Autoimmune hepatitis type 2 and hepatitis C virus infection: study of HLA antigens

Jurado, Aurora; Cárdaba, Blanca; Jara, Paloma; Cuadrado, Pilar; Hierro, Loreto; Andrés, Belen de; Pozo, Victoria del; Cortegano, M; Gallardo, Soledad; Camarena, C.; Bárcena, Rafael; Castañer, J.; Alvarez, Rita; Lahoz, Carlos; Palomino, Pilar

doi:10.1016/s0168-8278(97)80106-7

Cited by 43 publications

(23 citation statements)

References 37 publications

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“…Among the host factors, HLA appears to play an important role in the association with HCV infection, mainly HLA class II antigens [Minton et al, 1998], which are crucial for antigen presentation of the T helper lymphocytes [Hü e et al, 2002]. Some of the HLA alleles are associated with HCV infection [Jurado et al, 1997], with the development of chronicity [Thursz et al, 1999] or response to therapy [Almarri et al, 1998]. …”

Section: Discussionmentioning

confidence: 99%

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Allelic frequencies of HPA‐1 to 5 human platelet antigens in patients infected with hepatitis C virus

Verdichio-Moraes

Toralles-Pereira

Grotto

et al. 2009

Journal of Medical Virology

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Studies have suggested that hepatitis C virus (HCV) may infect not only hepatocytes but may also be carried by platelets. Platelets express more than 20 polymorphic antigenic determinants on their surface, which are called human platelet antigens (HPA). To determine the allele frequency of the HPA-1 to -5 in patients infected with HCV, blood samples were collected from 257 blood donors for the control group and from 191 patients infected with HCV. DNA was isolated and amplified for genes HPA-1 to -4 using PCR Sequence Specific Primers (PCR-SSP) and HPA-5 using PCR-Restriction Fragment Length Polymorphism (PCR-RFLP). The allelic and genotypic frequency of HPA-5a in patients infected with HCV was found to be significantly lower (P < 0.05) than in the controls, and HPA-5b from patients infected with HCV was significantly higher (P < 0.05) than in controls. The increase in HPA-5b allelic frequency in HCV infection may indicate a possible association between HCV infection and HPAs.

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Section: Discussionmentioning

confidence: 99%

“…On the other hand, other alleles can have a protective effect against HCV infection [Jurado et al, 1997]. Similarly, HPAs are also associated with diseases.…”

Section: Discussionmentioning

confidence: 99%

Allelic frequencies of HPA‐1 to 5 human platelet antigens in patients infected with hepatitis C virus

Verdichio-Moraes

Toralles-Pereira

Grotto

et al. 2009

Journal of Medical Virology

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“…A meta-analysis of 694 cases of autoimmune hepatitis and 1769 normal subjects reported from South America has implicated DQB1*02, DQB1*0603, DRB1*0405, and DRB1*1301 as the principal susceptibility alleles in this region [72]. DRB1*07 is associated with type 2 autoimmune hepatitis in Brazil [39,40,70,73], Britain [74], and Germany [75], and HLA DRB1*03 and HLA DQ2 are associated with type 2 autoimmune hepatitis in Spain [76] (Table 1). DQB1*0201 is in strong linkage disequilibrium with DRB1*07 and DRB1*03, and this allele has been proposed as the principal genetic determinant of type 2 autoimmune hepatitis [53].…”

Section: Insights Into the Genetic Predispositions For Autoimmune Hepmentioning

confidence: 99%

Transitioning from Idiopathic to Explainable Autoimmune Hepatitis

Czaja

2015

Dig Dis Sci

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Autoimmune hepatitis lacks an identifiable cause, and its diagnosis requires the exclusion of etiologically defined diseases that resemble it. Insights into its pathogenesis are moving autoimmune hepatitis from an idiopathic to explainable disease, and the goal of this review is to describe the insights that are hastening this transition. Two types of autoimmune hepatitis are justified by serological markers, but they also have distinctive genetic associations (DRB1 and DQB1 genes) and autoantigens. DRB1 alleles are the principal susceptibility factors in white adults, and a six amino acid sequence encoded in the antigen-binding groove of class II molecules of the major histocompatibility complex can influence the selection of autoantigens. Polymorphisms, including variants of SH2B3 and CARD10 genes, may affect immune reactivity and disease severity. The cytochrome mono-oxygenase, CYP2D6, is the autoantigen associated with type 2 autoimmune hepatitis, and it shares homologies with multiple viruses that might promote self-intolerance by molecular mimicry. Chemokines, especially CXCL9 and CXCL10, orchestrate the migration of effector cells to sites of injury and are associated with disease severity. Cells of the innate and adaptive immune responses promote tissue damage, and possible deficiencies in the number and function of regulatory T cells may facilitate the injurious process. Receptor-mediated apoptosis is the principal mechanism of hepatocyte loss, and cell-mediated and antibody-dependent mechanisms of cytotoxicity also contribute. Insights that explain autoimmune hepatitis will allow triggering exogenous antigens to be characterized, risk management to be improved, prognostic indices to be refined, and site-specific therapeutic interventions to emerge.

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“…47,92,97,98,109,[122][123][124][125][126][127][128][129][130][131][132] Two studies observed an association between DRB1*11 and the presence of cryoglobulins (OR not reported in Amaroso study; OR ¼ 3.4 in Cacoub study). 122,123 Both studies examined Italian populations.…”

Section: Studies Of Extrahepatic Manifestationsmentioning

confidence: 99%

Host genetic determinants in hepatitis C virus infection

2004

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In addition to viral and environmental/behavioural factors, host genetic diversity is believed to contribute to the spectrum of clinical outcomes in hepatitis C virus (HCV) infection. This paper reviews the literature with respect to studies of host genetic determinants of HCV outcome and attempts to highlight trends and synthesise findings. With respect to the susceptibility to HCV infection, several studies have replicated associations of the HLA class II alleles DQB1*0301 and DRB1*11 with selflimiting infection predominantly in Caucasian populations. Meta-analyses yielded summary estimates of 3.0 (95% CI: 1.8-4.8) and 2.5 (95% CI: 1.7-3.7) for the effects of DQB1*0301 and DRB1*11 on self-limiting HCV, respectively. Studies of genetics and the response to interferon-based therapies have largely concerned single-nucleotide polymorphisms and have been inconsistent. Regarding studies of genetics and the progression of HCV-related disease, there is a trend with DRB1*11 alleles and less severe disease. Studies of extrahepatic manifestations of chronic HCV have shown an association between DQB1*11 and DR3 with the formation of cryoglobulins. Some important initial observations have been made with respect to genetic determinants of HCV outcome. Replication studies are needed for many of these associations, as well as biological data on the function of many of these polymorphisms.

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Autoimmune hepatitis type 2 and hepatitis C virus infection: study of HLA antigens

Cited by 43 publications

References 37 publications

Allelic frequencies of HPA‐1 to 5 human platelet antigens in patients infected with hepatitis C virus

Allelic frequencies of HPA‐1 to 5 human platelet antigens in patients infected with hepatitis C virus

Transitioning from Idiopathic to Explainable Autoimmune Hepatitis

Host genetic determinants in hepatitis C virus infection

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