Table of Contents Author Guidelines Submit a Manuscript
Gastroenterology Research and Practice
Volume 2015 (2015), Article ID 796461, 9 pages
http://dx.doi.org/10.1155/2015/796461
Review Article

IFN-λ: A New Class of Interferon with Distinct Functions-Implications for Hepatitis C Virus Research

1Institute of Blood Transfusion, Chinese Academy of Medical Sciences, Peking Union Medical College, Chengdu, Sichuan 610052, China
2Toronto General Research Institute, University Health Network, University of Toronto, Toronto, ON, Canada M5G 1L6

Received 26 November 2014; Accepted 6 April 2015

Academic Editor: Anastasios Koulaouzidis

Copyright © 2015 Bing Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. M. F. Sorrell, E. A. Belongia, J. Costa et al., “National Institutes of Health consensus development conference statement: management of hepatitis B,” Hepatology, vol. 49, no. 5, pp. S4–S12, 2009. View at Publisher · View at Google Scholar · View at Scopus
  2. J. J. Feld, “The beginning of the end: what is the future of interferon therapy for chronic hepatitis C?” Antiviral Research, vol. 105, pp. 32–38, 2014. View at Publisher · View at Google Scholar
  3. P. Sheppard, W. Kindsvogel, W. Xu et al., “IL-28, IL-29 and their class II cytokine receptor IL-28R,” Nature Immunology, vol. 4, no. 1, pp. 63–68, 2003. View at Publisher · View at Google Scholar · View at Scopus
  4. S. V. Kotenko, G. Gallagher, V. V. Baurin et al., “IFN-λs mediate antiviral protection through a distinct class II cytokine receptor complex,” Nature Immunology, vol. 4, no. 1, pp. 69–77, 2003. View at Publisher · View at Google Scholar · View at Scopus
  5. L. Prokunina-Olsson, B. Muchmore, W. Tang et al., “A variant upstream of IFNL3 (IL28B) creating a new interferon gene IFNL4 is associated with impaired clearance of hepatitis C virus,” Nature Genetics, vol. 45, no. 2, pp. 164–171, 2013. View at Publisher · View at Google Scholar · View at Scopus
  6. T. R. O'Brien, L. Prokunina-Olsson, and R. P. Donnelly, “IFN-λ4: the paradoxical new member of the interferon lambda family,” Journal of Interferon & Cytokine Research, vol. 34, no. 11, pp. 829–838, 2014. View at Publisher · View at Google Scholar
  7. C. Kelly, P. Klenerman, and E. Barnes, “Interferon lambdas: the next cytokine storm,” Gut, vol. 60, no. 9, pp. 1284–1293, 2011. View at Publisher · View at Google Scholar · View at Scopus
  8. K. Witte, G. Gruetz, H.-D. Volk et al., “Despite IFN-λ receptor expression, blood immune cells, but not keratinocytes or melanocytes, have an impaired response to type III interferons: Implications for therapeutic applications of these cytokines,” Genes & Immunity, vol. 10, no. 8, pp. 702–714, 2009. View at Publisher · View at Google Scholar · View at Scopus
  9. C. Sommereyns, S. Paul, P. Staeheli et al., “IFN-Lambda (IFN-λ) is expressed in a tissue-dependent fashion and primarily acts on epithelial cells in vivo,” PLoS Pathogens, vol. 4, no. 3, Article ID e1000017, 2008. View at Publisher · View at Google Scholar
  10. A. Meager, K. Visvalingam, P. Dilger, D. Bryan, and M. Wadhwa, “Biological activity of interleukins-28 and -29: comparison with type I interferons,” Cytokine, vol. 31, no. 2, pp. 109–118, 2005. View at Publisher · View at Google Scholar · View at Scopus
  11. N. E. Pagliaccetti and M. D. Robek, “Interferon-λ in the immune response to hepatitis B virus and hepatitis C virus,” Journal of Interferon & Cytokine Research, vol. 30, no. 8, pp. 585–590, 2010. View at Publisher · View at Google Scholar · View at Scopus
  12. K. Wolk, K. Witte, E. Witte et al., “Maturing dendritic cells are an important source of IL-29 and IL-20 that may cooperatively increase the innate immunity of keratinocytes,” Journal of Leukocyte Biology, vol. 83, no. 5, pp. 1181–1193, 2008. View at Publisher · View at Google Scholar · View at Scopus
  13. S. Marukian, L. Andrus, T. P. Sheahan et al., “Hepatitis C virus induces interferon-λ and interferon-stimulated genes in primary liver cultures,” Hepatology, vol. 54, no. 6, pp. 1913–1923, 2011. View at Publisher · View at Google Scholar · View at Scopus
  14. F. J. D. Mennechet and G. Uzé, “Interferon-λ-treated dendritic cells specifically induce proliferation of FOXP3-expressing suppressor T cells,” Blood, vol. 107, no. 11, pp. 4417–4423, 2006. View at Publisher · View at Google Scholar · View at Scopus
  15. S. E. Doyle, H. Schreckhise, K. Khuu-Duong et al., “Interleukin-29 uses a type 1 interferon-like program to promote antiviral responses in human hepatocytes,” Hepatology, vol. 44, no. 4, pp. 896–906, 2006. View at Publisher · View at Google Scholar · View at Scopus
  16. K. Onoguchi, M. Yoneyama, A. Takemura et al., “Viral infections activate types I and III interferon genes through a common mechanism,” The Journal of Biological Chemistry, vol. 282, no. 10, pp. 7576–7581, 2007. View at Publisher · View at Google Scholar · View at Scopus
  17. Z. Makowska and M. H. Heim, “Interferon signaling in the liver during hepatitis C virus infection,” Cytokine, vol. 59, no. 3, pp. 460–466, 2012. View at Publisher · View at Google Scholar · View at Scopus
  18. P. I. Österlund, T. E. Pietilä, V. Veckman, S. V. Kotenko, and I. Julkunen, “IFN regulatory factor family members differentially regulate the expression of type III IFN (IFN-λ) genes,” The Journal of Immunology, vol. 179, no. 6, pp. 3434–3442, 2007. View at Publisher · View at Google Scholar · View at Scopus
  19. S. M. Horner and M. Gale Jr., “Regulation of hepatic innate immunity by hepatitis C virus,” Nature Medicine, vol. 19, no. 7, pp. 879–888, 2013. View at Publisher · View at Google Scholar · View at Scopus
  20. J. Wu and Z. J. Chen, “Innate immune sensing and signaling of cytosolic nucleic acids,” Annual Review of Immunology, vol. 32, no. 1, pp. 461–488, 2014. View at Publisher · View at Google Scholar · View at Scopus
  21. M. H. Heim, “Innate immunity and HCV,” Journal of Hepatology, vol. 58, no. 3, pp. 564–574, 2013. View at Publisher · View at Google Scholar · View at Scopus
  22. N. Jilg, W. Lin, J. Hong et al., “Kinetic differences in the induction of interferon stimulated genes by interferon-α and interleukin 28B are altered by infection with hepatitis C virus,” Hepatology, vol. 59, no. 4, pp. 1250–1261, 2014. View at Publisher · View at Google Scholar · View at Scopus
  23. R.-X. Shao, L. Zhang, Z. Hong et al., “SOCS1 abrogates IFN's antiviral effect on hepatitis C virus replication,” Antiviral Research, vol. 97, no. 2, pp. 101–107, 2013. View at Publisher · View at Google Scholar · View at Scopus
  24. V. François-Newton, G. M. de Freitas Almeida, B. Payelle-Brogard et al., “USP18-based negative feedback control is induced by type I and type III interferons and specifically inactivates interferon α response,” PLoS ONE, vol. 6, no. 7, Article ID e22200, 2011. View at Publisher · View at Google Scholar · View at Scopus
  25. C. Koh and T. J. Liang, “What is the future of ribavirin therapy for hepatitis C?” Antiviral Research, vol. 104, no. 1, pp. 34–39, 2014. View at Publisher · View at Google Scholar · View at Scopus
  26. M. Sarasin-Filipowicz, “Interferon therapy of hepatitis C: molecular insights into success and failure,” Swiss Medical Weekly, vol. 140, no. 1-2, pp. 3–11, 2010. View at Google Scholar · View at Scopus
  27. J. J. Feld and J. H. Hoofnagle, “Mechanism of action of interferon and ribavirin in treatment of hepatitis C,” Nature, vol. 436, no. 7053, pp. 967–972, 2005. View at Publisher · View at Google Scholar · View at Scopus
  28. F. Lin and H. A. Young, “Interferons: success in anti-viral immunotherapy,” Cytokine & Growth Factor Reviews, vol. 25, no. 4, pp. 369–376, 2014. View at Publisher · View at Google Scholar
  29. K. E. Sherman, S. L. Flamm, N. H. Afdhal et al., “Response-guided telaprevir combination treatment for hepatitis C virus infection,” The New England Journal of Medicine, vol. 365, no. 11, pp. 1014–1024, 2011. View at Publisher · View at Google Scholar · View at Scopus
  30. S. Zeuzem, P. Andreone, S. Pol et al., “Telaprevir for retreatment of HCV infection,” The New England Journal of Medicine, vol. 364, no. 25, pp. 2417–2428, 2011. View at Publisher · View at Google Scholar · View at Scopus
  31. J. Jaroszewicz, R. Flisiak, and G. Dusheiko, “A pill for HCV—myth or foreseeable future?” Liver International, vol. 34, no. 1, pp. 6–11, 2014. View at Publisher · View at Google Scholar · View at Scopus
  32. Z. Zhou, O. J. Hamming, N. Ank, S. R. Paludan, A. L. Nielsen, and R. Hartmann, “Type III interferon (IFN) induces a type I IFN-like response in a restricted subset of cells through signaling pathways involving both the Jak-STAT pathway and the mitogen-activated protein kinases,” Journal of Virology, vol. 81, no. 14, pp. 7749–7758, 2007. View at Publisher · View at Google Scholar · View at Scopus
  33. J. Pott, T. Mahlakõiv, M. Mordstein et al., “IFN-λ determines the intestinal epithelial antiviral host defense,” Proceedings of the National Academy of Sciences of the United States of America, vol. 108, no. 19, pp. 7944–7949, 2011. View at Publisher · View at Google Scholar · View at Scopus
  34. M. Sarasin-Filipowicz, X. Wang, M. Yan et al., “Alpha interferon induces long-lasting refractoriness of JAK-STAT signaling in the mouse liver through induction of USP18/UBP43,” Molecular and Cellular Biology, vol. 29, no. 17, pp. 4841–4851, 2009. View at Publisher · View at Google Scholar · View at Scopus
  35. H. Qashqari, A. Al-Mars, A. Chaudhary et al., “Understanding the molecular mechanism(s) of hepatitis C virus (HCV) induced interferon resistance,” Infection, Genetics and Evolution, vol. 19, pp. 113–119, 2013. View at Publisher · View at Google Scholar · View at Scopus
  36. Z. Makowska, F. H. T. Duong, G. Trincucci, D. F. Tough, and M. H. Heim, “Interferon-β and interferon-λ signaling is not affected by interferon-induced refractoriness to interferon-α in vivo,” Hepatology, vol. 53, no. 4, pp. 1171–1180, 2011. View at Publisher · View at Google Scholar · View at Scopus
  37. B. Edlich, G. Ahlenstiel, A. A. Zabaleta et al., “Early changes in interferon signaling define natural killer cell response and refractoriness to interferon-based therapy of hepatitis C patients,” Hepatology, vol. 55, no. 1, pp. 39–48, 2012. View at Publisher · View at Google Scholar · View at Scopus
  38. Z. Yin, J. Dai, J. Deng et al., “Type III IFNs are produced by and stimulate human plasmacytoid dendritic cells,” The Journal of Immunology, vol. 189, no. 6, pp. 2735–2745, 2012. View at Publisher · View at Google Scholar · View at Scopus
  39. D. Olagnier and J. Hiscott, “Type I and type III interferon-induced immune response: it's a matter of kinetics and magnitude,” Hepatology, vol. 59, no. 4, pp. 1225–1228, 2014. View at Publisher · View at Google Scholar · View at Scopus
  40. E. L. Ramos, “Preclinical and clinical development of pegylated interferon-lambda 1 in chronic hepatitis C,” Journal of Interferon and Cytokine Research, vol. 30, no. 8, pp. 591–595, 2010. View at Publisher · View at Google Scholar · View at Scopus
  41. A. J. Muir, M. L. Shiffman, A. Zaman et al., “Phase 1b study of pegylated interferon lambda 1 with or without ribavirin in patients with chronic genotype 1 hepatitis C virus infection,” Hepatology, vol. 52, no. 3, pp. 822–832, 2010. View at Publisher · View at Google Scholar · View at Scopus
  42. X. Wang, M. Hruska, P. Chan et al., “Derivation of Phase 3 dosing for peginterferon lambda-1a in chronic hepatitis C, Part 1: modeling optimal treatment duration and sustained virologic response rates,” The Journal of Clinical Pharmacology, vol. 55, no. 1, pp. 63–72, 2015. View at Publisher · View at Google Scholar
  43. M. Hruska, X. Wang, P. Chan et al., “Derivation of Phase 3 dosing for peginterferon lambda-1a in chronic hepatitis C, Part 2: exposure-response analyses for efficacy and safety variables,” The Journal of Clinical Pharmacology, vol. 55, no. 1, pp. 73–80, 2015. View at Publisher · View at Google Scholar
  44. D. Ge, J. Fellay, A. J. Thompson et al., “Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance,” Nature, vol. 461, no. 7262, pp. 399–401, 2009. View at Publisher · View at Google Scholar · View at Scopus
  45. I. McGilvray, J. J. Feld, L. Chen et al., “Hepatic cell-type specific gene expression better predicts HCV treatment outcome than IL28B genotype,” Gastroenterology, vol. 142, no. 5, pp. 1122.e1–1131.e1, 2012. View at Publisher · View at Google Scholar
  46. B. I. Chen L, J. Sun, M. Guindi et al., “Cell-type specific gene expression signature in liver underlies response to interferon therapy in chronic hepatitis C infection,” Gastroenterology, vol. 138, no. 3, pp. 1123–1133, 2010. View at Google Scholar
  47. P. V. Aka, M. H. Kuniholm, R. M. Pfeiffer et al., “Association of the IFNL4-ΔG allele with impaired spontaneous clearance of hepatitis C virus,” Journal of Infectious Diseases, vol. 209, no. 3, pp. 350–354, 2014. View at Publisher · View at Google Scholar · View at Scopus
  48. Y. Nagaoki, M. Imamura, Y. Kawakami et al., “Interferon lambda 4 polymorphism affects on outcome of telaprevir, pegylated interferon and ribavirin combination therapy for chronic hepatitis C,” Hepatology Research, vol. 44, no. 14, pp. E447–E454, 2014. View at Publisher · View at Google Scholar
  49. P. Simmonds, J. Bukh, C. Combet et al., “Consensus proposals for a unified system of nomenclature of hepatitis C virus genotypes,” Hepatology, vol. 42, no. 4, pp. 962–973, 2005. View at Publisher · View at Google Scholar · View at Scopus
  50. B. L. Pearlman and N. Traub, “Sustained virologic response to antiviral therapy for chronic hepatitis C virus infection: a cure and so much more,” Clinical Infectious Diseases, vol. 52, no. 7, pp. 889–900, 2011. View at Publisher · View at Google Scholar · View at Scopus
  51. M. G. Ghany, D. B. Strader, D. L. Thomas, and L. B. Seeff, “Diagnosis, management, and treatment of hepatitis C: an update,” Hepatology, vol. 49, no. 4, pp. 1335–1374, 2009. View at Publisher · View at Google Scholar · View at Scopus
  52. M. W. Fried, M. L. Shiffman, K. R. Reddy et al., “Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection,” The New England Journal of Medicine, vol. 347, no. 13, pp. 975–982, 2002. View at Publisher · View at Google Scholar · View at Scopus
  53. C. Sarrazin, C. Hézode, S. Zeuzem, and J.-M. Pawlotsky, “Antiviral strategies in hepatitis C virus infection,” Journal of Hepatology, vol. 56, supplement 1, pp. S88–S100, 2012. View at Publisher · View at Google Scholar · View at Scopus
  54. P. Halfon, A. U. Neumann, M. Bourlière et al., “Slow viral dynamics of hepatitis C virus genotype 4,” Journal of Viral Hepatitis, vol. 10, no. 5, pp. 351–353, 2003. View at Publisher · View at Google Scholar · View at Scopus
  55. H. Toyoda, T. Kumada, N. Shimada et al., “Baseline factors and early viral response (week 4) to antiviral therapy with peginterferon and ribavirin for predicting sustained virologic response in patients infected with hepatitis C virus genotype 1: a multicenter study,” Journal of Medical Virology, vol. 85, no. 1, pp. 65–70, 2013. View at Publisher · View at Google Scholar · View at Scopus
  56. M. W. Fried, S. J. Hadziyannis, M. L. Shiffman, D. Messinger, and S. Zeuzem, “Rapid virological response is the most important predictor of sustained virological response across genotypes in patients with chronic hepatitis C virus infection,” Journal of Hepatology, vol. 55, no. 1, pp. 69–75, 2011. View at Publisher · View at Google Scholar · View at Scopus
  57. Y. Wada, H. Tamai, A. Uno et al., “Prediction of efficacy to pegylated interferon-α-2b plus ribavirin in patients with genotype 2 hepatitis C virus using viral response within 2 weeks,” Hepatology Research, vol. 44, no. 2, pp. 179–186, 2014. View at Publisher · View at Google Scholar · View at Scopus
  58. J. Itakura, Y. Asahina, N. Tamaki et al., “Changes in hepatitis C viral load during first 14 days can predict the undetectable time point of serum viral load by pegylated interferon and ribavirin therapy,” Hepatology Research, vol. 41, no. 3, pp. 217–224, 2011. View at Publisher · View at Google Scholar · View at Scopus
  59. O. Stambouli, Hepatitis C Virus: Molecular Pathways and Treatments, 2014.
  60. N. Enomoto, I. Sakuma, Y. Asahina et al., “Comparison of full-length sequences of interferon-sensitive and resistant hepatitis C virus 1b: sensitivity to interferon is conferred by amino acid substitutions in the NS5A region,” The Journal of Clinical Investigation, vol. 96, no. 1, pp. 224–230, 1995. View at Publisher · View at Google Scholar · View at Scopus
  61. K. Hayashi, Y. Katano, M. Ishigami et al., “Mutations in the core and NS5A region of hepatitis C virus genotype 1b and correlation with response to pegylated-interferon-alpha 2b and ribavirin combination therapy,” Journal of Viral Hepatitis, vol. 18, no. 4, pp. 280–286, 2011. View at Publisher · View at Google Scholar · View at Scopus
  62. P. M. de Rueda, J. Casado, R. Patón et al., “Mutations in E2-PePHD, NS5A-PKRBD, NS5A-ISDR, and NS5A-V3 of hepatitis C virus genotype 1 and their relationships to pegylated interferon-ribavirin treatment responses,” Journal of Virology, vol. 82, no. 13, pp. 6644–6653, 2008. View at Publisher · View at Google Scholar · View at Scopus
  63. S. Kitamura, M. Tsuge, T. Hatakeyama et al., “Amino acid substitutions in core and NS5A regions of the HCV genome can predict virological decrease with pegylated interferon plus ribavirin therapy,” Antiviral Therapy, vol. 15, no. 8, pp. 1087–1097, 2010. View at Publisher · View at Google Scholar · View at Scopus
  64. R. Kozuka, M. Enomoto, H. Hai et al., “Changes in sequences of core region, interferon sensitivity-determining region and interferon and ribavirin resistance-determining region of hepatitis C virus genotype 1 during interferon-alpha and ribavirin therapy, and efficacy of retreatment,” Hepatology Research, vol. 42, no. 12, pp. 1157–1167, 2012. View at Publisher · View at Google Scholar · View at Scopus
  65. S. Sakamoto, J. Qin, A. Navarro et al., “Cells previously desensitized to type 1 interferons display different mechanisms of activation of stat-dependent gene expression from naïve cells,” The Journal of Biological Chemistry, vol. 279, no. 5, pp. 3245–3253, 2004. View at Publisher · View at Google Scholar · View at Scopus
  66. G. C. MacQuillan, W. B. de Boer, M. A. Platten et al., “Intrahepatic MxA and PKR protein expression in chronic hepatitis C virus infection,” Journal of Medical Virology, vol. 68, no. 2, pp. 197–205, 2002. View at Publisher · View at Google Scholar · View at Scopus
  67. T. Asselah, I. Bieche, S. Narguet et al., “Liver gene expression signature to predict response to pegylated interferon plus ribavirin combination therapy in patients with chronic hepatitis C,” Gut, vol. 57, no. 4, pp. 516–523, 2008. View at Publisher · View at Google Scholar · View at Scopus
  68. J. Hou, G. van Oord, Z. M. A. Groothuismink et al., “Gene expression profiling to predict and assess the consequences of therapy-induced virus eradication in chronic hepatitis C virus infection,” Journal of Virology, vol. 88, no. 21, pp. 12254–12264, 2014. View at Publisher · View at Google Scholar
  69. L. Chen, I. Borozan, J. Feld et al., “Hepatic gene expression discriminates responders and nonresponders in treatment of chronic hepatitis C viral infection,” Gastroenterology, vol. 128, no. 5, pp. 1437–1444, 2005. View at Publisher · View at Google Scholar · View at Scopus
  70. Y. Zhu, B. Qin, C. Xiao, X. Lu, and L. Chen, “Cell-type specific interferon stimulated gene staining in liver underlies response to interferon therapy in chronic hbv infected patients,” Digestive Diseases and Sciences, vol. 57, no. 9, pp. 2355–2361, 2012. View at Publisher · View at Google Scholar · View at Scopus
  71. G. Randall, L. Chen, M. Panis et al., “Silencing of USP18 potentiates the antiviral activity of interferon against hepatitis C virus infection,” Gastroenterology, vol. 131, no. 5, pp. 1584–1591, 2006. View at Publisher · View at Google Scholar · View at Scopus
  72. M. Sarasin-Filipowicz, E. J. Oakeley, F. H. T. Duong et al., “Interferon signaling and treatment outcome in chronic hepatitis C,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 19, pp. 7034–7039, 2008. View at Publisher · View at Google Scholar · View at Scopus
  73. T. Huang, K. Tu, Y. Shyr, C.-C. Wei, L. Xie, and Y.-X. Li, “The prediction of interferon treatment effects based on time series microarray gene expression profiles,” Journal of Translational Medicine, vol. 6, no. 1, article 44, 2008. View at Publisher · View at Google Scholar · View at Scopus
  74. N. I. Rallon, L. A. Lopez-Fernandez, M. I. Garcia et al., “Interferon-stimulated genes are associated with peginterferon/ribavirin treatment response regardless of IL28B alleles in hepatitis C virus/HIV-coinfected patients,” AIDS, vol. 27, no. 5, pp. 687–696, 2013. View at Publisher · View at Google Scholar · View at Scopus
  75. E. G. Meissner, D. Bon, L. Prokunina-Olsson et al., “IFNL4-ΔG genotype is associated with slower viral clearance in Hepatitis C, genotype-1 patients treated with sofosbuvir and ribavirin,” Journal of Infectious Diseases, vol. 209, no. 11, pp. 1700–1704, 2014. View at Publisher · View at Google Scholar · View at Scopus
  76. V. Suppiah, M. Moldovan, G. Ahlenstiel et al., “IL28B is associated with response to chronic hepatitis C interferon-α and ribavirin therapy,” Nature Genetics, vol. 41, no. 10, pp. 1100–1104, 2009. View at Publisher · View at Google Scholar · View at Scopus
  77. Y. Tanaka, N. Nishida, M. Sugiyama et al., “Genome-wide association of IL28B with response to pegylated interferon-α and ribavirin therapy for chronic hepatitis C,” Nature Genetics, vol. 41, no. 10, pp. 1105–1109, 2009. View at Publisher · View at Google Scholar · View at Scopus
  78. H. Ochi, T. Maekawa, H. Abe et al., “Il-28b predicts response to chronic hepatitis C therapy—fine-mapping and replication study in Asian populations,” Journal of General Virology, vol. 92, no. 5, pp. 1071–1081, 2011. View at Publisher · View at Google Scholar · View at Scopus
  79. K. Ray, “Hepatitis: new gene IFNL4 is associated with impaired clearance of HCV,” Nature Reviews Gastroenterology and Hepatology, vol. 10, no. 2, p. 63, 2013. View at Publisher · View at Google Scholar · View at Scopus
  80. O. J. Hamming, E. Terczyńska-Dyla, G. Vieyres et al., “Interferon lambda 4 signals via the IFNλ receptor to regulate antiviral activity against HCV and coronaviruses,” The EMBO Journal, vol. 32, no. 23, pp. 3055–3065, 2013. View at Publisher · View at Google Scholar · View at Scopus
  81. L. M. Real, K. Neukam, R. Herrero et al., “IFNL4 ss469415590 variant shows similar performance to rs12979860 as predictor of response to treatment against hepatitis C virus genotype 1 or 4 in Caucasians,” PLoS ONE, vol. 9, no. 4, Article ID e95515, 2014. View at Publisher · View at Google Scholar · View at Scopus
  82. H. Konishi, T. Motomura, Y. Matsumoto et al., “Interferon-lambda4 genetic polymorphism is associated with the therapy response for hepatitis C virus recurrence after a living donor liver transplant,” Journal of Viral Hepatitis, vol. 21, no. 6, pp. 397–404, 2014. View at Publisher · View at Google Scholar · View at Scopus
  83. S. Zeuzem, V. Soriano, T. Asselah et al., “Faldaprevir and deleobuvir for HCV genotype 1 infection,” The New England Journal of Medicine, vol. 369, no. 7, pp. 630–639, 2013. View at Publisher · View at Google Scholar · View at Scopus
  84. S. Franco, E. Aparicio, M. Parera, B. Clotet, C. Tural, and M. A. Martinez, “IFNL4 ss469415590 variant is a better predictor than rs12979860 of pegylated interferon-alpha/ribavirin therapy failure in hepatitis C virus/HIV-1 coinfected patients,” AIDS, vol. 28, no. 1, pp. 133–136, 2014. View at Publisher · View at Google Scholar · View at Scopus
  85. L. Covolo, S. Bibert, F. Donato et al., “The novel ss469415590 variant predicts virological response to therapy in patients with chronic hepatitis C virus type 1 infection,” Alimentary Pharmacology & Therapeutics, vol. 39, no. 3, pp. 322–330, 2014. View at Publisher · View at Google Scholar · View at Scopus
  86. S. Akkarathamrongsin, V. D. Thong, S. Payungporn et al., “IFNL3 (IL28B) and IFNL4 polymorphisms are associated with treatment response in Thai patients infected with HCV genotype 1, but not with genotypes 3 and 6,” Journal of Medical Virology, vol. 86, no. 9, pp. 1482–1490, 2014. View at Google Scholar