The relationship between HLA-G and viral loads in non-responder HCV-infected patients after combined therapy with IFN-α2α and ribavirin

Khorrami, Samaneh; Mohammadpour, Hemn; Shahzamani, Kiana; Zarif, Mahin Nikougoftar; Sharifi, Amir Houshang; Merat, Shahin

doi:10.1016/j.humimm.2014.12.012

Cited by 10 publications

(6 citation statements)

References 19 publications

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“…Various cytokines, such as IFNs, IL-10, IL-2, and TGF-β, influence HLA-G expression [ 17 , 18 ]. All these micro-environmental factors also play an effective role in the liver.…”

Section: Discussionmentioning

confidence: 99%

Outcomes of Interferon/Ribavirin Therapy in Patients with HCV Defined by Expression of Plasma Soluble Human Leukocyte Antigen-G but Not IL-37

Ding

et al. 2016

Med Sci Monit

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BackgroundChronic hepatitis C virus (HCV) infection leads to life-threatening complications worldwide. Immunomodulation signals the response to virus clearance. The immune-suppressive molecule human leukocyte antigen-G (HLA-G) has been shown to function in inhibiting both innate and adaptive immune responses. The objective of this study was to investigate the expression of HLA-G and IL-37 in sustained virological response (SVR) and non-SVR HCV-positive patients before and after complete treatment with a combination of pegylated interferon (IFN) and ribavirin (RBV).Material/MethodsOur study included 132 chronic hepatitis C patents who received combined therapy with IFN-α and RBV. Both SVR and non-SVR patients were included. The end-of-treatment response was defined as undetectable HCV RNA at week 48. Patients with end-of-treatment response were detected by HCV RNA at 24 weeks after therapy. The expression levels of HLA-G and IL-37 at the end and 24 weeks after treatment were detected by ELISA.ResultsPlasma HLA-G and IL-37 were significantly increased in HCV-infected patients compared with healthy individuals before treatment. Furthermore, HLA-G in SVR patients was noticeably decreased after treatment, while HLA-G in non-SVR patients had no changes after treatment. Additionally, both in SVR and non-SVR patients, the expression of IL-37 was remarkably reduced compared with baseline after treatment.ConclusionsThese findings suggest that elevation of HLA-G and IL-37 in HCV may play an important role in response to combined therapy with IFN-α and RBV. Monitoring the expression of HLA-G during therapy could contribute to adjusting the treatment program of HCV-infected patients.

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“…Various cytokines, such as IFNs, IL-10, IL-2, and TGF-β, influence HLA-G expression [ 17 , 18 ]. All these micro-environmental factors also play an effective role in the liver.…”

Section: Discussionmentioning

confidence: 99%

Outcomes of Interferon/Ribavirin Therapy in Patients with HCV Defined by Expression of Plasma Soluble Human Leukocyte Antigen-G but Not IL-37

Ding

et al. 2016

Med Sci Monit

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“…The tolerizing functions of HLA-G seem to be playing a significant role in viral clearance in non-responders to IFN-α2α and ribavirin therapy. Patients who are able to clear HCV infection express only low levels of HLA-G, while non-responders express drastically higher levels of HLA-G (268). Many patients with high levels of HLA-G who failed to respond to antiviral treatment also had a −1082 G/G genotype, resulting in overproduction of IL-10, higher levels of HLA-G, and inadequate viral clearance (267).…”

Section: The Complex Role Of Hla-g In Immunomodulationmentioning

confidence: 99%

Human Leukocyte Antigen (HLA) and Immune Regulation: How Do Classical and Non-Classical HLA Alleles Modulate Immune Response to Human Immunodeficiency Virus and Hepatitis C Virus Infections?

2017

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The genetic factors associated with susceptibility or resistance to viral infections are likely to involve a sophisticated array of immune response. These genetic elements may modulate other biological factors that account for significant influence on the gene expression and/or protein function in the host. Among them, the role of the major histocompatibility complex in viral pathogenesis in particular human immunodeficiency virus (HIV) and hepatitis C virus (HCV), is very well documented. We, recently, added a novel insight into the field by identifying the molecular mechanism associated with the protective role of human leukocyte antigen (HLA)-B27/B57 CD8+ T cells in the context of HIV-1 infection and why these alleles act as a double-edged sword protecting against viral infections but predisposing the host to autoimmune diseases. The focus of this review will be reexamining the role of classical and non-classical HLA alleles, including class Ia (HLA-A, -B, -C), class Ib (HLA-E, -F, -G, -H), and class II (HLA-DR, -DQ, -DM, and -DP) in immune regulation and viral pathogenesis (e.g., HIV and HCV). To our knowledge, this is the very first review of its kind to comprehensively analyze the role of these molecules in immune regulation associated with chronic viral infections.

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“…Additionally, HLA-G and IL-10 were higher in patients at the beginning of treatment than in healthy individuals. These findings suggested that increase of HLA-G and IL-10 in HCV infected patients might affect the response to combined therapy in HCV patients [ 44 ]. Laaribi and coworkers have analyzed HLA-G 14 bp ins/del polymorphism at the 3′ UTR of HLA-G in patients with chronic Hepatitis B virus (HBV) infection, and they found an association between the 14 bp ins/del polymorphism and an enhanced HBV activity, with high HBV DNA levels.…”

Section: Hla-g In Infectious Diseasesmentioning

confidence: 99%

Recent Advances in Our Understanding of HLA-G Biology: Lessons from a Wide Spectrum of Human Diseases

Morandi

Rizzo

Fainardi

et al. 2016

Journal of Immunology Research

109

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HLA-G is a HLA-class Ib molecule with potent immunomodulatory activities, which is expressed in physiological conditions, where modulation of the immune response is required to avoid allograft recognition (i.e., maternal-fetal interface or transplanted patients). However, HLA-G can be expressed de novo at high levels in several pathological conditions, including solid and hematological tumors and during microbial or viral infections, leading to the impairment of the immune response against tumor cells or pathogens, respectively. On the other hand, the loss of HLA-G mediated control of the immune responses may lead to the onset of autoimmune/inflammatory diseases, caused by an uncontrolled activation of the immune effector cells. Here, we have reviewed novel findings on HLA-G functions in different physiological and pathological settings, which have been published in the last two years. These studies further confirmed the important role of this molecule in the modulation of the immune system.

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The relationship between HLA-G and viral loads in non-responder HCV-infected patients after combined therapy with IFN-α2α and ribavirin

Cited by 10 publications

References 19 publications

Outcomes of Interferon/Ribavirin Therapy in Patients with HCV Defined by Expression of Plasma Soluble Human Leukocyte Antigen-G but Not IL-37

Outcomes of Interferon/Ribavirin Therapy in Patients with HCV Defined by Expression of Plasma Soluble Human Leukocyte Antigen-G but Not IL-37

Human Leukocyte Antigen (HLA) and Immune Regulation: How Do Classical and Non-Classical HLA Alleles Modulate Immune Response to Human Immunodeficiency Virus and Hepatitis C Virus Infections?

Recent Advances in Our Understanding of HLA-G Biology: Lessons from a Wide Spectrum of Human Diseases

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