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  • Review Article
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Mechanisms of Disease: HCV-induced liver injury

Nature Clinical Practice Gastroenterology & Hepatology volume 4, pages 622–634 (2007)Cite this article

Abstract

HCV persistently infects the majority of patients exposed to it and can cause irreversible fibrosis, leading to the onerous clinical sequelae of cirrhosis. In this Review, we discuss the direct effects of HCV on hepatocytes and the role of the immune system in liver damage. HCV, like many viruses, has developed methods by which to subvert host innate and adaptive immune responses to infection. HCV proteins seem to modulate apoptosis and steatosis, ultimately leading to hepatic stellate cell activation, fibrosis and hepatocellular carcinoma. In addition, HCV manipulates the immune system, disrupting both innate and adaptive immunity to establish persistent infection. The immune system initially attempts to eradicate the virus, but, in the setting of chronic infection, probably promotes hepatocyte damage and fibrosis through direct cellular toxicity and the release of inflammatory cytokines. Multiple types of cytotoxic lymphocytes, comprising the unique immune hepatic microenvironment, are likely to be important in the pathogenesis of HCV-induced liver damage. The net liver damage from HCV infection depends on the balance between the host's antiviral mechanisms and the virus' ability to subvert them.

Key Points

  • Liver damage in patients with a chronic HCV infection results from the direct effects of HCV proteins on hepatocytes and stellate cells, as well as the host immune response to the virus

  • HCV proteins can cause steatosis, activate stellate cells leading to fibrosis, inhibit the intracellular hepatocyte interferon response to infection, and modulate apoptosis leading to hepatocellular carcinoma; these effects seem to be overlapping and interrelated

  • Cytotoxic lymphocytes have an essential role in the host immune response to HCV as well as liver damage—cytotoxic T lymphocytes directly damage infected hepatocytes by apoptosis and probably indirectly damage the liver by cytokine secretion, and natural killer cells can stimulate cytotoxic-T-lymphocyte killing but might have antifibrotic and protective effects

  • The ultimate outcome in patients infected with HCV depends on the balance between host mechanisms of viral clearance and the virus's ability to persist, and the equilibrium between normal wound healing and fibrosis

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Figure 1: Interactions among HCV proteins, the apoptosis pathway and the RIG-I–MAVS pathway in hepatocytes.
Figure 2: Altered wound repair and telomere shortening lead to hepatic stellate cell activation and fibrosis.
Figure 3: HCV proteins can trigger inflammation, steatosis and fibrogenesis, and regulate apoptosis.
Figure 4: HCV-specific CD8+ T-cell responses to acute infection.
Figure 5: Natural killer cell involvement in HCV-related liver injury.
Figure 6: Hepatic γδ T cells in HCV infection.
Figure 7: Competing forces determine liver injury in hepatitis C infection.

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References

  1. Rosen HR (2003) Hepatitis C pathogenesis: mechanisms of viral clearance and liver injury. Liver Transpl 9: S35–S43

    Article  PubMed  Google Scholar 

  2. Thomas DL and Seeff LB (2005) Natural history of hepatitis C. Clin Liver Dis 9: 383–398

    Article  PubMed  Google Scholar 

  3. Bantel H and Schulze-Osthoff K (2003) Apoptosis in hepatitis C virus infection. Cell Death Differ 10 (Suppl 1): S48–S58

    Article  CAS  PubMed  Google Scholar 

  4. Bantel H et al. (2004) Detection of apoptotic caspase activation in sera from patients with chronic HCV infection is associated with fibrotic liver injury. Hepatology 40: 1078–1087

    Article  CAS  PubMed  Google Scholar 

  5. Canbay A et al. (2004) Apoptosis: the nexus of liver injury and fibrosis. Hepatology 39: 273–278

    Article  PubMed  Google Scholar 

  6. Canbay A et al. (2003) Apoptotic body engulfment by a human stellate cell line is profibrogenic. Lab Invest 83: 655–663

    Article  CAS  PubMed  Google Scholar 

  7. Baskin-Bey ES and Gores GJ (2005) Caspase-8, death-receptor signaling, and hepatocarcinogenesis: the Fas and the furious. Gastroenterology 129: 1790–1792

    Article  CAS  PubMed  Google Scholar 

  8. Fimia GM et al. (2003) Transgenic models for hepatitis C virus pathogenesis. Cell Death Differ 10 (Suppl 1): S16–S18

    Article  CAS  PubMed  Google Scholar 

  9. Saito K et al. (2006) Hepatitis C virus core protein inhibits tumor necrosis factor alpha-mediated apoptosis by a protective effect involving cellular FLICE inhibitory protein. J Virol 80: 4372–4379

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Moriya K et al. (1997) Hepatitis C virus core protein induces hepatic steatosis in transgenic mice. J Gen Virol 78: 1527–1531

    Article  CAS  PubMed  Google Scholar 

  11. Moriya K et al. (1998) The core protein of hepatitis C virus induces hepatocellular carcinoma in transgenic mice. Nat Med 4: 1065–1067

    Article  CAS  PubMed  Google Scholar 

  12. Lai MM (2002) Hepatitis C virus proteins: direct link to hepatic oxidative stress, steatosis, carcinogenesis and more. Gastroenterology 122: 568–571

    Article  PubMed  Google Scholar 

  13. Lerat H et al. (2002) Steatosis and liver cancer in transgenic mice expressing the structural and nonstructural proteins of hepatitis C virus. Gastroenterology 122: 352–365

    Article  CAS  PubMed  Google Scholar 

  14. Szabo G (2006) Hepatitis C virus NS5A protein—a master regulator? Gastroenterology 130: 995–999

    Article  CAS  PubMed  Google Scholar 

  15. Nanda SK et al. (2006) Src homology 3 domain of hepatitis C virus NS5A protein interacts with Bin1 and is important for apoptosis and infectivity. Gastroenterology 130: 794–809

    Article  CAS  PubMed  Google Scholar 

  16. Zhang N et al. (2005) The role of apoptosis in the development and function of T lymphocytes. Cell Res 15: 749–769

    Article  CAS  PubMed  Google Scholar 

  17. Kumar V et al. (2005) Robbins and Cotran: Pathologic Basis of Disease, edn 7. Philadelphia: Elsevier Saunders

    Google Scholar 

  18. Afford SC and Adams DH (2005) Following the TRAIL from hepatitis C virus and alcohol to fatty liver. Gut 54: 1518–1520

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Malhi H et al. (2006) Apoptosis and necrosis in the liver: a tale of two deaths? Hepatology 43 (Suppl 1): S31–S44

    Article  CAS  PubMed  Google Scholar 

  20. Kaplowitz N (2006) Liver biology and pathobiology. Hepatology 43 (Suppl 1): S235–S238

    Article  CAS  PubMed  Google Scholar 

  21. Ogasawara J et al. (1993) Lethal effect of the anti-Fas antibody in mice. Nature 364: 806–809

    Article  CAS  PubMed  Google Scholar 

  22. Okazaki M et al. (1996) Hepatic Fas antigen expression before and after interferon therapy in patients with chronic hepatitis C. Dig Dis Sci 41: 2453–2458

    Article  CAS  PubMed  Google Scholar 

  23. Hiramatsu N et al. (1994) Immunohistochemical detection of Fas antigen in liver tissue of patients with chronic hepatitis C. Hepatology 19: 1354–1359

    Article  CAS  PubMed  Google Scholar 

  24. Iken K et al. (2006) Apoptosis of activated CD4+ and CD8+ T cells is enhanced by co-culture with hepatocytes expressing hepatitis C virus (HCV) structural proteins through FasL induction. Virology 346: 363–372

    Article  CAS  PubMed  Google Scholar 

  25. Tillmann HL et al. (2005) Merging models of hepatitis C virus pathogenesis. Semin Liver Dis 25: 84–92

    Article  CAS  PubMed  Google Scholar 

  26. Asselah T et al. (2006) Steatosis in chronic hepatitis C: why does it really matter? Gut 55: 123–130

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Yoon EJ and Hu KQ (2006) Hepatitis C virus (HCV) infection and hepatic steatosis. Int J Med Sci 3: 53–56

    Article  PubMed  PubMed Central  Google Scholar 

  28. Kim KH et al. (2007) HCV core protein induces hepatic lipid accumulation by activating SREBP1 and PPARgamma. Biochem Biophys Res Commun 355: 883–888

    Article  CAS  PubMed  Google Scholar 

  29. Waris G et al. (2007) Hepatitis C virus induces proteolytic cleavage of sterol regulatory element binding proteins and stimulates their phosphorylation via oxidative stress. J Virol 81: 8122–8130

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Hui JM et al. (2003) Insulin resistance is associated with chronic hepatitis C virus infection and fibrosis progression [corrected]. Gastroenterology 125: 1695–1704

    Article  CAS  PubMed  Google Scholar 

  31. Walsh MJ et al. (2006) Non-response to antiviral therapy is associated with obesity and increased hepatic expression of suppressor of cytokine signalling 3 (SOCS-3) in patients with chronic hepatitis C, viral genotype 1. Gut 55: 529–535

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Mundt B et al. (2005) Tumour necrosis factor related apoptosis inducing ligand (TRAIL) induces hepatic steatosis in viral hepatitis and after alcohol intake. Gut 54: 1590–1596

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Lee SH et al. (2005) E2 of hepatitis C virus inhibits apoptosis. J Immunol 175: 8226–8235

    Article  CAS  PubMed  Google Scholar 

  34. Rockey DC (2005) Stellate cell/HCV interactions in hepatic fibrosis. Gastroenterology 129: 2117–2118

    Article  PubMed  Google Scholar 

  35. Schuppan D et al. (2003) Hepatitis C and liver fibrosis. Cell Death Differ 10 (Suppl 1): S59–S67

    Article  CAS  PubMed  Google Scholar 

  36. Gawrieh S et al. (2005) Early hepatic stellate cell activation predicts severe hepatitis C recurrence after liver transplantation. Liver Transpl 11: 1207–1213

    Article  PubMed  Google Scholar 

  37. Russo MW et al. (2005) Early hepatic stellate cell activation is associated with advanced fibrosis after liver transplantation in recipients with hepatitis C. Liver Transpl 11: 1235–1241

    Article  PubMed  Google Scholar 

  38. Schulze-Krebs A et al. (2005) Hepatitis C virus-replicating hepatocytes induce fibrogenic activation of hepatic stellate cells. Gastroenterology 129: 246–258

    Article  CAS  PubMed  Google Scholar 

  39. Purohit V and Brenner DA (2006) Mechanisms of alcohol-induced hepatic fibrosis: a summary of the Ron Thurman Symposium. Hepatology 43: 872–878

    Article  CAS  PubMed  Google Scholar 

  40. Bataller R et al. (2004) Hepatitis C virus core and nonstructural proteins induce fibrogenic effects in hepatic stellate cells. Gastroenterology 126: 529–540

    Article  CAS  PubMed  Google Scholar 

  41. Mazzocca A et al. (2005) Binding of hepatitis C virus envelope protein E2 to CD81 up-regulates matrix metalloproteinase-2 in human hepatic stellate cells. J Biol Chem 280: 11329–11339

    Article  CAS  PubMed  Google Scholar 

  42. Gong G et al. (2001) Human hepatitis C virus NS5A protein alters intracellular calcium levels, induces oxidative stress, and activates STAT-3 and NF-kappa B. Proc Natl Acad Sci USA 98: 9599–9604

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Moriya K et al. (2001) Oxidative stress in the absence of inflammation in a mouse model for hepatitis C virus-associated hepatocarcinogenesis. Cancer Res 61: 4365–4370

    CAS  PubMed  Google Scholar 

  44. Rockey DC (2006) Hepatic fibrosis, stellate cells, and portal hypertension. Clin Liver Dis 10: 459–479

    Article  PubMed  Google Scholar 

  45. Winau F et al. (2007) Ito cells are liver-resident antigen-presenting cells for activating T cell responses. Immunity 26: 117–129

    Article  CAS  PubMed  Google Scholar 

  46. Hiscott J et al. (2006) MasterCARD: a priceless link to innate immunity. Trends Mol Med 12: 53–56

    Article  CAS  PubMed  Google Scholar 

  47. Meylan E et al. (2005) Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus. Nature 437: 1167–1172

    Article  CAS  PubMed  Google Scholar 

  48. Seth RB et al. (2005) Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-kappa B and IRF 3. Cell 122: 669–682

    Article  CAS  PubMed  Google Scholar 

  49. Waterhouse NJ et al. (2004) Cytotoxic lymphocytes; instigators of dramatic target cell death. Biochem Pharmacol 68: 1033–1040

    Article  CAS  PubMed  Google Scholar 

  50. Kagi D and Hengartner H (1996) Different roles for cytotoxic T cells in the control of infections with cytopathic versus noncytopathic viruses. Curr Opin Immunol 8: 472–477

    Article  CAS  PubMed  Google Scholar 

  51. Guidotti LG and Chisari FV (2001) Noncytolytic control of viral infections by the innate and adaptive immune response. Annu Rev Immunol 19: 65–91

    Article  CAS  PubMed  Google Scholar 

  52. Bowen DG and Walker CM (2005) Adaptive immune responses in acute and chronic hepatitis C virus infection. Nature 436: 946–952

    Article  CAS  PubMed  Google Scholar 

  53. Cabrera R et al. (2004) An immunomodulatory role for CD4(+)CD25(+) regulatory T lymphocytes in hepatitis C virus infection. Hepatology 40: 1062–1071

    Article  CAS  PubMed  Google Scholar 

  54. Boettler T et al. (2005) T cells with a CD4+CD25+ regulatory phenotype suppress in vitro proliferation of virus-specific CD8+ T cells during chronic hepatitis C virus infection. J Virol 79: 7860–7867

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Rushbrook SM et al. (2005) Regulatory T cells suppress in vitro proliferation of virus-specific CD8+ T cells during persistent hepatitis C virus infection. J Virol 79: 7852–7859

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  56. Shoukry NH et al. (2003) Memory CD8+ T cells are required for protection from persistent hepatitis C virus infection. J Exp Med 197: 1645–1655

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  57. Cox AL et al. (2005) Cellular immune selection with hepatitis C virus persistence in humans. J Exp Med 201: 1741–1752

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  58. Bertoletti A and Maini MK (2000) Protection or damage: a dual role for the virus-specific cytotoxic T lymphocyte response in hepatitis B and C infection? Curr Opin Microbiol 3: 387–392

    Article  CAS  PubMed  Google Scholar 

  59. Urbani S et al. (2005) Heterologous T cell immunity in severe hepatitis C virus infection. J Exp Med 201: 675–680

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  60. Rehermann B and Shin EC (2005) Private aspects of heterologous immunity. J Exp Med 201: 667–670

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  61. Lechner F et al. (2000) CD8+ T lymphocyte responses are induced during acute hepatitis C virus infection but are not sustained. Eur J Immunol 30: 2479–2487

    Article  CAS  PubMed  Google Scholar 

  62. Thimme R et al. (2001) Determinants of viral clearance and persistence during acute hepatitis C virus infection. J Exp Med 194: 1395–1406

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Safadi R (2004) Immune stimulation of hepatic fibrogenesis by CD8 cells and attenuation by transgenic interleukin-10 from hepatocytes. Gastroenterology 127: 870–882

    Article  CAS  PubMed  Google Scholar 

  64. Frese M et al. (2002) Interferon-gamma inhibits replication of subgenomic and genomic hepatitis C virus RNAs. Hepatology 35: 694–703

    Article  CAS  PubMed  Google Scholar 

  65. Napoli J et al. (1996) Progressive liver injury in chronic hepatitis C infection correlates with increased intrahepatic expression of Th1-associated cytokines. Hepatology 24: 759–765

    Article  CAS  PubMed  Google Scholar 

  66. Afford SC et al. (1999) CD40 activation induces apoptosis in cultured human hepatocytes via induction of cell surface fas ligand expression and amplifies fas-mediated hepatocyte death during allograft rejection. J Exp Med 189: 441–446

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  67. Ljunggren HG and Karre K (1990) In search of the 'missing self': MHC molecules and NK cell recognition. Immunol Today 11: 237–244

    Article  CAS  PubMed  Google Scholar 

  68. Karre K (1997) How to recognize a foreign submarine. Immunol Rev 155: 5–9

    Article  CAS  PubMed  Google Scholar 

  69. Lanier LL (2005) NK cell recognition. Annu Rev Immunol 23: 225–274

    Article  CAS  PubMed  Google Scholar 

  70. Golden-Mason L and Rosen HR (2006) Natural killer cells: primary target for hepatitis C virus immune evasion strategies? Liver Transpl 12: 363–372

    Article  PubMed  Google Scholar 

  71. Doherty DG and O' Farrelly C (2000) Innate and adaptive lymphoid cells in the human liver. Immunol Rev 174: 5–20

    Article  CAS  PubMed  Google Scholar 

  72. Tay CH and Welsh RM (1997) Distinct organ-dependent mechanisms for the control of murine cytomegalovirus infection by natural killer cells. J Virol 71: 267–275

    CAS  PubMed  PubMed Central  Google Scholar 

  73. Guidotti LG et al. (1999) Noncytopathic clearance of lymphocytic choriomeningitis virus from the hepatocyte. J Exp Med 189: 1555–1564

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  74. Liu ZX et al. (2000) NK cells cause liver injury and facilitate the induction of T cell-mediated immunity to a viral liver infection. J Immunol 164: 6480–6486

    Article  CAS  PubMed  Google Scholar 

  75. Hayakawa Y et al. (2004) NK cell TRAIL eliminates immature dendritic cells in vivo and limits dendritic cell vaccination efficacy. J Immunol 172: 123–129

    Article  CAS  PubMed  Google Scholar 

  76. Mirandola P et al. (2004) Activated human NK and CD8+ T cells express both TNF-related apoptosis-inducing ligand (TRAIL) and TRAIL receptors but are resistant to TRAIL-mediated cytotoxicity. Blood 104: 2418–2424

    Article  CAS  PubMed  Google Scholar 

  77. Shigeno M et al. (2003) Interferon-alpha sensitizes human hepatoma cells to TRAIL-induced apoptosis through DR5 upregulation and NF-kappa B inactivation. Oncogene 22: 1653–1662

    Article  CAS  PubMed  Google Scholar 

  78. Mundt B (2003) Involvement of TRAIL and its receptors in viral hepatitis. FASEB J 17: 94–96

    Article  CAS  PubMed  Google Scholar 

  79. Pernollet M et al. (2002) Simultaneous evaluation of lymphocyte subpopulations in the liver and in peripheral blood mononuclear cells of HCV-infected patients: relationship with histological lesions. Clin Exp Immunol 130: 518–525

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  80. Deignan T et al. (2002) Decrease in hepatic CD56(+) T cells and V alpha 24(+) natural killer T cells in chronic hepatitis C viral infection. J Hepatol 37: 101–108

    Article  CAS  PubMed  Google Scholar 

  81. Tran A et al. (1997) Phenotyping of intrahepatic and peripheral blood lymphocytes in patients with chronic hepatitis C. Dig Dis Sci 42: 2495–2500

    Article  CAS  PubMed  Google Scholar 

  82. Melhem A et al. (2006) Anti-fibrotic activity of NK cells in experimental liver injury through killing of activated HSC. J Hepatol 45: 60–71

    Article  CAS  PubMed  Google Scholar 

  83. Radaeva S et al. (2006) Natural killer cells ameliorate liver fibrosis by killing activated stellate cells in NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent manners. Gastroenterology 130: 435–452

    Article  CAS  PubMed  Google Scholar 

  84. Morishima C et al. (2006) Decreased NK cell frequency in chronic hepatitis C does not affect ex vivo cytolytic killing. Hepatology 43: 573–580

    Article  PubMed  Google Scholar 

  85. Hayday A and Tigelaar R (2003) Immunoregulation in the tissues by gammadelta T cells. Nat Rev Immunol 3: 233–242

    Article  CAS  PubMed  Google Scholar 

  86. Kenna T et al. (2004) Distinct subpopulations of gamma delta T cells are present in normal and tumor-bearing human liver. Clin Immunol 113: 56–63

    Article  CAS  PubMed  Google Scholar 

  87. Nikolopoulou V et al. (1995) An increased number of circulating gamma/delta TCR + T cells in patients with chronic viral hepatitis. FEMS Immunol Med Microbiol 10: 115–118

    CAS  PubMed  Google Scholar 

  88. Yonekura K (2000) Liver-infiltrating CD56 positive T lymphocytes in hepatitis C virus infection. Liver 20: 357–365

    Article  CAS  PubMed  Google Scholar 

  89. Agrati C et al. (2001) Vdelta1 T lymphocytes expressing a Th1 phenotype are the major gammadelta T cell subset infiltrating the liver of HCV-infected persons. Mol Med 7: 11–19

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  90. Tseng CT et al. (2001) Characterization of liver T-cell receptor gammadelta T cells obtained from individuals chronically infected with hepatitis C virus (HCV): evidence for these T cells playing a role in the liver pathology associated with HCV infections. Hepatology 33: 1312–1320

    Article  CAS  PubMed  Google Scholar 

  91. Fu YX et al. (1994) Immune protection and control of inflammatory tissue necrosis by gamma delta T cells. J Immunol 153: 3101–3115

    CAS  PubMed  Google Scholar 

  92. Exley MA and Koziel MJ (2004) To be or not to be NKT: natural killer T cells in the liver. Hepatology 40: 1033–1040

    Article  PubMed  Google Scholar 

  93. Blumberg RS et al. (1995) Structure and function of the CD1 family of MHC-like cell surface proteins. Immunol Rev 147: 5–29

    Article  CAS  PubMed  Google Scholar 

  94. Kakimi K et al. (2000) Natural killer T cell activation inhibits hepatitis B virus replication in vivo. J Exp Med 192: 921–930

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  95. Nuti S et al. (1998) Dynamics of intra-hepatic lymphocytes in chronic hepatitis C: enrichment for Valpha24+ T cells and rapid elimination of effector cells by apoptosis. Eur J Immunol 28: 3448–3455

    Article  CAS  PubMed  Google Scholar 

  96. Durante-Mangoni E et al. (2004) Hepatic CD1d expression in hepatitis C virus infection and recognition by resident proinflammatory CD1d-reactive T cells. J Immunol 173: 2159–2166

    Article  CAS  PubMed  Google Scholar 

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Authors and Affiliations

  1. and HR Rosen is the Waterman Professor of Medicine and Immunology and Division Head, Division of Gastroenterology and Hepatology, Department of Medicine, JA Mengshol is a NIH training grant supported Clinical and Research Fellow in Gastroenterology and Hepatology, L Golden-Mason is an Assistant Professor of Gastroenterology and Hepatology, and Integrated Program in Immunology, University of Colorado Health Sciences Center, Denver, CO, USA.,

    John A Mengshol, Lucy Golden-Mason & Hugo R Rosen

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Correspondence to Hugo R Rosen.

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Mengshol, J., Golden-Mason, L. & Rosen, H. Mechanisms of Disease: HCV-induced liver injury. Nat Rev Gastroenterol Hepatol 4, 622–634 (2007). https://doi.org/10.1038/ncpgasthep0961

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