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      Correlations between polymorphisms in the uridine diphosphate-glucuronosyltransferase 1A and C-C motif chemokine receptor 5 genes and infection with the hepatitis B virus in three ethnic groups in China

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          Abstract

          Objective

          To determine whether genetic polymorphisms in the uridine diphosphate-glucuronosyltransferase 1A ( UGT1A) and the C-C motif chemokine receptor 5 ( CCR5) genes are associated with hepatitis B virus (HBV) infection in Yi, Yao and Han ethnic groups in the Guizhou Province of China.

          Methods

          The study enrolled subjects with and without HBV infection. Whole blood was used for DNA genotyping using standard techniques. The study determined the frequencies of several polymorphic alleles ( UGT1A6 [rs2070959], UGT1A1 [rs8175347], CCR5-59029 [rs1799987] and CCR5Δ32 [rs333]) and then characterized their relationship with HBV infection.

          Results

          A total of 404 subjects were enrolled in the study: 138 from the Yao group, 101 from the Yi group and 165 from the Han group. There was a significant difference in the frequency of UGT1A1 rs8175347 polymorphisms among the three groups. The rates of 7TA carriers of UGT1A1 rs8175347 in all three groups were significantly higher than the other genotypes. Individuals with genotype AA of UGT1A6 rs2070959 in the Yi group had a higher risk for HBV infection than in the Yao and Han groups. The frequency of genotype GG in CCR5-59029 in the Yao group was significantly higher than in the Yi group. The genotypes of CCR5Δ32 were not associated with HBV infection.

          Conclusion

          These findings provide genetic and epidemiological evidence for an association of UGT1A and CCR5-59029 polymorphisms with HBV infection in Chinese Yi and Yao populations.

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          Human UDP-glucuronosyltransferases: metabolism, expression, and disease.

          R H Tukey, C P Strassburg (2000)
          In vertebrates, the glucuronidation of small lipophilic agents is catalyzed by the endoplasmic reticulum UDP-glucuronosyltransferases (UGTs). This metabolic pathway leads to the formation of water-soluble metabolites originating from normal dietary processes, cellular catabolism, or exposure to drugs and xenobiotics. This classic detoxification process, which led to the discovery nearly 50 years ago of the cosubstrate UDP-glucuronic acid (19), is now known to be carried out by 15 human UGTs. Characterization of the individual gene products using cDNA expression experiments has led to the identification of over 350 individual compounds that serve as substrates for this superfamily of proteins. This data, coupled with the introduction of sophisticated RNA detection techniques designed to elucidate patterns of gene expression of the UGT superfamily in human liver and extrahepatic tissues of the gastrointestinal tract, has aided in understanding the contribution of glucuronidation toward epithelial first-pass metabolism. In addition, characterization of the UGT1A locus and genetic studies directed at understanding the role of bilirubin glucuronidation and the biochemical basis of the clinical symptoms found in unconjugated hyperbilirubinemia have uncovered the structural gene polymorphisms associated with Crigler-Najjar's and Gilbert's syndrome. The role of the UGTs in metabolism and different disease states in humans is the topic of this review.
          Article 0 comments Cited 187 times – based on 0 reviews     Review now
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            Intracellular inactivation of the hepatitis B virus by cytotoxic T lymphocytes.

            Marcia Hobbs, Luca Guidotti, R Schreiber … (1995)
            It is widely believed that viral clearance is mediated principally by the destruction of infected cells by CTLs. In this report, we use a transgenic mouse model of HBV replication to demonstrate that this assumption may not be true for all viruses. We find that adoptively transferred virus-specific CTLs can abolish HBV gene expression and replication in the liver without killing the hepatocytes. This antiviral function is mediated by IFN gamma and TNF alpha secreted by the CTL or by the antigen-nonspecific macrophages and T cells that they activate following antigen recognition. These cytokines activate two independent virocidal pathways: the first pathway eliminates HBV nucleocapsid particles and their cargo of replicating viral genomes, while the second pathway destabilizes the viral RNA. Intracellular viral inactivation mechanisms such as these could greatly amplify the protective effects of the immune response, while failure of such mechanisms could lead to viral persistence or to the death of the host.
            Article 0 comments Cited 127 times – based on 0 reviews     Review now
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              Natural Killer T Cell Activation Inhibits Hepatitis B Virus Replication in Vivo

              Kazuhiro Kakimi, Luca Guidotti, Yasuhiko Koezuka … (2000)
              We have previously reported that hepatitis B virus (HBV)–specific CD8+ cytotoxic T lymphocytes and CD4+ helper T lymphocytes can inhibit HBV replication in the liver of HBV transgenic mice by secreting interferon (IFN)-γ when they recognize viral antigen. To determine whether an activated innate immune system can also inhibit HBV replication, in this study we activated natural killer T (NKT) cells in the liver of HBV transgenic mice by a single injection of α-galactosylceramide (α-GalCer), a glycolipid antigen presented to Vα14+NK1.1+ T cells by the nonclassical major histocompatibility complex class I–like molecule CD1d. Within 24 h of α-GalCer injection, IFN-γ and IFN-α/β were detected in the liver of HBV transgenic mice and HBV replication was abolished. Both of these events were temporally associated with the rapid disappearance of NKT cells from the liver, presumably reflecting activation-induced cell death, and by the recruitment of activated NK cells into the organ. In addition, prior antibody-mediated depletion of CD4+ and CD8+ T cells from the mice did not diminish the ability of α-GalCer to trigger the disappearance of HBV from the liver, indicating that conventional T cells were not downstream mediators of this effect. Finally, the antiviral effect of α-GalCer was inhibited in mice that are genetically deficient for either IFN-γ or the IFN-α/β receptor, indicating that most of the antiviral activity of α-GalCer is mediated by these cytokines. Based on these results, we conclude that α-GalCer inhibits HBV replication by directly activating NKT cells and by secondarily activating NK cells to secrete antiviral cytokines in the liver. In view of these findings, we suggest that, if activated, the innate immune response, like the adaptive immune response, has the potential to control viral replication during natural HBV infection. In addition, the data suggest that therapeutic activation of NKT cells may represent a new strategy for the treatment of chronic HBV infection.
              Article 0 comments Cited 114 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Int Med Res
                Journal ID (iso-abbrev): J. Int. Med. Res
                Journal ID (publisher-id): IMR
                Journal ID (hwp): spimr
                Title: The Journal of International Medical Research
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Print): 0300-0605
                ISSN (Electronic): 1473-2300
                Publication date (Electronic): 20 September 2017
                Publication date (Print): February 2018
                Volume: 46
                Issue: 2
                Pages: 739-751
                Affiliations
                [1 ]The Key Laboratory of Endemic and Ethnic Diseases of the Ministry of Education of PR China (Guizhou Medical University), Guiyang, Guizhou Province, China
                [2 ]Department of Pathology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, China
                [3 ]Reproduction Centre of Luoyang Centre Hospital Affiliated to Zhengzhou University, Zhengzhou, Henan Province, China
                Author notes
                [#]

                These authors contributed equally to this work.

                [*]Zhi-Zhong Guan, Department of Pathology, Affiliated Hospital of Guizhou Medical University, First Hospital Building, 9 Beijing Road, Guiyang 550004, Guizhou Province, China. Email: 1457658298@ 123456qq.com
                Article
                Publisher ID: 10.1177_0300060517730174
                DOI: 10.1177/0300060517730174
                PMC ID: 5971517
                PubMed ID: 29239247
                SO-VID: e2c32898-ba4b-41a8-9694-aaea5a2af9df
                Copyright © © The Author(s) 2017
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 3 January 2017
                Date accepted : 16 August 2017
                Categories
                Subject: Research Reports

                Keywords: c-c motif chemokine receptor 5 (ccr5),ethnic minorities,gene polymorphisms,hepatitis b virus infection,uridine diphosphate-glucuronosyltransferase 1a (ugt-1a)
                Data availability:
                Keywords: c-c motif chemokine receptor 5 (ccr5), ethnic minorities, gene polymorphisms, hepatitis b virus infection, uridine diphosphate-glucuronosyltransferase 1a (ugt-1a)

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