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  1. Article ; Online: Mutational modifications of hepatitis A virus proteins 2B and 2C described for cell culture-adapted and attenuated virus are present in wild-type virus populations.

    Weilandt, Rebecca / Paulmann, Dajana / Schlottau, Kore / Vallbracht, Angelika / Dotzauer, Andreas

    Archives of virology

    2014  Volume 159, Issue 10, Page(s) 2699–2704

    Abstract: Studies have identified certain mutations in the 2B and 2C proteins of hepatitis A virus (HAV) as being essential for efficient growth in cultured cells, and it is assumed that these mutations contribute to the attenuated phenotype. We found that ... ...

    Abstract Studies have identified certain mutations in the 2B and 2C proteins of hepatitis A virus (HAV) as being essential for efficient growth in cultured cells, and it is assumed that these mutations contribute to the attenuated phenotype. We found that mutations supporting cell culture growth already exist in wild-type HAV populations. This suggests that these variants are not entirely generated de novo but are selected from the wild-type population. In a prolonged case of hepatitis A, we found that sequences associated with cell culture adaptation predominated later in infection. This might suggest selection of an attenuated virus population during a prolonged clinical infection.
    MeSH term(s) Adaptation, Physiological/genetics ; Base Sequence ; Carrier Proteins/genetics ; Cell Line ; Child, Preschool ; Feces/virology ; Hepatitis A Virus, Human ; Hepatitis A virus/genetics ; Hepatitis A virus/isolation & purification ; Humans ; Male ; Mutation ; RNA, Viral/analysis ; Sequence Analysis, RNA ; Viral Nonstructural Proteins/genetics ; Virus Replication/genetics
    Chemical Substances 2B protein, hepatitis A virus ; Carrier Proteins ; RNA, Viral ; Viral Nonstructural Proteins ; 2C protein, viral (EC 3.6.1.-)
    Language English
    Publishing date 2014-10
    Publishing country Austria
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 7491-3
    ISSN 1432-8798 ; 0304-8608
    ISSN (online) 1432-8798
    ISSN 0304-8608
    DOI 10.1007/s00705-014-2103-6
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  2. Article: NF-κB activation induced by hepatitis A virus and Newcastle disease virus occurs by different pathways depending on the structural pattern of viral nucleic acids

    Paulmann, Dajana / Bortmann, Simone / Grimm, Florian / Berk, Iris / Kraemer, Leena / Vallbracht, Angelika / Dotzauer, Andreas

    Archives of virology. 2014 July, v. 159, no. 7

    2014  

    Abstract: NF-κB is activated by hepatitis B virus and hepatitis C virus and is assumed to contribute to viral persistence, leading to the development of hepatocellular cancer by inhibition of apoptosis mediated by cytotoxic T cells. Whether hepatitis A virus (HAV), ...

    Abstract NF-κB is activated by hepatitis B virus and hepatitis C virus and is assumed to contribute to viral persistence, leading to the development of hepatocellular cancer by inhibition of apoptosis mediated by cytotoxic T cells. Whether hepatitis A virus (HAV), which does not cause chronic infection, activates NF-κB is a topic of controversy. Here, we confirm that HAV activates NF-κB and show that HAV enhances the activation of NF-κB by poly(I-C), but it inhibits the activation of NF-κB by Newcastle disease virus (NDV), a paramyxovirus. In addition, HAV inhibits NF-κB activation induced by overexpressed MAVS (mitochondrial antiviral signaling protein). We conclude from these findings that NF-κB induction occurs in cells infected with HAV by dsRNA, independently of mitochondrial-transduced RIG-I/MDA-5 signaling, whereas the induction of NF-κB in cells infected by NDV is mediated by RIG-I signaling, independenly of viral dsRNA. This is supported by experiments in which the different RNA inducers of RIG-I and MDA-5 are sequestered and which also show that poly(I-C) and HAV, but not NDV, are functionally equivalent in inducing NF-κB activity. Furthermore, we demonstrate that HAV interferes with the protein kinase R (PKR) activity and PKR activation induced by dsRNA, and that HAV-induced activation of NF-κB therefore does not take place via the PKR-induced pathway. As assumed for hepatitis B and C virus infections, NF-κB activation could attenuate the effects of cytotoxic T cells and may contribute to prolonged as well as relapsing courses of hepatitis A.
    Keywords Hepatitis A virus ; Hepatitis B virus ; Hepatitis C virus ; Newcastle disease virus ; T-lymphocytes ; apoptosis ; cytotoxicity ; double-stranded RNA ; hepatitis A ; hepatitis B ; hepatoma ; protein kinases ; viruses
    Language English
    Dates of publication 2014-07
    Size p. 1723-1733.
    Publishing place Springer-Verlag
    Document type Article
    ZDB-ID 7491-3
    ISSN 1432-8798 ; 0304-8608
    ISSN (online) 1432-8798
    ISSN 0304-8608
    DOI 10.1007/s00705-014-1993-7
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  3. Article: Mutational modifications of hepatitis A virus proteins 2B and 2C described for cell culture-adapted and attenuated virus are present in wild-type virus populations

    Weilandt, Rebecca / Paulmann, Dajana / Schlottau, Kore / Vallbracht, Angelika / Dotzauer, Andreas

    Archives of virology. 2014 Oct., v. 159, no. 10

    2014  

    Abstract: Studies have identified certain mutations in the 2B and 2C proteins of hepatitis A virus (HAV) as being essential for efficient growth in cultured cells, and it is assumed that these mutations contribute to the attenuated phenotype. We found that ... ...

    Abstract Studies have identified certain mutations in the 2B and 2C proteins of hepatitis A virus (HAV) as being essential for efficient growth in cultured cells, and it is assumed that these mutations contribute to the attenuated phenotype. We found that mutations supporting cell culture growth already exist in wild-type HAV populations. This suggests that these variants are not entirely generated de novo but are selected from the wild-type population. In a prolonged case of hepatitis A, we found that sequences associated with cell culture adaptation predominated later in infection. This might suggest selection of an attenuated virus population during a prolonged clinical infection.
    Keywords Hepatitis A virus ; cell culture ; cultured cells ; hepatitis A ; mutation ; phenotype ; proteins ; viruses
    Language English
    Dates of publication 2014-10
    Size p. 2699-2704.
    Publishing place Springer-Verlag
    Document type Article
    ZDB-ID 7491-3
    ISSN 1432-8798 ; 0304-8608
    ISSN (online) 1432-8798
    ISSN 0304-8608
    DOI 10.1007/s00705-014-2103-6
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  4. Article ; Online: NF-κB activation induced by hepatitis A virus and Newcastle disease virus occurs by different pathways depending on the structural pattern of viral nucleic acids.

    Paulmann, Dajana / Bortmann, Simone / Grimm, Florian / Berk, Iris / Kraemer, Leena / Vallbracht, Angelika / Dotzauer, Andreas

    Archives of virology

    2014  Volume 159, Issue 7, Page(s) 1723–1733

    Abstract: NF-κB is activated by hepatitis B virus and hepatitis C virus and is assumed to contribute to viral persistence, leading to the development of hepatocellular cancer by inhibition of apoptosis mediated by cytotoxic T cells. Whether hepatitis A virus (HAV), ...

    Abstract NF-κB is activated by hepatitis B virus and hepatitis C virus and is assumed to contribute to viral persistence, leading to the development of hepatocellular cancer by inhibition of apoptosis mediated by cytotoxic T cells. Whether hepatitis A virus (HAV), which does not cause chronic infection, activates NF-κB is a topic of controversy. Here, we confirm that HAV activates NF-κB and show that HAV enhances the activation of NF-κB by poly(I-C), but it inhibits the activation of NF-κB by Newcastle disease virus (NDV), a paramyxovirus. In addition, HAV inhibits NF-κB activation induced by overexpressed MAVS (mitochondrial antiviral signaling protein). We conclude from these findings that NF-κB induction occurs in cells infected with HAV by dsRNA, independently of mitochondrial-transduced RIG-I/MDA-5 signaling, whereas the induction of NF-κB in cells infected by NDV is mediated by RIG-I signaling, independenly of viral dsRNA. This is supported by experiments in which the different RNA inducers of RIG-I and MDA-5 are sequestered and which also show that poly(I-C) and HAV, but not NDV, are functionally equivalent in inducing NF-κB activity. Furthermore, we demonstrate that HAV interferes with the protein kinase R (PKR) activity and PKR activation induced by dsRNA, and that HAV-induced activation of NF-κB therefore does not take place via the PKR-induced pathway. As assumed for hepatitis B and C virus infections, NF-κB activation could attenuate the effects of cytotoxic T cells and may contribute to prolonged as well as relapsing courses of hepatitis A.
    MeSH term(s) Animals ; Cell Line ; Gene Expression Regulation, Viral/immunology ; Hepatitis A virus/immunology ; Humans ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Newcastle disease virus/immunology ; RNA, Viral/genetics ; RNA, Viral/metabolism
    Chemical Substances NF-kappa B ; RNA, Viral
    Language English
    Publishing date 2014-07
    Publishing country Austria
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 7491-3
    ISSN 1432-8798 ; 0304-8608
    ISSN (online) 1432-8798
    ISSN 0304-8608
    DOI 10.1007/s00705-014-1993-7
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  5. Article: IgA-coated particles of Hepatitis A virus are translocalized antivectorially from the apical to the basolateral site of polarized epithelial cells via the polymeric immunoglobulin receptor.

    Dotzauer, Andreas / Brenner, Meike / Gebhardt, Ulrike / Vallbracht, Angelika

    The Journal of general virology

    2005  Volume 86, Issue Pt 10, Page(s) 2747–2751

    Abstract: Although Hepatitis A virus (HAV) is transmitted by the faecal-oral route, its target for replication is the liver. Little is known of its interactions with cells of the gastrointestinal tract, and it is not known by which mechanisms HAV crosses the ... ...

    Abstract Although Hepatitis A virus (HAV) is transmitted by the faecal-oral route, its target for replication is the liver. Little is known of its interactions with cells of the gastrointestinal tract, and it is not known by which mechanisms HAV crosses the intestinal epithelium. In this study, it is shown that HAV associated with IgA is translocated from the apical to the basolateral compartment of polarized epithelial cells via the polymeric immunoglobulin receptor by IgA-mediated reverse transcytosis. The relevance of this mechanism, by which HAV-IgA complexes may overcome the intestinal barrier and contribute to infections of the liver, results from the fact that HAV-IgA complexes are infectious for hepatocytes and that significant amounts of intestinal HAV-IgA are present during acute infections, which are also partly transmitted. Besides supporting the primary infection, this mechanism may play a role in relapsing infections by establishing an enterohepatic cycle for HAV.
    MeSH term(s) Antigen-Antibody Complex/chemistry ; Biological Transport ; Cell Membrane/virology ; Cell Polarity ; Epithelial Cells/virology ; Hepatovirus/immunology ; Hepatovirus/metabolism ; Humans ; Immunoglobulin A/immunology ; Receptors, Polymeric Immunoglobulin/physiology ; Tumor Cells, Cultured
    Chemical Substances Antigen-Antibody Complex ; Immunoglobulin A ; Receptors, Polymeric Immunoglobulin
    Language English
    Publishing date 2005-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 219316-4
    ISSN 1465-2099 ; 0022-1317
    ISSN (online) 1465-2099
    ISSN 0022-1317
    DOI 10.1099/vir.0.81157-0
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  6. Article: Time course of hepatitis A viremia and viral load in the blood of human hepatitis A patients.

    Normann, Andrea / Jung, Christian / Vallbracht, Angelika / Flehmig, Bertram

    Journal of medical virology

    2004  Volume 72, Issue 1, Page(s) 10–16

    Abstract: The hepatitis A virus (HAV) is the most common etiological cause of acute hepatitis infections in humans in industrialized countries. Investigations into the viral load during HAV viremia, however, are rare. Therefore, correlation studies between viral ... ...

    Abstract The hepatitis A virus (HAV) is the most common etiological cause of acute hepatitis infections in humans in industrialized countries. Investigations into the viral load during HAV viremia, however, are rare. Therefore, correlation studies between viral load, biochemical, and specific serological markers have been undertaken. The group of sera comprised a series of multiple consecutive blood samples drawn from 11 patients at different times after onset of the disease. During the period up to 70 days after the onset of icterus, the individual range was at 1 x 10(3) to 3 x 10(4) HAV genome equivalents/ml. From day 75 until 120 after onset of the disease, the levels traced were at 10(3). In one case, it was possible to trace 1.25 x 10(4) genome equivalents/ml up to 180 days after onset of icterus and in two cases even up to 408 and 490 days viral load levels of 5 x 10(3) and 4 x 10(4) were detected, respectively. The same sera were used to measure IgM class antibodies to hepatitis A virus and the total anti-HAV. The results demonstrate that a direct correlation to peak levels of viral load exists with peak serum transaminase levels, but neither with peak anti-HAV IgM levels nor with total anti-HAV. Decreasing amounts of anti-HAV IgM tend to occur with decreasing amounts of HAV genome equivalents; and, vice versa, increasing amounts of total anti-HAV are accompanied by decreasing amounts of HAV genome equivalents. The longest duration of viremia was found in patients infected with HAV genotype IA.
    MeSH term(s) Acute Disease ; Adult ; Female ; Genotype ; Hepatitis A/physiopathology ; Hepatitis A/virology ; Hepatitis A Antibodies/blood ; Hepatitis A Virus, Human/genetics ; Hepatitis A Virus, Human/immunology ; Hepatitis A Virus, Human/isolation & purification ; Humans ; Immunoglobulin M/blood ; Male ; RNA, Viral/blood ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Viral Load ; Viremia/physiopathology ; Viremia/virology
    Chemical Substances Hepatitis A Antibodies ; Immunoglobulin M ; RNA, Viral
    Language English
    Publishing date 2004-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 752392-0
    ISSN 1096-9071 ; 0146-6615
    ISSN (online) 1096-9071
    ISSN 0146-6615
    DOI 10.1002/jmv.10532
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  7. Article: Hepatitis A virus suppresses monocyte-to-macrophage maturation in vitro.

    Wünschmann, Sabina / Becker, Britta / Vallbracht, Angelika

    Journal of virology

    2001  Volume 76, Issue 9, Page(s) 4350–4356

    Abstract: To analyze the pathogenetic mechanism of hematopoietic dysregulation associated with hepatitis A virus (HAV) infections, we studied the influence of HAV on monocyte (MO)-to-macrophage (MAC) maturation in vitro. Exposure of peripheral blood-derived ... ...

    Abstract To analyze the pathogenetic mechanism of hematopoietic dysregulation associated with hepatitis A virus (HAV) infections, we studied the influence of HAV on monocyte (MO)-to-macrophage (MAC) maturation in vitro. Exposure of peripheral blood-derived mononuclear cells (MNC) to HAV led to diminished adherence of MO to plastic. Furthermore, HAV inhibited the ability of peripheral blood MO to differentiate toward MAC. Freshly isolated and 14-day-old MO cultures demonstrated reduced differentiation and decreased phagocytic capacity after challenge with HAV. Viral replication in MO/MAC cultures was confirmed by titration of infectious virus. We also determined the influence of HAV on the MO/MAC population in human long-term bone marrow cultures (LTBMCs). Inoculation of bone marrow MNC with HAV suppressed the establishment of an adherent stromal layer containing a reduced number of MAC. Furthermore, increased MO numbers in the nonadherent fraction of HAV-challenged LTBMCs are indicative of the disturbance of MO adherence. These findings suggest that HAV infection leads to a disorder of the mononuclear phagocytic system which may contribute to functional abnormalities of the bone marrow stroma.
    MeSH term(s) Cell Adhesion ; Cell Differentiation ; Cells, Cultured ; Hepatitis A/virology ; Hepatitis A Virus, Human/pathogenicity ; Humans ; Macrophages/virology ; Monocytes/cytology ; Monocytes/virology ; Phagocytosis ; Virus Replication
    Language English
    Publishing date 2001-05-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/jvi.76.9.4350-4356.2002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 609: Show issues Location:
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  8. Article ; Online: The role of immunoglobulin A in prolonged and relapsing hepatitis A virus infections.

    Dotzauer, Andreas / Heitmann, Alke / Laue, Thomas / Kraemer, Leena / Schwabe, Kerstin / Paulmann, Dajana / Flehmig, Bertram / Vallbracht, Angelika

    The Journal of general virology

    2011  Volume 93, Issue Pt 4, Page(s) 754–760

    Abstract: Hepatitis A virus (HAV) infections result in different courses of the disease, varying between normal, prolonged and relapsing. However, the reason for these heterogeneous clinical appearances is not understood. As HAV-anti-HAV IgA immunocomplexes (HAV- ... ...

    Abstract Hepatitis A virus (HAV) infections result in different courses of the disease, varying between normal, prolonged and relapsing. However, the reason for these heterogeneous clinical appearances is not understood. As HAV-anti-HAV IgA immunocomplexes (HAV-IgA) infect hepatocytes, IgA was postulated as a carrier supporting hepatotropic transport of HAV, and it was speculated that this carrier mechanism contributes to the various clinical outcomes. In this study, the IgA-carrier mechanism was investigated in a mouse model. We show that HAV-IgA immunocomplexes efficiently reached the liver not only in HAV-seronegative mice, but also, and this is in contrast to free-HAV particles, in immunized HAV-seropositive animals. This IgA-mediated transport of HAV to the liver in the presence of immunity depended on the stage of development of the immune response. We conclude that over a period of several weeks after infection, anti-HAV IgA is able to promote an enterohepatic cycling of HAV, resulting in continuous endogenous reinfections of the liver. Our experiments indicate that highly avid IgG antibodies, which are present at later times of the infection, can terminate the reinfections. However, the endogenous reinfections in the presence of a developing neutralizing immunity might contribute to prolonged as well as to relapsing courses of HAV infections. Furthermore, the results show that serum IgA may act as an infection protracting factor.
    MeSH term(s) Animals ; Antibodies, Neutralizing/immunology ; Hepatitis A/immunology ; Hepatitis A/virology ; Hepatitis A Vaccines/immunology ; Hepatitis A virus/immunology ; Hepatitis A virus/physiology ; Humans ; Immunity, Humoral/immunology ; Immunoglobulin A/immunology ; Liver/virology ; Male ; Mice ; Mice, Inbred C3H ; Recurrence
    Chemical Substances Antibodies, Neutralizing ; Hepatitis A Vaccines ; Immunoglobulin A
    Language English
    Publishing date 2011-12-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 219316-4
    ISSN 1465-2099 ; 0022-1317
    ISSN (online) 1465-2099
    ISSN 0022-1317
    DOI 10.1099/vir.0.038406-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Hepatitis A virus protein 2B suppresses beta interferon (IFN) gene transcription by interfering with IFN regulatory factor 3 activation.

    Paulmann, Dajana / Magulski, Thomas / Schwarz, Rebecca / Heitmann, Lisa / Flehmig, Bertram / Vallbracht, Angelika / Dotzauer, Andreas

    The Journal of general virology

    2006  Volume 89, Issue Pt 7, Page(s) 1593–1604

    Abstract: Hepatitis A virus (HAV) antagonizes the innate immune response by inhibition of retinoic acid-inducible gene I-mediated and melanoma differentiation-associated gene 5-mediated beta interferon (IFN-beta) gene expression. This study showed that this is due ...

    Abstract Hepatitis A virus (HAV) antagonizes the innate immune response by inhibition of retinoic acid-inducible gene I-mediated and melanoma differentiation-associated gene 5-mediated beta interferon (IFN-beta) gene expression. This study showed that this is due to an interaction of HAV with mitochondrial antiviral signalling protein (MAVS)-dependent signalling, in which the viral non-structural protein 2B and the protein intermediate 3ABC recently suggested in this context seem to be involved, cooperatively affecting the activities of MAVS and the kinases TANK-binding kinase 1 (TBK1) and the inhibitor of NF-kappaB kinase epsilon (IKKepsilon). In consequence, interferon regulatory factor 3 (IRF-3) is not activated. As IRF-3 is necessary for IFN-beta transcription, inhibition of this factor results in efficient suppression of IFN-beta synthesis. This ability might be of vital importance for HAV, which is an exceptionally slow growing virus sensitive to IFN-beta, as it allows the virus to establish infection and maintain virus replication for a longer period of time.
    MeSH term(s) Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Animals ; Cell Line ; Hepatitis A virus/physiology ; I-kappa B Kinase/antagonists & inhibitors ; Interferon Regulatory Factor-3/antagonists & inhibitors ; Interferon-beta/antagonists & inhibitors ; Macaca mulatta ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Transcription, Genetic ; Viral Nonstructural Proteins/metabolism
    Chemical Substances 2B protein, hepatitis A virus ; 3ABC protein, virus ; Adaptor Proteins, Signal Transducing ; Interferon Regulatory Factor-3 ; Viral Nonstructural Proteins ; Interferon-beta (77238-31-4) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; I-kappa B Kinase (EC 2.7.11.10)
    Language English
    Publishing date 2006-04-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 219316-4
    ISSN 1465-2099 ; 0022-1317
    ISSN (online) 1465-2099
    ISSN 0022-1317
    DOI 10.1099/vir.0.83521-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Book ; Thesis: Neurovirulenz in einem Influenza-A-Rekombinationssystem

    Vallbracht, Angelika

    1977  

    Author's details Angelika Vallbracht
    Language Undetermined
    Size 68 S
    Document type Book ; Thesis
    Thesis / German Habilitation thesis @Tübingen, Univ., Fachbereich Biologie, Diss. : 1977
    Database Former special subject collection: coastal and deep sea fishing

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