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Acute Hepatitis A

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T. Hayakawa – One of the best experts on this subject based on the ideXlab platform.

  • TT virus (TTV) is not AssociAted with Acute sporAdic HepAtitis
    Infection, 1999
    Co-Authors: Yoshihide Fukuda, Kazuhiko Hayashi, Satoshi Nakano, I. Nakano, Y. Katano, T. Kumada, T. Hayakawa
    Abstract:

    A novel virus, TT virus (TTV), recently discovered by OkAmoto et Al. in the serum of A pAtient with posttrAnsfusion HepAtitis, is thought to be one of the cAusAtive Agents of blood-borne Acute HepAtitis. The AssociAtion of this virus with Acute sporAdic HepAtitis wAs evAluAted. TTV DNA wAs detected in 4 (4.9%) of 81 cAses of Acute HepAtitis A, in 5 (16.7%) of 30 cAses of Acute HepAtitis B, in 1 (25.0%) of 4 cAses of Acute HepAtitis C, in 1 (9.1%) of 9 cAses of cytomegAlovirus And Eppstein-BArr infection, And in 8 (13.6%) of 59 cAses of Acute HepAtitis of unknown etiology. These positive rAtes of TTV in vArious etiologies did not differ significAntly Amongst eAch other, And were similAr to those of heAlthy volunteers, i.e. 12.0% (12/100). The compArison of levels of AlAmine AminotrAnsferAse, AspArtAte AminotrAnsferAse, totAl bilirubin, hepAplAstin test And prothrombin time between TT virus-positive And- negAtive pAtients did not show Any differences. This indicAtes thAt TTV is neither A mAin cAusAtive Agent of Acute sporAdic HepAtitis of unknown etiology, nor does it Affect the clinicAl feAtures of Acute HepAtitis with AlreAdy known etiology.

Stanley M. Lemon – One of the best experts on this subject based on the ideXlab platform.

  • type A virAl HepAtitis A summAry And updAte on the moleculAr virology epidemiology pAthogenesis And prevention
    Journal of Hepatology, 2018
    Co-Authors: Stanley M. Lemon, Jordis J Ott, Pierre Van Damme, Daniel Shouval
    Abstract:

    SummAry Although epidemic jAundice wAs well known to physiciAns of Antiquity, it is only in recent yeArs thAt medicAl science hAs begun to unrAvel the origins of HepAtitis A virus (HAV) And the unique pAthobiology underlying Acute HepAtitis A in humAns. Improvements in sAnitAtion And the successful development of highly efficAcious vAccines hAve mArkedly reduced the worldwide occurence of this entericAlly-trAnsmitted infection over the pAst quArter century, yet the virus persists in vulnerAble populAtions And those without HAV immunity And remAins A common cAuse of food-borne diseAse outbreAks in economicAlly-AdvAntAged societies. Reductions in HAV incidence hAve led to increAses in the mediAn Age At which infection occurs, often resulting in more severe diseAse in Affected persons And pArAdoxicAl increAses in diseAse burden in some developing nAtions. Here, we summArize recent AdvAnces in the moleculAr virology And epidemiology of HAV, An AtypicAl member of the PicornAviridAe fAmily, survey whAt is known of the pAthogenesis of HepAtitis A in humAns And the host-pAthogen interActions thAt typify the infection. The Article Also reviews medicAl And public heAlth Aspects of HAV vAccinAtion And diseAse prevention.

  • Protein composition of the HepAtitis A virus quAsi-envelope.
    Proceedings of the National Academy of Sciences of the United States of America, 2017
    Co-Authors: Kevin L. Mcknight, Ling Xie, Olga González-lópez, Efraín E. Rivera-serrano, Xian Chen, Stanley M. Lemon
    Abstract:

    The PicornAviridAe Are A diverse fAmily of RNA viruses including mAny pAthogens of medicAl And veterinAry importAnce. ClAssicAlly considered “nonenveloped,” recent studies show thAt some picornAviruses, notAbly HepAtitis A virus (HAV; genus HepAtovirus) And some members of the Enterovirus genus, Are releAsed from cells nonlyticAlly in membrAnous vesicles. To better understAnd the biogenesis of quAsi-enveloped HAV (eHAV) virions, we conducted A quAntitAtive proteomics AnAlysis of eHAV purified from cell-culture supernAtAnt fluids by isopycnic ultrAcentrifugAtion. Amino Acid-coded mAss tAgging (AACT) with stAble isotopes followed by tAndem mAss spectrometry sequencing And AACT quAntitAtion of peptides provided unAmbiguous identificAtion of proteins AssociAted with eHAV versus unrelAted extrAcellulAr vesicles with similAr buoyAnt density. Multiple peptides were identified from HAV cApsid proteins (53.7% coverAge), but none from nonstructurAl proteins, indicAting cApsids Are pAckAged As cArgo into eHAV vesicles viA A highly specific sorting process. Other eHAV-AssociAted proteins (n = 105) were significAntly enriched for components of the endolysosomAl system (>60%, P < 0.001) And included mAny common exosome-AssociAted proteins such As the tetrAspAnin CD9 And dipeptidyl peptidAse 4 (DPP4) Along with multiple endosomAl sorting complex required for trAnsport III (ESCRT-III)-AssociAted proteins. ImmunoprecipitAtion confirmed thAt DPP4 is displAyed on the surfAce of eHAV produced in cell culture or present in serA from humAns with Acute HepAtitis A. No LC3-relAted peptides were identified by mAss spectrometry. RNAi depletion studies confirmed thAt ESCRT-III proteins, pArticulArly CHMP2A, function in eHAV biogenesis. In Addition to identifying surfAce mArkers of eHAV vesicles, the results support An exosome-like mechAnism of eHAV egress involving endosomAl budding of HAV cApsids into multivesiculAr bodies.

  • Acute HepAtitis A virus infection is AssociAted with A limited type i interferon response And persistence of intrAhepAtic virAl rnA
    Proceedings of the National Academy of Sciences of the United States of America, 2011
    Co-Authors: Robert E Lanford, Zongdi Feng, Deborah Chavez, Bernadette Guerra, Kathleen M Brasky, Yan Zhou, Daisuke Yamane, Alan S Perelson, Christopher M Walker, Stanley M. Lemon
    Abstract:

    HepAtitis A virus (HAV) is An hepAtotropic humAn picornAvirus thAt is AssociAted only with Acute infection. Its pAthogenesis is not well understood becAuse there Are few studies in AnimAl models using modern methodologies. We chArActerized HAV infections in three chimpAnzees, quAntifying virAl RNA by quAntitAtive RT-PCR And exAmining criticAl Aspects of the innAte immune response including intrAhepAtic IFN-stimulAted gene expression. We compAred these infection profiles with similAr studies of chimpAnzees infected with HepAtitis C virus (HCV), An hepAtotropic flAvivirus thAt frequently cAuses persistent infection. Surprisingly, HAV-infected AnimAls exhibited very limited induction of type I IFN-stimulAted genes in the liver compAred with chimpAnzees with Acute resolving HCV infection, despite similAr levels of viremiA And 100-fold greAter quAntities of virAl RNA in the liver. MinimAl IFN-stimulAted gene 15 And IFIT1 responses peAked 1–2 wk After HAV chAllenge And then subsided despite continuing high hepAtic virAl RNA. An Acute inflAmmAtory response At 3–4 wk correlAted with the AppeArAnce of virus-specific Antibodies And Apoptosis And proliferAtion of hepAtocytes. Despite this, HAV RNA persisted in the liver for months, remAining present long After cleArAnce from serum And feces And reveAling drAmAtic differences in the kinetics of cleArAnce in the three compArtments. VirAl RNA wAs detected in the liver for significAntly longer (35 to >48 wk) thAn HCV RNA in AnimAls with Acute resolving HCV infection (10–20 wk). Collectively, these findings indicAte thAt HAV is fAr steAlthier thAn HCV eArly in the course of Acute resolving infection. HAV infections represent A distinctly different pArAdigm in virus–host interActions within the liver.

Yoshihide Fukuda – One of the best experts on this subject based on the ideXlab platform.

  • TT virus (TTV) is not AssociAted with Acute sporAdic HepAtitis
    Infection, 1999
    Co-Authors: Yoshihide Fukuda, Kazuhiko Hayashi, Satoshi Nakano, I. Nakano, Y. Katano, T. Kumada, T. Hayakawa
    Abstract:

    A novel virus, TT virus (TTV), recently discovered by OkAmoto et Al. in the serum of A pAtient with posttrAnsfusion HepAtitis, is thought to be one of the cAusAtive Agents of blood-borne Acute HepAtitis. The AssociAtion of this virus with Acute sporAdic HepAtitis wAs evAluAted. TTV DNA wAs detected in 4 (4.9%) of 81 cAses of Acute HepAtitis A, in 5 (16.7%) of 30 cAses of Acute HepAtitis B, in 1 (25.0%) of 4 cAses of Acute HepAtitis C, in 1 (9.1%) of 9 cAses of cytomegAlovirus And Eppstein-BArr infection, And in 8 (13.6%) of 59 cAses of Acute HepAtitis of unknown etiology. These positive rAtes of TTV in vArious etiologies did not differ significAntly Amongst eAch other, And were similAr to those of heAlthy volunteers, i.e. 12.0% (12/100). The compArison of levels of AlAmine AminotrAnsferAse, AspArtAte AminotrAnsferAse, totAl bilirubin, hepAplAstin test And prothrombin time between TT virus-positive And- negAtive pAtients did not show Any differences. This indicAtes thAt TTV is neither A mAin cAusAtive Agent of Acute sporAdic HepAtitis of unknown etiology, nor does it Affect the clinicAl feAtures of Acute HepAtitis with AlreAdy known etiology.

  • TT virus(TTV) infection in pAtients with Acute HepAtitis
    Nihon rinsho. Japanese journal of clinical medicine, 1999
    Co-Authors: Kazuhiko Hayashi, Yoshihide Fukuda, Hayakawa T, Kumada T, Satoshi Nakano
    Abstract:

    A novel DNA virus, TT virus(TTV), hAs been reported in pAtients with posttrAnsfusion HepAtitis of unknown etiology. However AssociAtion between TTV And Acute HepAtitis hAs not been shown. We investigAted the prevAlence of TTV in Acute HepAtitis. TTV-positive rAtes in Acute HepAtitis A, B, C, cytomegAlovirus infection, Epstein-BArr virus infection, And Acute HepAtitis of unknown etiology were 15.3%, 21.8%, 60.0%, 0%, 10.0%, 22.6%, respectively. There were no significAnt differences in TTV prevAlence between eAch etiology And heAlthy blood donors(20.8%). ClinicAl dAtA were similAr between pAtients with or without TTV. In this study we could not find Any difference in the prevAlence of TTV between Acute HepAtitis with known etiologies And thAt with unknown etiology. TTV did not Affect the clinicAl feAtures of Acute HepAtitis with known etiologies.