Skip to main content

Increased levels of circulating IL-10 in persons recovered from hepatitis C virus (HCV) infection compared with persons with active HCV infection



Approximately 70% of all hepatitis C (HCV) infections develop chronic disease. Active or exacerbated chronic hepatitis C infection subsequently progress to liver disease. The role of T-cells secretions in achieving viral clearance is still not well understood. Thus, the current study was set to determine the relationship between the T cell cytokine profiles, biochemical parameters and persistent HCV infection or spontaneous recovery.


Twenty-five percent (41/163) of the anti-HCV positive participants had recovered from HCV and had significantly higher concentration of IL-10 compared to those with active HCV infection (P < 0.012). Other circulating cytokines measured; IL-2, IFN gamma, TNF alpha, IL-5 and IL-17 were similar in both groups. Participants with active HCV infection had significantly higher aspartate transaminase (AST) (35 units) and alanine transaminase (46 units) compared to those in the recovered state (P < 0.001). Thus, serum levels of IL10 could be explored in larger prospective cohort study as a predictive marker of recovering from an active HCV infection.


Hepatitis is a leading cause of morbidity and mortality in developing countries. Majority of these liver diseases are known to be of viral origin of which hepatitis C virus (HCV) is the second highest viral causal agent. It is estimated that 0.5% to 3.5% of the world’s population, representing 36–266 million people are infected with hepatitis C [1, 2]. Out of all infected individuals, 54–80% result in chronic forms of hepatitis C and subsequently lead to severe acute liver inflammation and damage [3, 4].

HCV is distributed worldwide, but with uneven geographical spread [5]. In Africa, the overall sero-prevalence is estimated to be between 0 and 66% [5,6,7,8,9,10,11,12,13,14]. In Ghana, the prevalence of hepatitis C varies between 0.3 and 23.2% across different locations. [11, 15].

Chronic or active forms of hepatitis C infection is achieved through successful evasion of the body’s immune surveillance system [16,17,18]. There is limited data on the immunopathology of HCV infection in the Sub-Saharan Africa. The few data available have been from relatively low endemic regions. T-cells are thought to play a role in active HCV infection or spontaneously recovering from it, but the mechanism by which the virus is able to maintain viral perseverance in more than 50% of exposed individuals is still not well understood. Thus, there is the need to determine biomarkers, including serum cytokines which contribute to immunopathogenesis of hepatitis C virus infection and their capability to predict the outcome of HCV infection. The objective of the present study was to determine and analyse the relationship between the T cells cytokine profiles, biochemical parameters and persistence HCV infection or recovery using a single observation design.

Main text


Study population/design

The study employed cross-sectional observation design. The study population was derived from individuals who had tested for HCV positive based on a rapid serological assay test. These individuals were recruited from three different sites in Ghana; the Transfusion unit of Komfo Anokye Teaching Hospital, Obuasi municipality and Daboya community. We recalled 322 individuals using records obtained from the previous work which was carried out between 2013 and 2014 (unpublished). Komfo Anokye Teaching Hospital (KATH) is the second largest tertiary medical facility in Ghana. The Blood Transfusion Medicine Unit serves KATH and other health facilities in Ashanti Region. Obuasi Municipality is a big cosmopolitan municipal in Ashanti region with varying intercultural background due to ongoing mining activities and an estimated population of 169,000. Daboya community is a district capital with an estimated population of 6,510 in the Northern part of Ghana (Fig. 1).

Fig. 1
figure 1

Map of Ghana with selected areas of study. The map was adapted and modified from our previously published manuscript [44]

Inclusion and exclusion

Participants who were 18 years and above who voluntarily gave written informed consent were included. Participants should not have initiated HCV treatment at the time of enrolment. Participants who refused to provide consent were excluded from the study.

Consent and ethics

Ethics approval was granted by the Kwame Nkrumah University of Science and Technology and the Komfo Anokye Teaching Hospital research ethics review committee (Reference; CHRPE/AP/134/13, CHRPE/AP/443/13 and CHRPE/AP/162/15). Written consent was obtained from all participants above 18 years. Confidentiality of participant information was maintained at each level of the study.

Sample collection and processing

At least 5 ml of venous blood samples were collected from all HCV seropositive participants. Blood were collected into EDTA and serum vacutainers, transported to the laboratory and further processed for serum.

Anti-HCV screening confirmation

All samples collected were further confirmed for HCV sero-positivity using ORTHO® HCV Version 3.0 ELISA Test System (Ortho Clinicals Incorporated, USA) according to the manufacturer’s protocol. The test determined antibodies to recombinant hepatitis C encoded antigens c22-3, c200 and NS5 regions which is precoated in microwell-plates.

HCV quantification

Samples that were confirmed to be anti-HCV positive were further tested for HCV RNA and quantified using the Abbott Real-time RT-PCR (Abbott, IL, USA) automated system according to the manufacturer’s instructions.

HBsAg screening and confirmation

All the anti-HCV confirmed positive samples were serologically assessed for hepatitis B virus surface antibody (anti-HBsAg). The test assay was done using GS HBsAg EIA 3.0 (BIO-RAD, Redmond, Washington. USA) and according to the manufacturers protocol.

HIV screening

All the anti-HCV confirmed positive samples were further serologically assessed for HIV-1 and HIV-2 antigen and antibodies. The test assay was done using GS HIV Combo Ag/Ab EIA (BIO-RAD Clinical Diagnostic group, Redmond, Washington. USA) and according to the manufacturers protocol. The tests determined antigens and antibodies to HIV 1&2 using microwell-plates precoated with monoclonal antibodies to HIV p24 (mouse) and HIV-1 and HIV-2 antigens.

Biochemical analysis

Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured using ALT/GPT 4 + 1 SL (ELITech Clinical Systems) on Selectra ProS automated chemistry analyser (ELITech company, Japan) per protocol.

Analysis of serum cytokines

Samples from participants with known HCV status were analysed for their cytokine levels. The relative expression levels of T cell cytokines (Interleukin 2 (IL-2), Interferon (IFN) gamma, Tumour necrosis factor (TNF) alpha, Th2 (Interleukin 5 (IL-5), Th17 cytokines (Interleukin 17 (IL-17) and Interleukin 10 (IL-10) were determined. Cytokines were quantitated using commercially available ELISA assay (Affymetrix eBioscience ELISA Ready-SET-Go, San Diego–California) according to the manufacturer’s instructions. High protein binding ELISA plates were coated with specific capture monoclonal antibody to determine the cytokines (analytes) in the serum samples.

Definitions for hepatitis C infection

For purposes assessing the immunological and biochemical markers in hepatitis C, we classified our study subjects into recovered and active HCV states of infection. Subjects were considered recovered when the serological test was positive but HCV RNA was negative. Subjects were considered as having active HCV infections when the serological test and HCV RNA were both positive. These classifications were based on previous reports [19].

Data collection and statistical analysis

Socio-demographic information was collected through face–face interview with participants. The socio-demographic study variables determined were sex, age, use of alcohol and hepatitis B status. All categorical variables were analysed using Chi square test. Continuous variables and their subcategories were also analysed using either parametric or non-parametric methods based on the distribution of the variables. Statistical analyses were performed using IBM SPSS Statistics v.12 (IBM Computer hardware company, New York, USA) and p value of ≤ 0.05 was considered statistically significant.


A total of 163 participants who agreed to participate in the study were confirmed to be HCV sero-positive. Of the 163, 97 (59.5%) were from KATH, 38 (23.3%) were from Obuasi and 28 (17.7%) were from Daboya. Ninety-eight (98; 60.1%) of the study subjects were males and 65 (39.9%) were females. The overall mean age of participants was 36. Table 1 shows the socio-demographic characteristics of participants.

Table 1 Socio-demographic characteristics of participants

Of the 163 seropositive participants, 122 (74.84%; 95%CI 67.46–81.30) had active HCV infection and 41 (25.15%; 95%CI 18.69–32.53) were in the recovery state. The mean hepatitis C viral load of participants with active HCV infection was 5.5 log10 IU/ml (± 1.0 IU). Table 2 shows a comparison of sex, age, HBsAg status, HIV status, alcohol use and median liver marker enzymes (AST and ALT) between active and recovered HCV infected individuals. The active HCV infected participants had significantly higher AST (35 U/L) and ALT (46 U/L) compared to those in the recovery state (P < 0.001).

Table 2 Characteristics and immunological parameters of active and recovered HCV participants

Cytokine responses

In order to determine the variation in the levels of cytokine among study participants, serum samples were analysed for Th1 (IL-2, IFN gamma and TNF alpha), Th2 (IL-5), Th17 (IL-17A) and Treg (IL-10) cytokines. From the analysis, anti-HCV positive participants who had recovered from the infection had significantly higher [67.2 (50.6–113.1) pg/ml] concentration of IL-10 compared to those with active infection (48.5 (30.3–63.2) pg/ml) p = 0.012. All other cytokines were similar for the two groups. The comparison in levels of cytokines between recovered and active HCV infected participants are shown in Table 2.


Acute infection with HCV often begins as asymptomatic and a large proportion of these infected participants are not able to recover completely. They enter into the chronic phase with active infection. The exact mechanisms underlying spontaneous recovery from HCV is unclear. Therefore, we aimed our study at determining some specific serum cytokines that could play a role in spontaneous recovery from HCV infection.

We determined levels of T cell cytokines IL-2, IFN-γ, TNFα, IL-5, IL-10 and IL-17A among active HCV participants and HCV spontaneously recovered participants. Our study results showed significantly increased levels of IL-10 among spontaneously HCV recovered participants compared with active HCV infection. IL-10 is known to account for appropriate balance of the T helper cytokines necessary for the natural elimination of the hepatitis C viruses. This is consistent with observations made by Mangia et al. and Shaker et al., who demonstrated that heterogeneity in the promoter region as well as SNPs of the IL-10 gene influences the determination of spontaneous or treatment induced favourable outcome of HCV infection [20, 21]. IL-10 produced by stimulated regulatory T cells regulates Th1 and Th2 by inhibiting their inflammatory responses [22]. IL10 controls the differentiation and proliferation of B cells, T cells, antigen-presenting cells, mast cells and granulocytes but negatively regulates Natural killer cells. IL-10 promotes development of type 2 cytokines by inhibiting IFN-γ production [23].

Contrary to our study, Osburn et al. reported decreased levels of IL-10 and IL-2 in individuals who had cleared HCV infection among high risk adults as compared to those who had chronic infection [24]. This outcome differs from our study possibly due to the study design, differences in the age groups of the study populations, environmental exposures and host genetic make-up. We did not observe differences in the interferon, IL-17 and IL-2 levels detected in the serum of recovered and actively infected subjects. IL-2 is known to function by promoting the differentiation of immature T cells into effector and regulatory T cells which may positively affect the outcome of infection. [25, 26]. Interferons exhibit antiviral activity, antiproliferative/antitumor and immunomodulatory effects [27]. Despite the apoptotic signalling pathway induced by TNFα, our study found to not play any role in recovery of HCV infected participants. This outcome is similar to the studies by Abdou et al. 2015 and Costantini et al. 2010 [28,29,30]. Sex and age did not show any significant difference among active HCV infection and spontaneous recovery. This is consistent with observations made by Cho et al. and Kim et al. who could not find any statistically significant role played by sex in spontaneous viral clearance of HCV in a Korean population [31, 32]. Tsui et al. made a similar observation in an adult population [33]. However, Bulteel et al. in their retrospective study identified females within the younger age group showing positive association with spontaneous clearance [34]. The variation could be due to the difference in the geographical location and limited sample size of our study population. In this study there was no statistically significant relationship between spontaneous HCV cleared infection and co-infection with HBV or HIV. But in other studies, co-infection with other viruses had an effect on the natural history of HCV infections leading to variation in detection of serum nucleic acid levels of HCV RNA [35,36,37,38,39,40,41,42]. The study did not established a significant relationship between alcohol consumption and spontaneous HCV clearance or active infection even though alcohol have some immunosuppressive properties [33, 37, 43]. The outcome of the study suggest that serum levels of AST and ALT could be employed as a predictive measure of the status of HCV infection in seropositive subjects.


In the present study, age, sex, co-infection with hepatitis B or HIV variables were not found to be associated with spontaneous HCV clearance in the selected Ghanaian population. The levels of IL-2, IFN-γ, TNFα, IL-5 and IL-17A in the serum of HCV sero-positive are not associated with active HCV infection or spontaneously recovered infection. The levels of IL-10 was high in spontaneously recovered HCV persons, therefore could be explored as a predictive measure of HCV status in anti-HCV positive persons.


The limitations of this study could be conducting a cross-sectional study and the small sample size used. Longitudinal studies that employs a larger population size could provide useful information that would further strengthen the findings of this study.

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.





Hepatitis C virus


Garden City University College


Kumasi Centre for Collaborative Research in Tropical Medicine


Kwame Nkrumah University of Science and Technology


Interferon gamma


Komfo Anokye Teaching Hospital


Ethylenediaminetetraacetic acid


Committee for Human Research, Publications and Ethics


Enzyme linked immunosorbent assay


Ribonucleic acid


Real time polymerase chain reaction


Hepatitis C surface antigens


Human immunodeficiency virus


  1. Thomas DL. Global control of hepatitis C: Where challenge meets opportunity. Nat Med. 2013;19(7):850–8.

    Article  CAS  Google Scholar 

  2. WHO. Hepatitis C—Fact Sheet. 2017. p. October.

  3. Chen AY, Hoare M, Shankar AN, Allison M, Alexander GJM, Michalak TI, et al. Persistence of hepatitis C virus traces after spontaneous resolution of hepatitis C. PLoS ONE. 2015;10(10):1–16.

    Google Scholar 

  4. Zhang M, Rosenberg PS, Brown DL, Preiss L, Konkle BA, Eyster ME, et al. Correlates of spontaneous clearance of hepatitis C virus among people with hemophilia. Vol. 107, Blood. 2006. p. 892–7.

  5. Shepard CW, Finelli L, Alter MJ. Global epidemiology of hepatitis C virus infection. Lancet Infect Dis. 2005. 5(9):558–67.

  6. Arcjentini ARC, Kouruma F, Chionne P, Ucjo ED, Sabbatanp ESSDS, Rapicetta M. Heterogeneity of hepatitis C virus genotype 2 variants in West Central Africa (Guinea Conakry). J Gen Virol. 1996;77:2073–6.

  7. Genovese D, Dettori S, Argentini C, Villano U, Chionne P, Angelico M, et al. Molecular epidemiology of hepatitis C virus genotype 4 isolates in egypt and analysis of the variability of envelope proteins E1 and E2 in patients with chronic hepatitis. J Clin Microbiol. 2005;43(4):1902.

    Article  CAS  Google Scholar 

  8. Menendez C, Sanchez-tapias JM, Kahigwa E, Mshinda H, Costa J, Vidal J, et al. Prevalence and mother-to-infant transmission of hepatitis viruses B, C, and E in Southern Tanzania. J Med Virol. 1999;58(3):215–20.

    Article  CAS  Google Scholar 

  9. Njouom R, Pasquier C, Ayouba A, Tejiokem MC, Vessiere A, Mfoupouendoun J, et al. Low Risk of mother-to-child transmission of hepatitis C virus in Yaode, Cameroo: The ANRS 1262 Study. Am Soc Trop Med Hyg. 2005;73(2):460–6.

    Article  Google Scholar 

  10. Averhoff FM, Glass N, Holtzman D. Global burden of hepatitis C: considerations for healthcare providers in the United States. Clin Infect Dis [Internet]. 2012 Jul [cited 2013 Jun 10]; 55(Suppl 1):S10–5.

  11. Adjei AA, Armah HB, Gbagbo F, Ampofo WK, Quaye IKE, Hesse IFA, et al. Prevalence of human immunodeficiency virus, hepatitis B virus, hepatitis C virus and syphilis among prison inmates and officers at Nsawam and Accra Ghana. J Med Microbiol. 2006;55(5):593–7.

    Article  Google Scholar 

  12. Candotti D, Temple J, Sarkodie F, Allain J. Frequent recovery and broad genotype 2 diversity characterize hepatitis C virus infection in Ghana West Africa. J Virol. 2003;77(14):7914–23.

    Article  CAS  Google Scholar 

  13. Madhava V, Burgess C, Drucker E. Review Epidemiology of chronic hepatitis C virus infection in sub-Saharan Africa. Lancet Infect Dis. 2002;2(5):293–302.

    Article  Google Scholar 

  14. Nelson PK, Mathers BM, Cowie B, Hagan H, Jarlais D, Horyniak D, et al. Global epidemiology of hepatitis B and hepatitis C in people who inject drugs : results of systematic reviews. Lancet. 2010;378(9791):571–83.

    Article  Google Scholar 

  15. Sarkodie F, Adarkwa M, Adu-Sarkodie Y, Candotti D, Acheampong JW, Allain JP. Screening for viral markers in volunteer and replacement blood donors in West Africa. Vox Sang. 2001;80(3):142–7.

    Article  CAS  Google Scholar 

  16. Kew MC. Epidemiology of hepatocellular carcinoma in sub-Saharan Africa. Ann Hepatol. 2013;12(2):173–82.

    Article  Google Scholar 

  17. Petruzziello A. Epidemiology of Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) Related Hepatocellular Carcinoma. Open Virol J [Internet]. 2018. 12(Suppl-1, M3):26–32.

  18. Mittal S, El-Serag HB. Epidemiology of HCC: Consider the Population. J Clin Gastroenterol. 2013;47:1–10.

    Article  Google Scholar 

  19. Coppola N, Pisapia R, Marrocco C, Martini S, Vatiero LM, Messina V, et al. Anti-HCV IgG avidity index in acute hepatitis C. J Clin Virol. 2007;40(2):110–5.

    Article  CAS  Google Scholar 

  20. Mangia A, Santoro R, Piattelli M, Pazienza V, Grifa G, Iacobellis A, et al. IL-10 haplotypes as possible predictors of spontaneous clearance of HCV infection. Cytokine. 2004;25(3):103–9.

    Article  CAS  Google Scholar 

  21. Shaker OG, Nassar YH, Nour ZA, El Raziky M. Single-nucleotide polymorphisms of IL-10 and IL-28B as predictors of the response of IFN therapy in HCV genotype 4-infected children. J Pediatr Gastroenterol Nutr. 2013;57(2):155–60.

    Article  CAS  Google Scholar 

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

    Article  CAS  Google Scholar 

  23. Ouyang W, Rutz S, Crellin NK, Valdez PA, Hymowitz SG. Regulation and functions of the IL-10 family of cytokines in inflammation and disease. Annu Rev Immunol. 2011;29:71–109.

    Article  CAS  Google Scholar 

  24. Osburn WO, Levine JS, Chattergoon MA, Thomas DL, Cox AL. Anti-inflammatory cytokines, pro-fibrogenic chemokines and persistence of acute HCV infection. J Viral Hepat. 2013;20(6):404–13.

    Article  CAS  Google Scholar 

  25. Capobianco MP, Cassiano GC, Furini AA da C, Melo LMS de, Machado CRBD, Dantas RL, et al. Human Interleukin 2 (IL-2) Promotion of Immune Regulation and Clinical Outcomes: A Review. J Cytokine Biol. 2016. 1(109):14–7.

  26. Schlaak JF, Schramm C, Radecke K, zum Buschenfelde K-HM, Gerken G. Sustained suppression of HCV replication and inflammatory activity after interleukin-2 therapy in patients with HIV/hepatitis C virus coinfection. J Acquir Immune Defic Syndr. 2002. 29(2):145–8.

  27. Fensterl V, Sen GC. Interferons and viral infections. BioFactors. 2009;35(1):14–20.

    Article  CAS  PubMed  Google Scholar 

  28. Abdou AG, Asaad NY, Ehsan N, Eltahmody M, El-Sabaawy MM, Elkholy S, et al. The role of IL-28, IFN-gamma, and TNF-alpha in predicting response to pegylated interferon/ribavirin in chronic HCV patients. APMIS. 2015;123(1):18–27.

    Article  CAS  Google Scholar 

  29. Costantini S, Capone F, Guerriero E, Maio P, Colonna G, Castello G. Serum cytokine levels as putative prognostic markers in the progression of chronic HCV hepatitis to cirrhosis. Eur Cytokine Netw. 2010;21(4):251–6.

    CAS  PubMed  Google Scholar 

  30. Pompili M, Biolato M, Miele L, Grieco A. Tumor necrosis factor-alpha inhibitors and chronic hepatitis C: a comprehensive literature review. World J Gastroenterol. 2013;19(44):7867–73.

    Article  Google Scholar 

  31. Kim JY, Won JE, Jeong S-H, Park SJ, Hwang SG, Kang S-K, et al. Acute hepatitis C in Korea: different modes of infection, high rate of spontaneous recovery, and low rate of seroconversion. J Med Virol. 2011;83(7):1195–202.

    Article  Google Scholar 

  32. Cho Y-K, Kim YN, Song B-C. Predictors of spontaneous viral clearance and outcomes of acute hepatitis C infection. Clin Mol Hepatol. 2014. 20(4):368–75.

  33. Tsui JI, Mirzazadeh A, Hahn JA, Maher L, Bruneau J, Grebely J, et al. The effects of alcohol on spontaneous clearance of acute hepatitis C virus infection in females versus males. Drug Alcohol Depend. 2016;169:156–62.

    Article  CAS  Google Scholar 

  34. Bulteel N, Partha Sarathy P, Forrest E, Stanley AJ, Innes H, Mills PR, et al. Factors associated with spontaneous clearance of chronic hepatitis C virus infection. J Hepatol. 2016;65(2):266–72.

    Article  Google Scholar 

  35. Hernandez and Sherman. HIV/HCV coinfection natural history and disease progression, a review of the most recent literature. Curr Opin HIV AIDS. 2011;6(6):478–82.

    Article  Google Scholar 

  36. Mastroianni CM, Lichtner M, Mascia C, Zuccalà P, Vullo V. Molecular mechanisms of liver fibrosis in HIV/HCV coinfection. Int J Mol Sci. 2014;15(6):9184–208.

    Article  CAS  Google Scholar 

  37. Piasecki BA, Lewis JD, Reddy KR, Bellamy SL, Porter SB, Weinrieb RM, et al. Influence of alcohol use, race, and viral coinfections on spontaneous HCV clearance in a US veteran population. Hepatology. 2004;40(4):892–9.

    Article  Google Scholar 

  38. Nguyen LH, Ko S, Wong SS, Tran PS, Trinh HN, Garcia RT, et al. Ethnic differences in viral dominance patterns in patients with hepatitis B virus and hepatitis C virus dual infection. Hepatology. 2011;53(6):1839–45.

    Article  Google Scholar 

  39. Liu C-J. Treatment of patients with dual hepatitis C virus and hepatitis B virus infection: Resolved and unresolved issues. J Gastroenterol Hepatol [Internet]. 2014. 29(1):26–30.

  40. Hung C-H, Lu S-N, Wang J-H, Hu T-H, Chen C-H, Huang C-M, et al. Sustained HCV clearance by interferon-based therapy reduces hepatocellular carcinoma in hepatitis B and C dually-infected patients. Antivir Ther. 2011;16(7):959–68.

    Article  CAS  Google Scholar 

  41. Arends JE, van Assen S, Stek CJ, Wensing AM, Fransen JH, Schellens IM, et al. Pegylated interferon-alpha monotherapy leads to low response rates in HIV-infected patients with acute hepatitis C. Antivir Ther. 2011;16(7):979–88.

    Article  CAS  Google Scholar 

  42. Matthews GV, Dore GJ. HIV and hepatitis C coinfection. J Gastroenterol Hepatol. 2008;23(7 Pt 1):1000–8.

    Article  Google Scholar 

  43. Szabo G, Mandrekar P. A recent perspective on alcohol, immunity, and host defense. Alcohol Clin Exp Res. 2009;33(2):220–32.

    Article  CAS  PubMed  Google Scholar 

  44. Layden JE, Phillips RO, Owusu-Ofori S, Sarfo FS, Kliethermes S, Mora N, et al. High frequency of active HCV infection among seropositive cases in West Africa and evidence for multiple transmission pathways. Clin Infect Dis. 2015;60(7):1033–41.

    Article  Google Scholar 

Download references


The authors thank all the study participants. We are thankful to Professor Jennifer Layden of Loyola University Medical Center, Chicago and her team for the provision of some logistics used in the study. Thanks to Dr. Mrs. Shirley Owusu-Ofori of the Blood Donor Unit, KATH and all the study team members for their cooperation and great support during the study.


This research received no external funding.

Author information

Authors and Affiliations



DOO was the lead for the study, DOO, RP, MO and MF made conceptual contributions; DOO, RP and FSS designed the methodology of the work; MO, DOO and FSS analysed the study results; DOO and MO drafted the work; RP, MF and FSS substantively revised the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Dorcas Ohui Owusu.

Ethics declarations

Ethics approval and consent to participate

The Research was performed in accordance with the Declaration of Helsinki. The study obtained written consent from all study participants. Research ethics approval was obtained from Kwame Nkrumah University of Science and Technology and the Komfo Anokye Teaching Hospital research ethics review committee before commencement (Reference; CHRPE/AP/134/13, CHRPE/AP/443/13 and CHRPE/AP/162/15). Confidentiality of participants information was maintained at each level of the study.

Consent for publication

Not applicable. There are no details relating to an individual person.

Competing interests

The authors declare that they have no competing interests” in this section.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Owusu, D.O., Phillips, R., Owusu, M. et al. Increased levels of circulating IL-10 in persons recovered from hepatitis C virus (HCV) infection compared with persons with active HCV infection. BMC Res Notes 13, 472 (2020).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: