Co., 1986.

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Mayfield, Eleanor. Protecting patients and professionals from blood-borne disease. [Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, Office of Public Affairs, 1993.

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Mayfield, Eleanor. Protecting patients and professionals from blood-borne disease. [Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, Office of Public Affairs, 1993.

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Mohamed Hatem Fathi El-Saied Wali. Natural history, factors affecting severity and progression rate of hepatitis c virus (HCV) infection in liver transplanted and non-transplanted patients. University of Birmingham, 2002.

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Book chapters on the topic "Hepatitis E virus (HEV)"

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Ruggeri, Franco Maria, Ilaria Di Bartolo, Fabio Ostanello, and Marcello Trevisani. "Epidemiology of the Human HEV Infection." In Hepatitis E Virus. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7522-4_3.

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Ruggeri, Franco Maria, Ilaria Di Bartolo, Fabio Ostanello, and Marcello Trevisani. "Epidemiology of HEV Infection in Animals." In Hepatitis E Virus. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7522-4_5.

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Ehling, A., B. Gierten, and T. Arndt. "Hepatitis E-Virus (HEV)." In Springer Reference Medizin. Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1431.

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Ehling, A., B. Gierten, and T. Arndt. "Hepatitis E-Virus (HEV)." In Lexikon der Medizinischen Laboratoriumsdiagnostik. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1431-1.

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Rösen-Wolff, Angela. "Hepatitis E Virus (HEV)." In Lexikon der Infektionskrankheiten des Menschen. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-39026-8_455.

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Cencič, Avrelija, and Walter Chingwaru. "Hepatitis E Virus (HEV) – An Emerging Viral Pathogen." In Detection of Bacteria, Viruses, Parasites and Fungi. Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-8544-3_11.

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Deterding, Katja, Heiner Wedemeyer, and Michael P. Manns. "Acute HCV." In Chronic Hepatitis C Virus. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1192-5_2.

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Reyes, G. R., C. C. Huang, A. W. Tam, and M. A. Purdy. "Molecular organization and replication of hepatitis E virus (HEV)." In Unconventional Agents and Unclassified Viruses. Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-9300-6_2.

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Young, Hugh, and Marie Ogilvie. "Hepatitis D virus (HDV) (Hepatitis delta)." In Genitourinary Infections. Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-017-5080-6_6.

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Longer, Charles F., Mrigendra P. Shrestha, Phillip O. MacArthy, et al. "Epidemiology of Hepatitis E Virus (HEV): A Cohort Study in Kathmandu, Nepal." In Viral Hepatitis and Liver Disease. Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-68255-4_104.

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Conference papers on the topic "Hepatitis E virus (HEV)"

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Letellier, A., S. Quessy, C. Suprenant, and P. Buholzer. "Detection of hepatitis e virus (HEV) antibiodies in swine herds in Québec, Canada." In Safe Pork 2015: Epidemiology and control of hazards in pork production chain. Iowa State University, Digital Press, 2015. http://dx.doi.org/10.31274/safepork-180809-305.

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Clemens, R., G. Wirl, C. Velten, and H. J. Röthig. "VIRUS SAFETY OF ANTITHROMBIN III CONCENTRATE KYBERNIN P - APROSPECTIVE CLINICAL TRIAL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644148.

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In 13 healthy male volunteers a prospective clinical trial was performed to evaluate virus safety of the antithrombin III concentrate Kybernin P in regard to hepatitis B, non-A/non-Band HIV transmission. As the volunteers were participants of a pharmacokinetic study they received either a fixed dosage of 1000 units Kybernin P asbolus injection or a dosage of 50 units per kg body weight as short-term infusion. Two different batches of Kybernin P were used.Whereas in all 13 volunteers virussafety in hepatitis non-A/non-B and HAV transmission could be monitored, only those volunteers who were not vaccinated (n=3) against hepatitis B or who had no protecting antibodies of anti-HB type despite vaccination (n=3)were to be included in the hepatitis B monitoring.All 13 volunteers were followed-upfor 1 year according to the standardsof the International Committee on Thrombosis and Hemostasis (ICTH). For detection of a potential hepatitis non-A/non-B transmission transaminases (AST, ALT) were determined in biweekly intervals during the first 6 months of the observation period and thereafter in monthly intervals. Hepatitis B seromar-kers as well as anti-HIV wereassessed bimonthly. Furthermore, all volunteers were clinically examined at every follow-up.None of the 13 volunteers revealedan increase of transaminases to the 2.5 fold of the upper normal level which is considered to be the borderlinelevel for hepatitis non-A/non-B diagnosis. Furthermore, in none of the volunteers a seroconversion for hepatitis B or HIV could be detected. Thus, Kybernin P is to be considered as hepatitis B, hepatitis non-A/non-B and HIV safe.
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Kipiani, E., M. Butsashvili, G. Kamkamidze, and G. Abashidze. "STUDY OF RISK FACTORS AFFECTING HBV VACCINE EFFICIENCY AMONG CHILDREN IN GEORGIA." In International Trends in Science and Technology. RS Global Sp. z O.O., 2020. http://dx.doi.org/10.31435/rsglobal_conf/30122020/7346.

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In the conditions of mass vaccination of hepatitis B, all over the world, including in Georgia, in the vaccinated population, the numberof those individuals who could not develop Anti-HBs are growing every day. According to the literature, the main reason for the ineffective vaccination of hepatitis B is considered to be an increase in the prevalence of express mutants among the hepatitisB virus population, which is of a similar intensity throughout the world. In parallel with a detailed analysis of literature sources, the scientific article for the first time studied the seroprevalence of Anti-HBs in the population of Georgian vaccinatedchildren.
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Evatt, B. L. "VIRUS INACTIVATION AND COAGULATION FACTOR PREPARATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644754.

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Nonheat-treated factor concentrates were used for the therapy of congenital and acquired coagulation deficiencies until 1984. These unheated factor crticentrates, which are manufactured from pooled plasma obtained from between 2500 and 25,000 blood or plasma donors, have been epidemiologically implicated in exposure of large numbers of hemophilia patients to several viral infections Including human immunodeficiency virus (HIV), hepatitis B, and non-A non-B hepatitis. Of these, HIV has been fdund to be very heat labile. After the introduction in 1984-85 of heat treatment of concentrates to reduce the risk of! hepatitis to recipients, several studies documented a lack of HIV serconversion in patients treated with clotting-fadtor concentrates. However, subsequent reports described a few hemophilia patients who had seroconverted to HIV! after receiving heat-treated concentrate from unscreened donors. To determine the significance of these seroconvers(ions, an international survey was conducted on 11 hemophilia treatment centers in Europe, Canada, and the United Kingdcpn whose total patient population comprised more than 2300 hemophilia A patients and 400 hemophilia B patients. Only three patients were found who seroconverted beyond a 6-month period after switching to heat-treated material, a(nd no seroconversions have occurred in these centers between November 1985 and February 1987. In addition no cases of seroconversion on donor screened heat-treated concentrate have been reported since its widespread introduction to the hemophilia patients during 1985-1986. Other modes of viral inactivation are currently being tested, and they appeiar to be effective in inactivating HIV and hepatitis B virus. Some of these methods have shown some promise for the inactivation of non-A and non-B hepatitis, but more data are needed for final assessment of these methods.
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Nasrallah, Gheyath, Laila Hedaya, Fatima Ali, et al. "Is it the time for Hepatitis E virus (HEV) Testing for Blood Donors in Qatar?" In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbsp2838.

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Horowtz, M. S., M. W. Hilgartner, R. A. Lipton, C. Rooks, and B. Horowitz. "VIRAL SAFETY OF SOLVENT/DETERGENT-TREATED AHF IN PATIENTS WITH HEMOPHILIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644151.

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The safety of an Antihemophilic Factor concentrate (Factor VIII-SD) treated with the organic solvent tri(n-butyl) phosphate (TNBP) and sodium cholate is being assessed with respect to transmission of non-A, non-B hepatitis virus (NANBHV) and human immunodeficiency virus (HIV). TNBP/cholate treatment has been previously shown to inactivate at least 10,000 infectious doses each of hepatitis B virus (HBV) and NANBHV using a chimpanzee model, and 30,000 tissue culture infectious doses of HIV.Patients enrolled in the study have had no previous exposure to blood products made from plasma pools, although some have received small quantities of single-donor products. They have normal alanine amino transferase (ALT) levels and no markers of prior HIV infection and have all been vaccinated against HBV. Each has been treated, as required, with an individual lot of Factor VIII-SD prepared at the New York Blood Center by an FDA-licensed procedure. ALT levels and HIV antibody have been monitored bi-weekly for two months and monthly until the end of six months. Seven patients who have received 475 -20,000 units of AHF(total units 38,255, median dose ∽3400 units) have been followed for at least three months. There has been no indication in these patients ofinfection with either NANBHV or HIV. An eighth patient who had an elevatedALT level prior to enrollment was followed for HIV antibody only. He remains HIV antibody negative through fivemonths of follow-up. Six additional patients have entered the study, but have not yet required treatment or have been followed for only a short time. These results suggest that the risk of virus infection associated with the use of AHF concentrates is significantly diminished by solvent/detergenttreatment.
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Heimburger, N., P. Fuhge, J. Hilfenhaus, G. Kumpe, and H. E. Karges. "EXPERIMENTAL STUDIES CONCERNING THE VIRUS SAFETY OF PASTEURIZED FIBRINOGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644153.

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Fibrinogen is available for substitution in afibrinogenaemic patientssince about 4 decades. However, it soon turned out that those concentrates bear a high risk of transmitting serum hepatitis. Over many years it was not possible to produce safe concentrates of fibrinogen. Hence, the therapy with this protein was limited to vital indications. We have now succeeded to stabilize fibrinogen inaqueous solution for pasteurization over 10 to 20 hours at 60°C.The efficacy of the virus inactivation was tested using various animal viruses. Following results were obtained.Tests in chimpanzees for hepatitis B safety revealed that this procedure inactivates and eliminates 105.2 CID50 of hepatitis B virus; HIV experiments are going on.By immunizing rabbits with the pasteurized fibrinogen and absorption of the antiserum obtained with the unpasteurized product, an exposition of neoantigens during heating in aqueous solution could be excluded. This result could be further confirmed using passive cutaneous anaphylaxis.The coagulability of the pasteurized fibrinogen is unchanged, compared to not pasteurized material. It iseasily soluble and can be used for both, i. v. infusion and as a tissue adhesive. The clinical tolerability is very good.
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Stephan, W., H. Dichtelmüller, A. M. Prince, L. Gürtler та F. Deinhardt. "INACTIVATION OF HEPATITIS VIRUSES AND HIV IN PLASMA AND PLASMA DERIVATIVES BY COMBINED TREATMENTWITH β-PR0PI0LACT0NE/UV-IRRADIATION". У XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644147.

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A combined treatment of plasma andplasma derivatives by β-Propiolactone (β-PL) /UV-irradiation is inuse at Biotest for the preparation ofthe virus safe serum preserve Bisekd® and coagulation factor concentrates.The efficacy of this sterilization procedure has been demonstrated for HAV(> 8.2 log10), HBV ( 7.0 log10) and HNANB (> 4.5 log10). As HIV has become a major problem tne inactivation of HIV by β-PL/UV in human plasma was tested. Pooled human plasma was spiked with 104.2 infectious units per ml of the Gallo strain of HIV/ HTLV-III and sterilized with 0.25 % β-PL, 60 min at pH 7.2 and subsequently UV-irradiated (4 × 20 W). After treatment with β-PL alone orβ-PL/UV no infectious HIV was detectable by reverse transcriptase assay in inoculated H-9 cultures after 14 days of cultivation (> 4.2 log10 inactivation). When the virucidal efficacy of ft-PL and UV was tested separately, β-PL inactivated > 3.5 log10, UV-irradiation another 2.5 log10 of HIV, as demonstrated by immunofluorescence tests in H-9 cultures 27 daysafter inoculation.When cryoprecipitate/F VUI-concentrate was sterilized by ft-PL and UV, > 4.5 log10 of HIV were inactivated by UV and > 3.5 log10 by α-PL. The results indicate, that the combined treatment by β-PL/UV inactivates all potentialtiters of HIV, which can be expected inscreened and pooled human plasma orcryoprecipitate, used for the preparation of virus safe plasma derivatives.
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Drechsel, L., M. Pefferkorn, K. Rother, et al. "Das mittlere Hepatitis B Virus (HBV) Oberflächenantigen (MHBs) als neuer Serummarker für das Ansprechen von Heptitis B/Hepatitis D Virus (HDV)-Koinfektionen auf eine Interferon (IFN)-basierte Behandlung." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695322.

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Kurniati, Nurul. "Analysis of Factors and Management of Hepatitis B Virus Screening in Mothers and Infants: A Scoping Review." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.03.67.

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ABSTRACT Background: The importance of screening for HBV infection is to identify the risk of perinatal transmission from infected mothers. People infected with HBV during infancy or childhood are more likely to suffer chronic infection to cirrhosis of the liver and liver cancer. Early detection and prompt treatment are essential for HBV infection. This study aimed to review the factors and management of hepatitis B virus screening in mothers and infants. Subjects and Method: A scoping review method was conducted in eight stages including (1) Identification of study problems; (2) Determining priority problem and study question; (3) Determining framework; (4) Literature searching; (5) Article selec­tion; (6) Critical appraisal; (7) Data extraction; and (8) Mapping. The search included PubMed, ScienceDirect, Wiley Online Library, and Scopus databases. The inclusion criteria were English/ Indonesian-language and full-text articles (scoping review, meta-analysis, systematic review)/ documents/ reports/ policy brief/ guidelines from WHO/ other organizations published between 2009 and 2019. The data were selected by the PRISMA flow chart. Results: The searched database obtained a total of 27.862 articles. After screening, 27.325 articles were excluded because of unmet the inclusion criteria. After conducting critical appraisal for the remaining 537 articles, only 11 articles were eligible for further review. The selected articles obtained from developing countries (China, South Africa, and Tanzania) and developed countries (Netherlands, Japan, Denmark, Northern Europe, and Canada) with quantitative studies design (cross-sectional, case series, and cohort) met the inclusion criteria. The findings emphasized on four main topics around hepatitis B virus screening in mothers and infants, namely demographic factors, risk factors, post-screening benefit, and challenges in screening uptake. Conclusion: Early detection of HBV infection with prenatal screening reduce the HBV prenatal transmission, especially from infected pregnancy. Screening plays an important role in the administration of universal infant HBV vaccination and postexposure prophylaxis with hepatitis B immune globulin (HBIG) at birth. Keywords: pregnant women, hepatitis B virus, perinatal transmission, screening Correspondence: Setianingsih. Universitas ‘Aisyiyah Yogyakarta. Jl. Siliwangi (Ringroad Barat) No. 63, Nogotirto, Gamping, Sleman, Yogyakarta, 55292. Email: nsetia580@gmail.com. Mobile: 082242081295. DOI: https://doi.org/10.26911/the7thicph.03.67
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Reports on the topic "Hepatitis E virus (HEV)"

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Kasorndorkbua, C., P. J. Thomas, Patrick G. Halbur, D. K. Guenette, F. F. Huang, and X. J. Meng. Infection of Pigs with Avian Hepatitis E Virus (HEV). Iowa State University, 2005. http://dx.doi.org/10.31274/ans_air-180814-1096.

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Sobsey, Mark D. Inactivation of Hepatitis A Virus (HAV) by Chlorine and Iodine in Water. Defense Technical Information Center, 1986. http://dx.doi.org/10.21236/ada199503.

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Sjogren, Maria H., and Kent Holtzmuller. Hepatitis C Virus Infection: Mechanism of Disease Progression. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada406083.

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Sjogren, Maria H. Hepatitis C. Virus Infection: Mechanism of Disease Progression. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada433067.

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Sjogren, Maria H., and Brooke Huntley. Hepatitis C. Virus Infection: Mechanisms of Disease Progression. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada477987.

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Kasorndorkbua, C., P. J. Thomas, Patrick G. Halbur, F. F. Huang, D. K. Guenette, and X. J. Meng. Routes of Transmission of Swine Hepatitis E virus in Pigs. Iowa State University, 2005. http://dx.doi.org/10.31274/ans_air-180814-1095.

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Koizumi, Yoshiki, Syo Nakajim, Hirofumi Ohash, et al. Quantifying antiviral activity optimizes drug combinations against hepatitis C virus infection. Office of Scientific and Technical Information (OSTI), 2016. http://dx.doi.org/10.2172/1242919.

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Pishmisheva, Maria, Magdalena Baymakova, Elitsa Golkocheva-Markova, et al. First Serological Study of Hepatitis E Virus Infection in Pigs in Bulgaria. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, 2018. http://dx.doi.org/10.7546/crabs.2018.07.18.

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Cook-Mills, Joan M., Hidayatulla G. Munshi, Robert L. Perlman, and Donald A. Chambers. Mouse Hepatitis Virus Infection Suppresses Modulation of Mouse Spleen T- Cell Activation. Defense Technical Information Center, 1988. http://dx.doi.org/10.21236/ada237464.

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Martinez-Chantar, Malu. Especial Premio Nobel de Medicina 2020: La ciencia vence al virus de la hepatitis C. Sociedad Española de Bioquímica y Biología Molecular, 2020. http://dx.doi.org/10.18567/sebbmdiv_rpc.2020.10.1.

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