Image description

Published yearly: 

4 Issues


ISSN: 2320-964X (Online) 

ISSN: 2320-7817  (Print)



Dr. Santosh Pawar 




Int. Journal of Life Sciences, 2017; 5(1):127- 132    |    Available online, 11 April, 2017

Role of IL-10 and IL28B in HCV Infected Patients: A Short Review

Amar Deep1,2, Ajay Kumar2#, Suchit Swaroop1


1Experimental and Public Health Lab, Department of Zoology, University of Lucknow,

2Department of Medical Gastroenterology, King George’s Medical University, Lucknow,

Received: 10.12.2016    |   Accepted: 29.01.2017    |     Published : 11.04.2017

The hepatitis C virus (HCV) infection is pandemic and has been systematically studied, characterized in North America and Europe, but this important public health problem has not received tantamount attention in other regions. Hepatitis C virus (HCV) was detected from the serum of infected animal by Choo et al (1989), it is now well accomplished that HCV infection pretends all countries, leading to a major global health problem that requires far-flung active interventions for its prevention and control. Subsequently HCV infection, the innate immune response is initially important for controlling viral replication with the adaptive immune reaction topping out at 8–weeks after infection. Finally, a coordinated attempt between the innate and adaptive immune responses is necessary to eliminate HCV from the liver. Cytokines play an important role in the regulation of immune response may influence the outcome of acute HCV infection. Interleukin-10 (IL-10) is having multiple function anti-inflammatory cytokine mainly produced by immune cells, such as T cells, monocytes, appropriately stimulated macrophages, some subsets of dendritic cells (DCs), and B cells. IL28B gene encodes a cytokine distantly related to type I interferon and the IL-10 family. IL-10, interleukin 28B (IL28B), and interleukin 29 (IL29) are three closely related cytokine genes that form a cytokine gene cluster on a chromosomal region mapped to 19q13. Expression of the cytokines encoded by the three genes can be induced by viral infection.


Keywords: Hepatitis C virus (HCV), Untranslated regions (UTRs), Interleukin, Cirrhosis.



Editor: Dr. Arvind Chavhan


Cite this article as:

Amar Deep, Ajay Kumar, Suchit Swaroop (2017) Role of IL-10 and IL28B in HCV Infected Patients: A Short Review, International J. of Life Sciences, 5 (1): 127-132.



I am deeply grateful to UGC for providing me UGC-BSR fellowship which help me conducting the experimental work smoothly and to the Prof. OMKAR, HOD of Zoology Department, University of Lucknow for all sources and materials used for reviewed this manuscript, for his valuable support and guidance.


Conflicts of interest: The authors stated that no conflicts of interest.



Copyright: © 2017 | Author(s), This is an open access article under the terms of the Creative Commons Attribution-Non-Commercial - No Derivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.


Abbas Z, Moatter T (2003) Interleukin (IL) 1beta and IL-10 gene polymorphism in chronic hepatitis C patients with normal or elevated alanine aminotransferase levels. J Pak Med Assoc;53: 59–62.

Alter HJ, Holland PV, Purcell RH, Lander JJ, Feinstone SM, et al. (1972) Post transfusion Hepatitis after exclusion of commercial and Hepatitis-B antigen-positive donors. Ann Intern Med 77: 691-699.

Alter HJ, Klein HG (2008) The hazards of blood transfusion in historical perspective. Blood 112: 2617-2626.

Alter HJ, Purcell RH, Holland PV, Popper H (1978) Transmissible agent in non-A, non-B Hepatitis. Lancet 1: 459-463.

Baron S (1996) Medical microbiology. 4th ed. Galveston, Tex.: University of Texas Medical Branch at Galveston.

Barrett S, Collins M, Kenny C et al. (2003) Polymorphisms in tumour necrosis factor-alpha, transforming growth factor-beta, interleukin-10, interleukin-6, interferon-gamma, and outcome of hepatitis C virus infection. J Med Virol; 71: 212–218.

Biron CA (1994) Cytokines in the generation of immune responses to, and resolution of virus infection. Curr Opin Immunol.;6:530–538.

Choo QL, Kuo G, Weiner AJ, Overby LR, Bradley DW, Houghton M. 1989. Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome. Science 244:359-362.

Constantini PK, Wawrzynowicz-Syczewska M, Clare M et al. (2002) Interleukin-1, interleukin-10 and tumour necrosis factor-alpha gene polymorphisms in hepatitis C virus infection: an investigation of the relationships with spontaneous viral clearance and response to alpha-interferon therapy. Liver; 22: 404–412.

Edwards-Smith CJ, Jonsson JR, Purdie DM et al. (1999) Interleukin-10 promoter polymorphism predicts initial response of chronic hepatitis C to interferon alfa. Hepatology; 30: 526–530.

Elizabeth J. Minton, David Smillie, Paula Smith, Suzanne Shipley, Michael W McKendrick, Dermot C Gleeson, James CE Underwood, Christopher Cannings, Anthony G Wilson, (2005) Clearance of Hepatitis C Virus Is Not Associated With Single Nucleotide Polymorphisms in the IL-1, -6, or -10 Genes. Human Immunology 2005; 66, 127–132.

Eskdale J, Kube D, Gallagher G (1996) A second polymorphic dinucleotide repeat in the 5_ flanking region of the human IL10 gene. Immunogenetics;45:82–83.

Flamm SL. Chronic hepatitis C virus infection. JAMA 2003; 289: 2413–2417.

Ge D, Fellay J, Thompson AJ, Simon JS, Shianna KV, Urban TJ, et al. (2009) Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance. Nature;461:399-401.

Gottwein JM, Scheel TK, Jensen TB, Lademann JB, Prentoe JC, Knudsen ML, et al, (2009) Development and characterization of hepatitis C virus genotype 1-7 cell culture systems: Role of hepatitis C virus genotype 1-7 cell culture systems: Role of cd81 and scavenger receptor class b type i and effect of antiviral drugs. Hepatol; 49 : 364-77.

Heydtmann M, Shields P, McCaughan G, Adams D: Cytokines and chemokines in the immune response to hepatitis C infection. Curr Opin Infect Dis 2001; 14:279.

Khachatoorian R, French SW (2016) Chaperones in hepatitis C virus infection. World J Hepatol., 8(1): 9­35.

Knapp S, Hennig BJ, Frodsham AJ et al. Interleukin-10 promoter polymorphisms and the outcome of hepatitis C virus infection. Immunogenetics 2003; 55: 362–369.

Kotenko SV, Gallagher G, Baurin VV et al. (2003) “IFN-λs mediate antiviral protection through a distinct class II cytokine receptor complex,” Nature Immunology, vol. 4, no. 1, pp. 69– 77.

Kuiken C, Simmonds P (2009) Nomenclature and numbering of the hepatitis C virus. Methods Mol Biol (Clifton) NJ; 510 : 33-53.

Lindenbach BD, Rice CM (2005) Unravelling hepatitis C virus replication from genome to function. Nature; 436: 933­938 [PMID: 16107832 DOI: 10.1038/nature04077].

Moore KW, de Waal Malefyt R, Coffman RL, O’Garra A. Interleukin-10 and the interleukin-10 receptor. Ann Rev Immunol 2001;19:683–765.

Mosmann TR, Sad S (1996) The expanding universe of T-cell subsets: Th1, Th2 and more. Immunol Today.;17:138–146.

Muhammad SA, Sadia T, Amna S, Tahir AB, Talha S, Najm US SZ, Ishtiaq Q (2011) Analysis of interleukin-10 gene polymorphisms and hepatitis C susceptibility in Pakistan. J Infect Dev Ctries, 5(6):473-479.

Olfat G. Shaker, Yasser H. Nassar, Zeinab A. Nour, and yMona El Raziky (2013) Single-Nucleotide Polymorphisms of IL-10 and IL-28B as Predictors of the Response of IFN Therapy in HCV Genotype 4–infected Children. JPGN;57: 155–160.

Persico M, Capasso M, Persico E, Masarone M, de Renzo A, Spano D, Bruno S, Iolascon A (2006) Interleukin-101082 GG polymorphism influences the occurrence and the clinical characteristics of hepatitis C virus infection Journal of Hepatology 45 : 779–785.

Rauch A, Kutalik Z, Descombes P, Cai T, di Iulio J, Mueller T, et al. (2010) Genetic variation in IL28B is associated with chronic hepatitis C and treatment failure: a genome-wide association study. Gastroenterology 2010;138:1338-1345.

Sheppard P, Kindsvogel W, Xu W et al. (2003) “IL-28, IL-29 and their class II cytokine receptor IL-28R,” Nature Immunology, vol. 4, no. 1, pp. 63–68.

Thio C (2008) Host Genetic Factors and Antiviral Immune Responses to HCV. Clin Liver Dis 12: 713-726.

Thomas DL, Thio CL, Martin MP, et al. (2009) Genetic variation in IL28B and spontaneous clearance of hepatitis C virus. Nature.;461(7265):798-801. doi:10.1038/nature08463.

Thomas DL, Thio CL, Martin MP, et al. (2009) Genetic variation in IL28B and spontaneous clearance of hepatitis C virus. Nature. Oct 8;461(7265):798–801. doi: 10.1038/nature08463.

Tough DF, Borrow P, Spent J (1996) Induction of bystander T cell proliferation by viruses and type I interferon in vivo. Science., 272:1947–1950.

Vidigal PG, Germer JJ, Zein NN (2002) Polymorphisms in the interleukin-10, tumor necrosis factor alpha, and transforming growth factor-beta1 genes in chronic hepatitis C patients treated with interferon and ribavirin. J Hepatol; 36: 271–277.

Wang C, Sarnow P, Siddiqui A (1993) Translation of human hepatitis C virus RNA in cultured cells is mediated by an internal ribosome binding mechanism. J Virol; 67: 3338­ 3344.

Yee LJ, Tang J, Gibson AW et al. Interleukin 10 polymorphisms as predictors of sustained response in antiviral therapy for chronic hepatitis C infection. Hepatology 2001; 33: 708–712.







    Origin & Evolution

    Print ISSN : 2320-7817 

    Online ISSN:2320-964X

    UGC Approved Journal No. 48951


    46, Guruwandan, Jawahar Nagar, 

    VMV Road, Amravati- 444604

    Maharashtra, India.

    Tel  + 91- 9970559438  |   9420775527  

    Email: |