Temporal Pathogenesis of Experimental Neonatal Woodchuck Hepatitis Virus Infection: Increased Initial Viral Load and Decreased Severity of Acute Hepatitis During the Development of Chronic Viral Infection
Hepatology, ISSN: 0270-9139, Vol: 32, Issue: 4, Page: 807-817
2000
- 50Citations
- 18Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations50
- Citation Indexes50
- 50
- CrossRef45
- Captures18
- Readers18
- 18
Article Description
Acute hepatitis B virus (HBV) infections either resolve or progress to chronicity. Identification of early deviations in host-virus responses associated with these outcomes can further differentiate cause-effect mechanisms that initiate and maintain chronicity. Neonatal woodchucks were infected experimentally with the woodchuck hepatitis virus (WHV) at 3 days of age. At 8 or 14 weeks of age ( i.e., the early- or mid-acute stage of infection), whole blood and large surgical biopsies of the liver were obtained from infected animals and uninfected controls. These were stored for later correlating histopathologic responses and viral load with the subsequently determined outcome of infection. As of 1 year postinfection, half of the surgically treated infected woodchucks had developed self-limited infections, while the other half developed chronic infections. The self-limited outcome was characterized by decreased viral load in acute-phase liver and plasma and a generally robust acute hepatic inflammatory response. Comparisons at the same early time points revealed that the chronic outcome was characterized by increasing initial viral load in liver and plasma, and a detectable, but diminished, acute hepatic inflammation. These cotemporal comparisons indicate that there is an early host-response deviation during the acute phase of a developing chronic infection. Continued analysis of the tissues banked from this study will facilitate further temporal characterization of acute-phase mechanisms that determine resolution versus chronicity in WHV infection. Understanding such mechanisms may be useful in the rational design of therapy for established chronic HBV infection. (Hepatology 2000;32:807-817.)
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0270913900089060; http://dx.doi.org/10.1053/jhep.2000.17681; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0033803194&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11003627; https://journals.lww.com/01515467-200010000-00018; https://dx.doi.org/10.1053/jhep.2000.17681; https://aasldpubs.onlinelibrary.wiley.com/doi/abs/10.1053/jhep.2000.17681
Ovid Technologies (Wolters Kluwer Health)
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