Hepatitis virus immunity. Mar 9, 2005 Rehermann and Nascimbeni review Crispe review

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1 Hepatitis virus immunity Mar 9, 2005 Rehermann and Nascimbeni review Crispe review

2 HBV & HCV infection outcomes Both viruses cause immune-mediated active and chronic hepatitis HBV Vertical transmission = chronic hepatitis Adult infection = protective immunity HCV Adult infection = 60-80% chronic hepatitis

3 Clinical features Feature Hepatitis B Hepatitis C Worldwide 350 million infected 170 million infected United States 1 million infected 4 million infected Vertical transmission Horizontal transmission Mother to neonate Chronic hepatitis IV drug use, parenteral, sexual Recovery Rare - IV drug use, parenteral, sexual Chronic hepatitis Vaccine Yes No

4 Molecular virology Feature HBV HCV Structure 42 nm enveloped partially dsdna 50 nm enveloped +stranded RNA Family Hepadnaviridae Flaviviridae Receptor Unknown Includes CD81 Mutation rate Low (10-5 /base) High (10-3 /base) Genotypes 8; low divergence 6 with >50 subtypes

5 Image removed for copyright reasons. Source: Figure 1 in Rehermann, B., and M. Nascimbeni. "Immunology of hepatitis B virus and hepatitis C virus infection." Nature Review Immunology 5, no. 3 (2005).

6 HBV molecular virology Relaxed circular 3.2-kb genome Full-length negative strand, 5 viral RT Partial positive strand, 5 oligoribonucleotide cccdna template for transcription of 4 viral RNAs in nucleus Exported to cytoplasm and translated Longest RNA also serves as template for HBV replication in nucleocapsids in the cytoplasm Some DNA and nucleocapsids return to nucleus Others bud into ER & are secreted via golgi

7 HCV molecular virology ssrna (+) 10K nucleotides Single long ORF flanked by 2 UTRs Replicates in the cytoplasm Translation initiated by internal ribosomal entry site in 5 UTR Polyprotein processed into structural and non-structural proteins Combine with viral RNA to form membraneassociated replication complexes Nucleocapsids bud into cytoplasmic vesicles

8 Acute HBV infection in adults HBV DNA is detectable in circulation within 1 month of infection Remains at a low level ( genome equivalents/ml) for up to 6 weeks HBeAg and HBsAg reach peak levels HBcAg-specific IgM appears early and IgG persists for life, regardless of outcome T cell-mediated liver damage begins to be apparent weeks after infection Most viral DNA is cleared by this time

9 Acute HBV infection in adults >90% of acutely infected adults resolve all clinical signs, develop HBeAg- and HBsAgspecific antibodies, clear HBeAg and HBsAg from circulation, and maintain lifelong protective immunity Despite complete clinical recovery, trace amounts of HBV DNA persist and are controlled by humoral and cellular immune responses

10 Acute HCV infection in adults HCV reaches high levels in serum within 1 week after infection Cellular immune response takes 1 month and humoral immune response 2 months Clinical signs associated with T cell-mediated liver damage are rare Liver enzymes indicating tissue damage are detectable 8-12 weeks after infection Viral RNA declines Development of HCV-specific Ig is variable

11 Acute HCV infection in adults HCV-specific antibodies do not indicate the outcome of infection Most individuals develop chronic hepatitis with relatively stable viral titers (2-3 logs below that in the acute phase) Only a small proportion of patients recover and test negative for viral RNA Whether complete eradication occurs is controversial

12 Protective immunity to HBV Clinical recovery is associated with lifelong protective immunity Trace amounts of virus persist Reactivation with immunosuppression Transmission via organ transplantation Trace virus may maintain immune response Controversy regarding need to boost to maintain vaccine-induced HBsAg-specific immunity

13 Protective immunity to HCV Recovery is associated with HCV-specific T cells B cell responses are variable, and may not persist Whether HCV is completely eradiated or trace amounts remain is controversial Protective immunity is not believed to be completely protective or lifelong But data in humans are limited

14 Liver tolerance Portal blood is rich in bacterial products and food-derived antigens Malaria, HBV, and HCV all persist Allogeneic liver grafts can be established and maintained without immunosuppression Local presentation of Ag causes T cell inactivation, tolerance, and apoptosis

15 Immune cells in the liver Resident macrophages = Kupffer cells Can sometimes be effective APCs Also seem to be involved in tolerance Intrahepatic lymphocytes CD8+ > CD4+ NK and NKT populations are enriched

16 Portal vein Arteriole Dendritic cell Bile duct Kupffer cell Central vein Lymphocyte Sinusoid Plate of hepatocytes Kupffer cell Space of Disse Hepatic Sinusoid PC Immature DC Blood from portal vein Hepatocyte LSEC Blood to central vein Lymph drains from space of Disse and enters lymphatic capillaries in the portal area Figure by MIT OCW.

17 NK cells in the liver Hepatic sinusoid T cell T cell NK CCL3 IL-12 IL-18 CXCL9 Kupffer cell Activated NK cell IFN-γ NK Space of Disse IFN -α/β Infected hepatocyte LSEC Important role in T cell recruitment In response to type 1 IFN, Kupffer cells produce CCL3 (MIP-1) Once activated by Kupffer cell IL-12, produce IFN-γ Induces other cells to secrete CXCL9 (MIG) Figure by MIT OCW.

18 DC trafficking in the liver CCR7 Hepatocyte CCR7 DC DC DC Hepatic sinusoid CCL3 pre-dc CCR5 CCR1 Lymphoid Tissue CCR1 CCR5 Kupffer cell LSEC Space of Disse Also in response to Kupffer cell CCL3, immature DC respond via CCR1 Downregulate CCR1 and CCR5, upregulate CCR7 and become responsive to CCL21 Migrate to lymphoid aggregates in portal tracts and to LN Figure by MIT OCW.

19 T cell tolerance in the liver A Space of Disse B Space of Disse Naive CD4 + T cell Partial activation (G0 G1: no IL-2) IL-14 Naive CD8 + T cell T Reg IL-10 Kupffer cell IL-13 Passive apoptosis Hepatic Sinusoid Phagocytosis Hepatocyte LSEC Hepatocyte Hepatic Sinusoid Figure by MIT OCW.

20 Overcoming base-line tolerance Infected hepatocyte IFN -α/β IL-15 IL-12 CD4 + T cell CD8 + T cell Hepatic sinusoid T H 1 Pro-inflammatory CD4 + T cell CD8 + T cell Viable cell Hypothesis that type 1 IFN allows liver sinusoidal endothelial cells to produce IL-12 Promotes differentiation of Th1 cells IL-15 serves as a survival factor for CD8+ T cells LSEC Space of Disse Figure by MIT OCW.

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