Molecular Biology

, Volume 52, Issue 2, pp 165–181 | Cite as

Human Genetic Predisposition to Diseases Caused by Viruses from Flaviviridae Family

  • N. S. Yudin
  • A. V. Barkhash
  • V. N. Maksimov
  • E. V. Ignatieva
  • A. G. Romaschenko


The identification of human predisposition genes to severe forms of infectious diseases is important for understanding the mechanisms of pathogenesis, as well as for the detection of the risk groups. This will allow one to carry out targeted vaccination and preventive therapy. The most common approaches to the genetic risk estimation include conducting association studies, in which the groups of patients and control individuals are compared using both preliminarily selected candidate genes and using genome-wide analysis. To search for genetic variants predisposed to severe forms of infectious diseases, it is expedient to form a control that consists of patients with clinically proven infections with asymptomatic or mild forms of the disease. The examples of the use of these approaches to identify genetic factors that predispose one to severe forms of infections caused by viruses from the Flaviviridae family are considered in the review. At present, a number of genetic markers associated with predisposition to tick-borne encephalitis, West Nile fever, and Dengue fever have already been detected. These associations must be confirmed in independent samples. Genetic variants, for which the association with spontaneous recovery during infection with hepatitis C virus, patient’s reaction on antiviral drugs, and the development of liver fibrosis was established, were also detected. The gene variants with more pronounced phenotypic effects will probably be found during further studies; they can be used in clinical practice as prognostic markers of the course and outcomes of infection with the Flaviviridae, as well as of the response to treatment.


Flaviviridae genomics candidate gene genome-wide association analysis tick-borne encephalitis West Nile virus Dengue virus hepatitis C virus 



genome-wide association study


single nucleotide polymorphism


tick-borne encephalitis virus


West Nile virus


Dengue virus


hepatitis C virus


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  1. 1.
    Khor C.C., Hibberd M.L. 2012. Host-pathogen interactions revealed by human genome-wide surveys. Trends Genet. 28, 233–243.PubMedCrossRefGoogle Scholar
  2. 2.
    Jack R.S. 2015. Evolution of immunity and pathogens. Results Probl. Cell Differ. 57, 1–20.PubMedCrossRefGoogle Scholar
  3. 3.
    Horby P., Nguyen N.Y., Dunstan S.J., et al. 2012. The role of host genetics in susceptibility to influenza: A systematic review. PLoS One. 7, e33180.PubMedPubMedCentralCrossRefGoogle Scholar
  4. 4.
    Spanevello F., Calistri A., Del Vecchio C., et al. 2016. Development of lentiviral vectors simultaneously expressing multiple siRNAs against CCR5, vif and tat/rev genes for an HIV-1 gene therapy approach. Mol. Ther. Nucleic Acids. 5, e312.PubMedPubMedCentralCrossRefGoogle Scholar
  5. 5.
    Mentzer A.J., O’Connor D., Pollard A.J., et al. 2015. Searching for the human genetic factors standing in the way of universally effective vaccines. Phil. Trans. R. Soc. Lond. B. 370, pii: 20140341.CrossRefGoogle Scholar
  6. 6.
    Loeb M. 2013. Host genomics in infectious diseases. Infect. Chemother. 45, 253–259.PubMedPubMedCentralCrossRefGoogle Scholar
  7. 7.
    Albright F.S., Orlando P., Pavia A.T., et al. 2008. Evidence for a heritable predisposition to death due to influenza. J. Infect. Dis. 197, 18–24.PubMedCrossRefGoogle Scholar
  8. 8.
    Hwang A.E., Hamilton A.S., Cockburn M.G., et al. 2012. Evidence of genetic susceptibility to infectious mononucleosis: A twin study. Epidemiol. Infect. 140, 2089–2095.PubMedCrossRefGoogle Scholar
  9. 9.
    Petersen L., Andersen P.K., Sørensen T.I. 2005. Premature death of adult adoptees: Analyses of a casecohort sample. Genet. Epidemiol. 28, 376–382.PubMedCrossRefGoogle Scholar
  10. 10.
    Pradier S., Lecollinet S., Leblond A. 2012. West Nile virus epidemiology and factors triggering change in its distribution in Europe. Rev. Sci. Tech. 31, 829–844.PubMedCrossRefGoogle Scholar
  11. 11.
    Hasan S., Jamdar S.F., Alalowi M., et al. 2016. Dengue virus: A global human threat. Review of literature. J. Int. Soc. Prev. Community Dent. 6, 1–6.PubMedCrossRefGoogle Scholar
  12. 12.
    Carabali M., Hernandez L.M., Arauz M.J., et al. 2015. Why are people with dengue dying? A scoping review of determinants for dengue mortality. BMC Infect Dis. 15,301.PubMedPubMedCentralCrossRefGoogle Scholar
  13. 13.
    Perelygin A.A., Scherbik S.V., Zhulin I.B., et al. 2002. Positional cloning of the murine flavivirus resistance gene. Proc. Natl. Acad. Sci. U. S. A. 99, 9322–9327.PubMedPubMedCentralCrossRefGoogle Scholar
  14. 14.
    Scherbik S.V., Pulit-Penaloza J.A., Basu M., et al. 2013. Increased early RNA replication by chimeric West Nile virus W956IC leads to IPS-1-mediated activation of NF-kB and insufficient virus-mediated counteraction of the resulting canonical type I interferon signaling. J. Virol. 87, 7952–7965.PubMedPubMedCentralCrossRefGoogle Scholar
  15. 15.
    Pulit-Penaloza J.A., Scherbik S.V., Brinton M.A. 2012. Type 1 IFN-independent activation of a subset of interferon stimulated genes in West Nile virus Eg101-infected mouse cells. Virology. 425, 82–94.PubMedPubMedCentralCrossRefGoogle Scholar
  16. 16.
    Mashimo T., Lucas M., Simon-Chazottes D., et al. 2002. A nonsense mutation in the gene encoding 2'-5'-oligoadenylate synthetase/L1 isoform is associated with West Nile virus susceptibility in laboratory mice. Proc. Natl. Acad. Sci. U. S. A. 99, 11555–11557.CrossRefGoogle Scholar
  17. 17.
    Brinton M.A., Perelygin A.A. 2003. Genetic resistance to flaviviruses. Adv. Virus Res. 60, 43–85.PubMedCrossRefGoogle Scholar
  18. 18.
    Courtney S.C., Di H., Stockman B.M., et al. 2012. Identification of novel host cell binding partners of Oas1b, the protein conferring resistance to flavivirusinduced disease in mice. J. Virol. 86, 7953–7963.PubMedPubMedCentralCrossRefGoogle Scholar
  19. 19.
    Graham J.B., Thomas S., Swarts J., et al. 2015. Genetic diversity in the collaborative cross model recapitulates human West Nile virus disease outcomes. MBio. 6, e00493–e00515.PubMedPubMedCentralCrossRefGoogle Scholar
  20. 20.
    Kumar V., Wijmenga C., Xavier R.J. 2014. Genetics of immune-mediated disorders: From genome-wide association to molecular mechanism. Curr. Opin. Immunol. 31, 51–57.PubMedPubMedCentralCrossRefGoogle Scholar
  21. 21.
    Boisson-Dupuis S., Bustamante J., El-Baghdadi J., et al. 2015. Inherited and acquired immunodeficiencies underlying tuberculosis in childhood. Immunol. Rev. 264, 103–120.PubMedPubMedCentralCrossRefGoogle Scholar
  22. 22.
    Donnelly R.P., Dickensheets H., O’Brien T.R. 2011. Interferon-lambda and therapy for chronic hepatitis C virus infection. Trends Immunol. 32, 443–450.PubMedPubMedCentralCrossRefGoogle Scholar
  23. 23.
    Lu Y.F., Mauger D.M., Goldstein D.B., et al. 2015. IFNL3 mRNA structure is remodeled by a functional non-coding polymorphism associated with hepatitis C virus clearance. Sci. Rep. 5, 16037.PubMedPubMedCentralCrossRefGoogle Scholar
  24. 24.
    Newport M.J., Finan C. 2011. Genome-wide association studies and susceptibility to infectious diseases. Brief Funct. Genomics. 10, 98–107.PubMedCrossRefGoogle Scholar
  25. 25.
    Iio E., Matsuura K., Nishida N., et al. 2015. Genomewide association study identifies a PSMD3 variant associated with neutropenia in interferon-based therapy for chronic hepatitis C. Hum. Genet. 134, 279–289.PubMedCrossRefGoogle Scholar
  26. 26.
    Amos W., Driscoll E., Hoffman J.I. 2011. Candidate genes versus genome-wide associations: which are better for detecting genetic susceptibility to infectious disease? Proc. Biol. Sci. 278, 1183–1188.CrossRefGoogle Scholar
  27. 27.
    Loeb M., Eskandarian S., Rupp M., et al. 2011. Genetic variants and susceptibility to neurological complications following West Nile virus infection. J. Infect. Dis. 204, 1031–1037.PubMedPubMedCentralCrossRefGoogle Scholar
  28. 28.
    Ioannidis J.P., Yu Y., Seddon J.M. 2012. Correction of phenotype misclassification based on high-discrimination genetic predictive risk models. Epidemiology. 23, 902–909.PubMedCrossRefGoogle Scholar
  29. 29.
    Munafo M.R., Gage S.H. 2013. Improving the reliability and reporting of genetic association studies. Drug Alcohol Depend. 132:411–413.PubMedCrossRefGoogle Scholar
  30. 30.
    Chen H., Wang C., Conomos M.P., et al. 2016. Control for population structure and relatedness for binary traits in genetic association studies via logistic mixed models. Am. J. Hum. Genet. 98, 653–666.PubMedPubMedCentralCrossRefGoogle Scholar
  31. 31.
    Burton P.R., Hansell A.L., Fortier I., et al. 2009. Size matters: just how big is BIG?: Quantifying realistic sample size requirements for human genome epidemiology. Int. J. Epidemiol. 38, 263–273.PubMedCrossRefGoogle Scholar
  32. 32.
    Daep C.A., Munoz-Jordan J.L., Eugenin E.A. 2014. Flaviviruses, an expanding threat in public health: focus on dengue, West Nile, and Japanese encephalitis virus. J. Neurovirol. 20, 539–560.PubMedPubMedCentralCrossRefGoogle Scholar
  33. 33.
    Klein R.S. 2008. A moving target: the multiple roles of CCR5 in infectious diseases. J. Infect. Dis. 197, 183–186.PubMedCrossRefGoogle Scholar
  34. 34.
    Kindberg E., Mickiene A., Ax C., et al. 2008. A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis. J. Infect. Dis. 197, 266–269.PubMedCrossRefGoogle Scholar
  35. 35.
    Mickiene A., Pakalniene J., Nordgren J., et al. 2014. Polymorphisms in chemokine receptor 5 and toll-like receptor 3 genes are risk factors for clinical tick-borne encephalitis in the Lithuanian population. PLOS ONE. 9, e106798.PubMedPubMedCentralCrossRefGoogle Scholar
  36. 36.
    Lim J.K., McDermott D.H., Lisco A., et al. 2010. CCR5 deficiency is a risk factor for early clinical manifestations of West Nile virus infection but not for viral transmission. J. Infect. Dis. 201, 178–185.PubMedPubMedCentralCrossRefGoogle Scholar
  37. 37.
    Liu H., Yu W., Liou L.Y., Rice A.P. 2003. Isolation and characterization of the human DC-SIGN and DC-SIGNR promoters. Gene 313, 149–159.PubMedCrossRefGoogle Scholar
  38. 38.
    Koizumi Y., Kageyama S., Fujiyama Y., et al. 2007. RANTES-28G delays and DC-SIGN-139C enhances AIDS progression in HIV type 1-infected Japanese hemophiliacs. AIDS Res. Hum. Retroviruses 23, 713–719.PubMedCrossRefGoogle Scholar
  39. 39.
    Barkhash A.V., Kochneva G.V., Chub E.V., et al. 2014. Association between polymorphisms in OAS2 and CD209 genes and predisposition to chronic hepatitis C in Russian population. Microbes Infect. 16, 445–449.PubMedCrossRefGoogle Scholar
  40. 40.
    Barkhash A.V., Perelygin A.A., Babenko V.N., et al. 2012. Single nucleotide polymorphism in the pro moter region of the CD209 gene is associated with human predisposition to severe forms of tick-borne encephalitis. Antiviral Res. 93, 64–68.PubMedCrossRefGoogle Scholar
  41. 41.
    Alagarasu K., Damle I.M., Bachal R.V., et al. 2013. Association of promoter region polymorphisms of CD209 gene with clinical outcomes of dengue virus infection in Western India. Infect. Genet. Evol. 17, 239–242.PubMedCrossRefGoogle Scholar
  42. 42.
    Sakuntabhai A., Turbpaiboon C., Casadémont I., et al. 2005. A variant in the CD209 promoter is associated with severity of dengue disease. Nat. Genet. 37, 507–513.PubMedCrossRefGoogle Scholar
  43. 43.
    Wang L., Chen R.F., Liu J.W., et al. 2011. DC-SIGN (CD209) Promoter -336 A/G polymorphism is associated with dengue hemorrhagic fever and correlated to DC-SIGN expression and immune augmentation. PLoS Negl. Trop. Dis. 5, e934.PubMedPubMedCentralCrossRefGoogle Scholar
  44. 44.
    Oliveira L.F., Lima C.P., Azevedo Rdo S., et al. 2014. Polymorphism of DC-SIGN (CD209) promoter in association with clinical symptoms of dengue fever. Viral Immunol. 27, 245–249.PubMedCrossRefGoogle Scholar
  45. 45.
    Noecker C.A., Amaya-Larios I.Y., Galeana-Hernández M., et al. 2014. Contrasting associations of polymorphisms in FcγRIIa and DC-SIGN with the clinical presentation of dengue infection in a Mexican population. Acta Trop. 138, 15–22.PubMedCrossRefGoogle Scholar
  46. 46.
    Bigham A.W., Buckingham K.J., Husain S., et al. 2011. Host genetic risk factors for West Nile virus infection and disease progression. PLoS ONE. 6, e24745.PubMedPubMedCentralCrossRefGoogle Scholar
  47. 47.
    Lim J.K., Lisco A., McDermott D.H., et al. 2009. Genetic variation in OAS1 is a risk factor for initial infection with West Nile virus in man. PLoS Pathog. 5, e1000321.PubMedPubMedCentralCrossRefGoogle Scholar
  48. 48.
    Alagarasu K., Honap T., Damle I.M., et al. 2013. Polymorphisms in the oligoadenylate synthetase gene cluster and its association with clinical outcomes of dengue virus infection. Infect. Genet. Evol. 14, 390–395.PubMedCrossRefGoogle Scholar
  49. 49.
    Thamizhmani R., Vijayachari P. 2014. Association of dengue virus infection susceptibility with polymorphisms of 2'-5'-oligoadenylatesynthetase genes: A case-control study. Braz. J. Infect. Dis. 18, 548–550.PubMedCrossRefGoogle Scholar
  50. 50.
    Lanteri M.C., Kaidarova Z., Peterson T., et al. 2011. Association between HLA class I and class II alleles and the outcome of West Nile virus infection: An exploratory study. PLoS ONE. 6, e22948.PubMedPubMedCentralCrossRefGoogle Scholar
  51. 51.
    Ranjith-Kumar C.T., Miller W., Sun J., et al. 2007. Effects of single nucleotide polymorphisms on Tolllike receptor 3 activity and expression in cultured cells. J. Biol. Chem. 282, 17696–17705.PubMedCrossRefGoogle Scholar
  52. 52.
    Barkhash A.V., Voevoda M.I., Romaschenko A.G. 2013. Association of single nucleotide polymorphism rs3775291 in the coding region of the TLR3 gene with predisposition to tick-borne encephalitis in a Russian population. Antiviral Res. 99, 136–138.PubMedCrossRefGoogle Scholar
  53. 53.
    Kindberg E., Vene S., Mickiene A., et al. 2011. A functional toll-like receptor 3 gene (TLR3. may be a risk factor for tick-borne encephalitis virus (TBEV) infection. J. Infect. Dis. 203, 523–528.PubMedGoogle Scholar
  54. 54.
    Alagarasu K., Bachal R.V., Memane R.S., et al. 2015. Polymorphisms in RNA sensing toll like receptor genes and its association with clinical outcomes of dengue virus infection. Immunobiology. 220, 164–168.PubMedCrossRefGoogle Scholar
  55. 55.
    Alagarasu K., Memane R.S., Shah P.S. 2015. Polymorphisms in the retinoic acid-1 like-receptor family of genes and their association with clinical outcome of dengue virus infection. Arch. Virol. 160, 1555–1560.PubMedCrossRefGoogle Scholar
  56. 56.
    Tanaka Y., Nishida N., Sugiyama M., et al. 2009. Genome-wide association of IL28B with response to pegylated interferon-alpha and ribavirin therapy for chronic hepatitis C. Nat. Genet. 41, 1105–1109.PubMedCrossRefGoogle Scholar
  57. 57.
    Keshvari M., Alavian S.M., Behnava B., et al. 2016. Impact of IFNL4 rs12979860 and rs8099917 polymorphisms on response to Peg-Interferon-a and Ribavirin in patients with congenital bleeding disorder and chronic hepatitis C. J. Clin. Lab. Anal. doi 10.1002/jcla.22063Google Scholar
  58. 58.
    Barkhash A.V., Babenko V.N., Voevoda M.I., et al. 2016. Association of IL28B and IL10 gene polymorphism with predisposition to tick-borne encephalitis in a Russian population. Ticks Tick-Borne Dis. 7, 808–812.PubMedCrossRefGoogle Scholar
  59. 59.
    Danial-Farran N., Eghbaria S., Schwartz N., et al. 2015. Genetic variants associated with susceptibility of Ashkenazi Jews to West Nile virus infection. Epidemiol. Infect. 143, 857–863.PubMedCrossRefGoogle Scholar
  60. 60.
    Yakub I., Lillibridge K.M., Moran A., et al. 2005. Single nucleotide polymorphisms in genes for 2'-5'-oligoadenylate synthetase and RNase L in patients hospitalized with West Nile virus infection. J. Infect. Dis. 192, 1741–1748.PubMedCrossRefGoogle Scholar
  61. 61.
    Alagarasu K., Honap T., Mulay A.P., et al. 2012. Association of vitamin D receptor gene polymorphisms with clinical outcomes of dengue virus infection. Hum. Immunol. 73, 1194–1199.PubMedCrossRefGoogle Scholar
  62. 62.
    Ampuero J., del Campo J.A., Rojas L., et al. 2015. Fine-mapping butyrophilin family genes revealed several polymorphisms influencing viral genotype selection in hepatitis C infection. Genes Immun. 16, 297–300.PubMedCrossRefGoogle Scholar
  63. 63.
    Duggal P., Thio C.L., Wojcik G.L., et al. 2013. Genome-wide association study of spontaneous resolution of hepatitis C virus infection: data from multiple cohorts. Ann. Intern. Med. 158, 235–245.PubMedPubMedCentralCrossRefGoogle Scholar
  64. 64.
    Ierusalimsky A.P. 2001. Tick-Borne Encephalitis (Manual for Physicians). Novosibirsk: State Medical Academy.Google Scholar
  65. 65.
    Randall R.E., Goodbourn S. 2008. Interferons and viruses: An interplay between induction, signalling, antiviral responses and virus countermeasures. J. Gen. Virol. 89 (1), 1–47.PubMedCrossRefGoogle Scholar
  66. 66.
    Kovalchuka L., Eglite J., Zalite M., et al. 2014. The frequency of HLA-DR alleles in patients with tickborne disease from Latvia. Res. J. Infect. Dis. 2,4.CrossRefGoogle Scholar
  67. 67.
    Goncharova I.A., Freidin M.B., Rudko A.A., et al. 2006. Genomic bases of susceptibility to infectious diseases. Vavilov J. Genet. Breed. 10, 540–552.Google Scholar
  68. 68.
    Barkhash A.V., Perelygin A.A., Babenko V.N., et al. 2010. Variability in the 2'-5'-oligoadenylate synthetase gene cluster is associated with human predisposition to tick-borne encephalitis virus-induced disease. J. Infect. Dis. 202, 1813–1818.PubMedCrossRefGoogle Scholar
  69. 69.
    Glass W.G., Lim J.K., Cholera R., et al. 2005. Chemokine receptor CCR5 promotes leukocyte traf ficking to the brain and survival in West Nile virus infection. J. Exp. Med. 202, 1087–1098.PubMedPubMedCentralCrossRefGoogle Scholar
  70. 70.
    Larena M., Regner M., Lobigs M. 2012. The chemokine receptor CCR5, a therapeutic target for HIV/AIDS antagonists, is critical for recovery in a mouse model of Japanese encephalitis. PLoS ONE. 7, e44834.PubMedPubMedCentralCrossRefGoogle Scholar
  71. 71.
    Marques R.E., Guabiraba R., Del Sarto J.L., et al. 2015. Dengue virus requires the CC-chemokine receptor CCR5 for replication and infection development. Immunology. 145, 583–596.PubMedPubMedCentralCrossRefGoogle Scholar
  72. 72.
    Hovanessian A.G., Justesen J. 2007. The human 2'-5'oligoadenylate synthetase family: Unique interferoninducible enzymes catalyzing 2'-5' instead of 3'-5' phosphodiester bond formation. Biochimie. 89, 779–788.PubMedCrossRefGoogle Scholar
  73. 73.
    Kristiansen H., Gad H.H., Eskildsen-Larsen S., et al. 2011. The oligoadenylate synthetase family: an ancient protein family with multiple antiviral activities. J. Interferon Cytokine Res. 31, 41–47.PubMedCrossRefGoogle Scholar
  74. 74.
    Choi U.Y., Kang J.S., Hwang Y.S., et al. 2015. Oligoadenylate synthase-like (OASL) proteins: Dual functions and associations with diseases. Exp. Mol. Med. 47, e144.PubMedPubMedCentralCrossRefGoogle Scholar
  75. 75.
    Zhang F., Ren S., Zuo Y. 2014. DC-SIGN, DC-SIGNR and LSECtin: C-type lectins for infection. Int. Rev. Immunol. 33, 54–66.PubMedCrossRefGoogle Scholar
  76. 76.
    Mason C.P., Tarr A.W. 2015. Human lectins and their roles in viral infections. Molecules. 20, 2229–2271.PubMedCrossRefGoogle Scholar
  77. 77.
    Ubol S., Phuklia W., Kalayanarooj S., et al. 2010. Mechanisms of immune evasion induced by a complex of dengue virus and preexisting enhancing antibodies. J. Infect. Dis. 201, 923–935.PubMedCrossRefGoogle Scholar
  78. 78.
    Woitas R.P., Petersen U., Moshage D., et al. 2002. HCV-specific cytokine induction in monocytes of patients with different outcomes of hepatitis C. World J. Gastroenterol. 8, 562–566.PubMedPubMedCentralCrossRefGoogle Scholar
  79. 79.
    Tsai T.T., Chuang Y.J., Lin Y.S., et al. 2013. An emerging role for the anti-inflammatory cytokine interleukin-10 in dengue virus infection. J. Biomed. Sci. 20,40.PubMedPubMedCentralCrossRefGoogle Scholar
  80. 80.
    Rau M., Baur K., Geier A. 2012. Host genetic variants in the pathogenesis of hepatitis C. Viruses. 4, 3281–3302.PubMedPubMedCentralCrossRefGoogle Scholar
  81. 81.
    Swiatek, B.J. 2012. Is interleukin-10 gene polymorphism a predictive marker in HCV infection? Cytokine Growth Factor Rev. 23, 47–59.PubMedCrossRefGoogle Scholar
  82. 82.
    Günther G., Haglund M., Lindquist L., et al. 2011. Tick-borne encephalitis is associated with low levels of interleukin-10 in cerebrospinal fluid. Infect. Ecol. Epidemiol. 1, 6029.CrossRefGoogle Scholar
  83. 83.
    Grygorczuk S., Parczewski M., Moniuszko A., et al. 2015. Increased concentration of interferon lambda-3, interferon beta and interleukin-10 in the cerebrospinal fluid of patients with tick-borne encephalitis. Cytokine. 71, 125–131.PubMedCrossRefGoogle Scholar
  84. 84.
    Barkhash A.V., Babenko V.N., Kobzev V.F., et al. 2010. Polymorphism of 2'-5'-oligoadenylate synthetase (OAS) genes, associated with predisposition to severe forms of tick-borne encephalitis, in human populations of North Eurasia. Mol. Biol. (Moscow). 44, 875–882.CrossRefGoogle Scholar
  85. 85.
    Barkhash A.V., Babenko V.N., Voevoda M.I., et al. 2016. Polymorphism of CD209 and TLR3 genes in populations of North Eurasia. Rus. J. Genet. 52, 603–609.CrossRefGoogle Scholar
  86. 86.
    Palus M., Vojtíšková J., Salát J., et al. 2013. Mice with different susceptibility to tick-borne encephalitis virus infection show selective neutralizing antibody response and inflammatory reaction in the central nervous system. J. Neuroinflammation. 10,77.PubMedPubMedCentralCrossRefGoogle Scholar
  87. 87.
    Bonnevie-Nielsen V., Field L.L., Lu S., et al. 2005. Variation in antiviral 2',5'-oligoadenylate synthetase (2'5'AS) enzyme activity is controlled by a singlenucleotide polymorphism at a splice-acceptor site in the OAS1 gene. Am. J. Hum. Genet. 76, 623–633.PubMedPubMedCentralCrossRefGoogle Scholar
  88. 88.
    Rios J.J., Fleming J.G., Bryant U.K., Carter C.N., et al. 2010. OAS1 polymorphisms are associated with susceptibility to West Nile encephalitis in horses. PLoS ONE. 5, e10537.PubMedPubMedCentralCrossRefGoogle Scholar
  89. 89.
    Sadler A.J., Williams B.R. 2008. Interferon-inducible antiviral effectors. Nat. Rev. Immunol. 8, 559–568.PubMedPubMedCentralCrossRefGoogle Scholar
  90. 90.
    Glass W.G., McDermott D.H., Lim J.K., et al. 2006. CCR5 deficiency increases risk of symptomatic West Nile virus infection. J. Exp. Med. 203, 35–40.PubMedPubMedCentralCrossRefGoogle Scholar
  91. 91.
    Coffey L.L., Mertens E., Brehin A.C., et al. 2009. Human genetic determinants of dengue virus susceptibility. Microbes Infect. 11, 143–156.PubMedCrossRefGoogle Scholar
  92. 92.
    Stephens H.A. 2010. HLA and other gene associations with dengue disease severity. Curr. Top. Microbiol. Immunol. 338, 99–114.PubMedGoogle Scholar
  93. 93.
    Loeb M. 2013. Genetic susceptibility to West Nile virus and dengue. Public Health Genomics. 16, 4–8.PubMedCrossRefGoogle Scholar
  94. 94.
    Thomas D.L., Thio C.L., Martin M.P., et al. 2009. Genetic variation in IL28B and spontaneous clearance of hepatitis C virus. Nature. 461, 798–801.PubMedPubMedCentralCrossRefGoogle Scholar
  95. 95.
    Li Q., Brass A.L., Ng A., Hu Z., et al. 2009. A genome-wide genetic screen for host factors required for hepatitis C virus propagation. Proc. Natl. Acad. Sci. U. S. A. 106, 16410–16415.PubMedPubMedCentralCrossRefGoogle Scholar
  96. 96.
    Zhou L.Y., Zhang L.L. 2016. Host restriction factors for hepatitis C virus. World J. Gastroenterol. 22, 1477–1486.PubMedPubMedCentralCrossRefGoogle Scholar
  97. 97.
    Stättermayer A.F., Scherzer T., Beinhardt S., et al. 2014. Review article: Genetic factors that modify the outcome of viral hepatitis. Aliment. Pharmacol. Ther. 39, 1059–1070.PubMedCrossRefGoogle Scholar
  98. 98.
    Heim M.H., Bochud P.Y., George J. 2016. Host-hepatitis C viral interactions: The role of genetics. J. Hepatol. 65 (Suppl. 1), S22–S32.PubMedCrossRefGoogle Scholar
  99. 99.
    Matsuura K., Tanaka Y. 2016. Host genetic variants influencing the clinical course of hepatitis C virus infection. J. Med. Virol. 88, 185–195.PubMedCrossRefGoogle Scholar
  100. 100.
    Ge D., Fellay J., Thompson A.J., et al. 2009. Genetic variation in IL28B predicts hepatitis C treatmentinduced viral clearance. Nature. 461, 399–401.PubMedCrossRefGoogle Scholar
  101. 101.
    Suppiah V., Moldovan M., Ahlenstiel G., et al. 2009. IL28B is associated with response to chronic hepatitis C interferon-alpha and ribavirin therapy. Nat. Genet. 41, 1100–1104.PubMedCrossRefGoogle Scholar
  102. 102.
    Rauch A., Kutalik Z., Descombes P., et al. 2010. Swiss Hepatitis C Cohort Study; Swiss HIV Cohort Study. Genetic variation in IL28B is associated with chronic hepatitis C and treatment failure: A genome-wide association study. Gastroenterology. 138, 1338–1345.PubMedGoogle Scholar
  103. 103.
    McCarthy J.J., Li J.H., Thompson A., et al. 2010. Replicated association between an IL28B gene variant and a sustained response to pegylated interferon and ribavirin. Gastroenterology. 138, 2307–2314.PubMedPubMedCentralCrossRefGoogle Scholar
  104. 104.
    El-Bendary M., Neamatallah M.A., Abd El-Maksoud M., et al. 2015. Interleukin 28B polymorphism predicts treatment outcome among Egyptian patients infected with HCV genotype 4. Hepatogastroenterology. 62, 947–950.PubMedGoogle Scholar
  105. 105.
    Fateh A., Aghasadeghi M.R., Keyvani H., et al. 2015. High resolution melting curve assay for detecting rs12979860 IL28B polymorphisms involved in response of Iranian patients to chronic hepatitis C treatment. Asian Pac. J. Cancer Prev. 16, 1873–1880.PubMedCrossRefGoogle Scholar
  106. 106.
    Khudayberganova D., Sugiyama M., Masaki N., et al. 2014. IL28B polymorphisms and clinical implications for hepatitis C virus infection in Uzbekistan. PLOS ONE. 9, e93011.PubMedPubMedCentralCrossRefGoogle Scholar
  107. 107.
    de Seixas Santos Nastri A.C., de Mello Malta F., Diniz M.A., et al. 2016. Association of IFNL3 and IFNL4 polymorphisms with hepatitis C virus infection in a population from southeastern Brazil. Arch. Virol. 161, 1477–1484.PubMedCrossRefGoogle Scholar
  108. 108.
    Indolfi G., Mangone G., Calvo P.L., et al. 2014. Interleukin 28B rs12979860 single-nucleotide polymorphism predicts spontaneous clearance of hepatitis C virus in children. J. Pediatr. Gastroenterol. Nutr. 58, 666–668.PubMedCrossRefGoogle Scholar
  109. 109.
    Bellanti F., Vendemiale G., Altomare E., et al. 2012. The impact of interferon lambda 3 gene polymorphism on natural course and treatment of hepatitis C. Clin. Dev. Immunol. 2012, 849373.PubMedPubMedCentralCrossRefGoogle Scholar
  110. 110.
    McFarland A.P., Horner S.M., Jarret A., et al. 2014. The favorable IFNL3 genotype escapes mRNA decay mediated by AU-rich elements and hepatitis C virusinduced microRNAs. Nat. Immunol. 15, 72–79.PubMedCrossRefGoogle Scholar
  111. 111.
    Miki D., Ochi H., Takahashi A., et al. 2013. HLADQB1* 03 confers susceptibility to chronic hepatitis C in Japanese: a genome-wide association study. PLOS ONE. 8, e84226.PubMedPubMedCentralCrossRefGoogle Scholar
  112. 112.
    Xu Y., Huang P., Yue M., et al. 2016. A novel polymorphism near HLA class II region is associated with spontaneous clearance of HCV and response to interferon treatment in Chinese patients. J. Hum. Genet. 61, 301–305.PubMedCrossRefGoogle Scholar
  113. 113.
    Fitzmaurice K., Hurst J., Dring M., et al. 2015. Additive effects of HLA alleles and innate immune genes determine viral outcome in HCV infection. Gut. 64, 813–819.PubMedCrossRefGoogle Scholar
  114. 114.
    Nitschke K., Barriga A., Schmidt J., et al. 2014. HLAB* 27 subtype specificity determines targeting and viral evolution of a hepatitis C virus-specific CD8+ T cell epitope. J. Hepatol. 60, 22–29.PubMedCrossRefGoogle Scholar
  115. 115.
    Rüeger S., Bochud P.Y., Dufour J.F., et al. 2015. Impact of common risk factors of fibrosis progression in chronic hepatitis C. Gut. 64, 1605–1615.PubMedCrossRefGoogle Scholar
  116. 116.
    Nelson D., Yoshida E.M., Paulson M.S., et al. 2014. Genome-wide association study to characterize serum bilirubin elevations in patients with HCV treated with GS-9256, an HCV NS3 serine protease inhibitor. Antivir. Ther. 19, 679–686.PubMedCrossRefGoogle Scholar
  117. 117.
    Bahassi E.M., Stambrook P.J. 2014. Next-generation sequencing technologies: Breaking the sound barrier of human genetics. Mutagenesis. 29, 303–310.CrossRefGoogle Scholar
  118. 118.
    Ramage H., Cherry S. 2015. Virus-host interactions: From unbiased genetic screens to function. Annu. Rev. Virol. 2, 497–524.PubMedCrossRefGoogle Scholar

Copyright information

© Pleiades Publishing, Inc. 2018

Authors and Affiliations

  • N. S. Yudin
    • 1
    • 2
    • 3
  • A. V. Barkhash
    • 1
  • V. N. Maksimov
    • 1
    • 2
  • E. V. Ignatieva
    • 1
    • 3
  • A. G. Romaschenko
    • 1
  1. 1.Federal Research Center Institute of Cytology and Genetics, Siberian BranchRussian Academy of SciencesNovosibirskRussia
  2. 2.Institute of Internal and Preventive MedicineNovosibirskRussia
  3. 3.Novosibirsk National Research State UniversityNovosibirskRussia

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