Literature DB >> 7914548

Woodchuck hepatitis virus infections: very rapid recovery after a prolonged viremia and infection of virtually every hepatocyte.

K Kajino1, A R Jilbert, J Saputelli, C E Aldrich, J Cullen, W S Mason.   

Abstract

Earlier studies have suggested that transient hepadnavirus infections in mammals are associated with virus replication in a large fraction of hepatocytes. Although the viremia that occurred during transient infections in some individuals would presumably lead to virus replication in all hepatocytes, these studies did not reveal if this was the case. The question of the extent of hepatocyte infection was therefore reinvestigated because of the implications of the results for the mechanisms of virus clearance. Woodchucks were inoculated with woodchuck hepatitis virus, and the course of hepatic infection was determined. These studies indicated that essentially 100% of the hepatocytes became infected in the majority of woodchucks. In 7 of 10 woodchucks, the viral infection was then rapidly cleared from the liver, generally in less than 4 weeks. In another three woodchucks, though productive infection was just as rapidly cleared, viral covalently closed circular DNA remained for weeks to months after other indicators of virus infection had disappeared from the liver. Bromodeoxyuridine labeling and anti-proliferating cell nuclear antigen staining to detect hepatocytes passing through S phase indicated an increase in hepatocyte proliferation during the recovery phase of infection. The rate of cell division appeared to be sufficient to replace no more than 2 to 3% of the hepatocytes per day, at the times at which the biopsies were performed. Histopathologic evaluation of the biopsy samples did not provide evidence for a massive amount of liver regeneration. Models to explain virus clearance, with or without massive immune system-mediated destruction of infected hepatocytes, are reviewed.

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Year:  1994        PMID: 7914548      PMCID: PMC236983     

Source DB:  PubMed          Journal:  J Virol        ISSN: 0022-538X            Impact factor:   5.103


  30 in total

1.  Hepatic stem cell compartment: activation and lineage commitment.

Authors:  S S Thorgeirsson; R P Evarts; H C Bisgaard; K Fujio; Z Hu
Journal:  Proc Soc Exp Biol Med       Date:  1993-12

2.  Laboratory assessment of hepatic injury in the woodchuck (Marmota monax).

Authors:  W E Hornbuckle; E S Graham; L Roth; B H Baldwin; C Wickenden; B C Tennant
Journal:  Lab Anim Sci       Date:  1985-08

3.  Core antigen and antibody in woodchucks after infection with woodchuck hepatitis virus.

Authors:  A Ponzetto; P J Cote; E C Ford; R H Purcell; J L Gerin
Journal:  J Virol       Date:  1984-10       Impact factor: 5.103

4.  Woodchuck hepatitis virus: experimental infection and natural occurrence.

Authors:  I Millman; L Southam; T Halbherr; H Simmons; C M Kang
Journal:  Hepatology       Date:  1984 Sep-Oct       Impact factor: 17.425

5.  Immunopathologic aspects of woodchuck hepatitis.

Authors:  D Frommel; D Crevat; L Vitvitsky; C Pichoud; O Hantz; M Chevalier; J A Grimaud; J Lindberg; C G Trépo
Journal:  Am J Pathol       Date:  1984-04       Impact factor: 4.307

6.  Interleukin-2 and alpha/beta interferon down-regulate hepatitis B virus gene expression in vivo by tumor necrosis factor-dependent and -independent pathways.

Authors:  L G Guidotti; S Guilhot; F V Chisari
Journal:  J Virol       Date:  1994-03       Impact factor: 5.103

7.  Cytotoxic T lymphocytes inhibit hepatitis B virus gene expression by a noncytolytic mechanism in transgenic mice.

Authors:  L G Guidotti; K Ando; M V Hobbs; T Ishikawa; L Runkel; R D Schreiber; F V Chisari
Journal:  Proc Natl Acad Sci U S A       Date:  1994-04-26       Impact factor: 11.205

8.  A precursor-product relationship exists between oval cells and hepatocytes in rat liver.

Authors:  R P Evarts; P Nagy; E Marsden; S S Thorgeirsson
Journal:  Carcinogenesis       Date:  1987-11       Impact factor: 4.944

9.  Replicative intermediates of hepatitis B virus in HepG2 cells that produce infectious virions.

Authors:  M A Sells; A Z Zelent; M Shvartsman; G Acs
Journal:  J Virol       Date:  1988-08       Impact factor: 5.103

10.  Systemic distribution of woodchuck hepatitis virus in the tissues of experimentally infected woodchucks.

Authors:  B E Korba; E J Gowans; F V Wells; B C Tennant; R Clarke; J L Gerin
Journal:  Virology       Date:  1988-07       Impact factor: 3.616

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  64 in total

1.  Half-life of the duck hepatitis B virus covalently closed circular DNA pool in vivo following inhibition of viral replication.

Authors:  William R Addison; Kathie-Anne Walters; Winnie W S Wong; John S Wilson; Danuta Madej; Lawrence D Jewell; D Lorne J Tyrrell
Journal:  J Virol       Date:  2002-06       Impact factor: 5.103

Review 2.  Immune escape by hepatitis B viruses.

Authors:  U Protzer; H Schaller
Journal:  Virus Genes       Date:  2000       Impact factor: 2.332

3.  Combination therapy with lamivudine and adenovirus causes transient suppression of chronic woodchuck hepatitis virus infections.

Authors:  T Zhou; J T Guo; F A Nunes; K L Molnar-Kimber; J M Wilson; C E Aldrich; J Saputelli; S Litwin; L D Condreay; C Seeger; W S Mason
Journal:  J Virol       Date:  2000-12       Impact factor: 5.103

Review 4.  Metabolism and function of hepatitis B virus cccDNA: Implications for the development of cccDNA-targeting antiviral therapeutics.

Authors:  Ju-Tao Guo; Haitao Guo
Journal:  Antiviral Res       Date:  2015-08-10       Impact factor: 5.970

Review 5.  Animal models and the molecular biology of hepadnavirus infection.

Authors:  William S Mason
Journal:  Cold Spring Harb Perspect Med       Date:  2015-04-01       Impact factor: 6.915

6.  Blockade of NKG2D on NKT cells prevents hepatitis and the acute immune response to hepatitis B virus.

Authors:  Sílvia Vilarinho; Kouetsu Ogasawara; Stephen Nishimura; Lewis L Lanier; Jody L Baron
Journal:  Proc Natl Acad Sci U S A       Date:  2007-11-08       Impact factor: 11.205

7.  The amount of hepatocyte turnover that occurred during resolution of transient hepadnavirus infections was lower when virus replication was inhibited with entecavir.

Authors:  William S Mason; Chunxiao Xu; Huey Chi Low; Jeffry Saputelli; Carol E Aldrich; Catherine Scougall; Arend Grosse; Richard Colonno; Sam Litwin; Allison R Jilbert
Journal:  J Virol       Date:  2008-12-10       Impact factor: 5.103

8.  Evidence that hepatocyte turnover is required for rapid clearance of duck hepatitis B virus during antiviral therapy of chronically infected ducks.

Authors:  I Fourel; J M Cullen; J Saputelli; C E Aldrich; P Schaffer; D R Averett; J Pugh; W S Mason
Journal:  J Virol       Date:  1994-12       Impact factor: 5.103

9.  The liver of woodchucks chronically infected with the woodchuck hepatitis virus contains foci of virus core antigen-negative hepatocytes with both altered and normal morphology.

Authors:  Chunxiao Xu; Toshiki Yamamoto; Tianlun Zhou; Carol E Aldrich; Katy Frank; John M Cullen; Allison R Jilbert; William S Mason
Journal:  Virology       Date:  2006-10-31       Impact factor: 3.616

10.  Tumor necrosis factor activates a conserved innate antiviral response to hepatitis B virus that destabilizes nucleocapsids and reduces nuclear viral DNA.

Authors:  Robyn Puro; Robert J Schneider
Journal:  J Virol       Date:  2007-05-02       Impact factor: 5.103

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