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Francis V. Chisari

Researcher at Scripps Research Institute

Publications -  322
Citations -  57527

Francis V. Chisari is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Hepatitis B virus & Virus. The author has an hindex of 123, co-authored 322 publications receiving 54772 citations. Previous affiliations of Francis V. Chisari include University of Otago & University of Parma.

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A function of the hepatitis B virus precore protein is to regulate the immune response to the core antigen

TL;DR: It is demonstrated that HBeAg elicits T cell tolerance, whereas HBcAg is nontolerogenic in this system, and the results suggest that hepadnaviruses have retained a secretory form of the nucleoprotein because it functions as a T cell tolerogen and regulates the immune response to the intracellular nucleocapsid.
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Intrahepatic induction of alpha/beta interferon eliminates viral RNA-containing capsids in hepatitis B virus transgenic mice.

TL;DR: The results indicate that IFN-α/β triggers intracellular events that either inhibit the assembly of pgRNA-containing capsids or accelerate their degradation, and that maturation and secretion of virus is responsible for clearance of HBV capsids and their cargo of replicative intermediates from the cytoplasm of the hepatocyte.
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Blocking Chemokine Responsive to γ–2/Interferon (IFN)-γ Inducible Protein and Monokine Induced by IFN-γ Activity In Vivo Reduces the Pathogenetic but not the Antiviral Potential of Hepatitis B Virus–specific Cytotoxic T Lymphocytes

TL;DR: In this paper, the authors showed that the chemokines responsive to γ-2/IFN-γ inducible protein ([Crg2]IP-10) and monokine induced by interferon-γ (Mig) are rapidly and strongly induced in the liver after CTL transfer.
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PD-1:PD-L1 Interactions Contribute to the Functional Suppression of Virus-Specific CD8+ T Lymphocytes in the Liver

TL;DR: Results indicate that PD-1:PD-L1 interactions contribute to the suppression of IFN-γ secretion observed following Ag recognition in the liver, which may reverse viral persistence and chronic infection in cases in which the CTL response is suppressed by this mechanism.
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Cytotoxic T Lymphocyte Response to a Wild Type Hepatitis B Virus Epitope in Patients Chronically Infected by Variant Viruses Carrying Substitutions within the Epitope

TL;DR: The data suggest that negative selection of mutant viral genomes might contribute to viral persistence in a subset of patients with chronic HBV infection who express a narrow repertoire of anti-HBV CTL responses.