Abstract

Hepatitis A Virus (HAV) and Human Immunodeficiency Virus (HIV) have been associated with development of autoantibodies and autoimmune manifestations in children. Autoimmune Hepatitis (AIH) is particularly aggressive in children/adolescents with a more severe outcome. Thus, studying the mechanisms of virus-related autoimmune disorders in children is a relevant topic of research. We aimed to study the prevalence of autoantibodies in plasma of children infected with either HAV or HIV comparing to healthy children. The relationship bet ween the presence of autoantibodies and biochemical markers of hepatic damage was also investigated. De tection of autoantibodies (SMA) was associated with HAV infection with a prevalence of 35%. Similar levels of hepatic enzymes were observed in sera of HAV-infected patients with reactivity against autoa ntigens as compared to those without autoantibodies . On the other hand, HIV infection showed broader aut oantibodies reactivities than HAV-infected patients and was associated with SMA (18%), ANCA (20%), ANCA-PR3 (15%) and ANCA-MPO (13%). Moreover, either RF or ANA was detected in 8% of HIV-infected children. Prevalence of autoantibodies was not associated with either gender or age of inf ected children. A high prevalence of SMA was observed in HAV- and HIV-infected patients. As HAV and SMA may persit in some patients and AIH can develop in susceptible children, it is recommen ded a follow up of virus infected patients. Since ANCA-PR3 and ANCA-MPO have been shown to be pathogenic, proinflammatory and associated with symptomatic HIV infection, further studies are requ ired to determine the role of these autoantibodies in the pathogenesis associated with viral infection in children.

Highlights

  • Hepatitis A Virus (HAV) and HumanImmunodeficiency Virus (HIV) infections have been recognized with the ability of breaking tolerance to selfantigens, promoting self-reactivity and autoimmune diseases (Dan and Yaniv, 1990; Roessler, 2007).Children are susceptible to infection with HAV and Human Immunodeficiency Virus (HIV) and to develop autoimmune diseases (Huppertz et al., 1995; Skoog et al, 2002; Adebajo, 1997)

  • As HAV and SMA may persit in some patients and Autoimmune Hepatitis (AIH)

  • Either HAV or HIV children coinfected with Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) were excluded from this study

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Summary

Introduction

Hepatitis A Virus (HAV) and HumanImmunodeficiency Virus (HIV) infections have been recognized with the ability of breaking tolerance to selfantigens, promoting self-reactivity and autoimmune diseases (Dan and Yaniv, 1990; Roessler, 2007).Children are susceptible to infection with HAV and HIV and to develop autoimmune diseases (Huppertz et al., 1995; Skoog et al, 2002; Adebajo, 1997). Immunodeficiency Virus (HIV) infections have been recognized with the ability of breaking tolerance to selfantigens, promoting self-reactivity and autoimmune diseases (Dan and Yaniv, 1990; Roessler, 2007). Children are susceptible to infection with HAV and HIV and to develop autoimmune diseases (Huppertz et al., 1995; Skoog et al, 2002; Adebajo, 1997). Navarta and Nelson Acosta-Rivero, Laboratorio de Virología, Hospital Central de Mendoza, Science Publications. Navarta et al / American Journal of Immunology 10 (3): 144-155, 2014. Autoimmune and systemic diseases that have been described in HIV-infected patients (ZandmanGoddard and Shoenfeld, 2002) include: Vasculitis, immune cytopenias, rheumatic diseases, lupus, sarcoidosis, thyroid diseases, hepatic diseases and antiphospholipid syndrome (Iordache et al, 2014). Several autoantibodies have been associated with these pathologies including Antinuclear (ANA), Antimitochondrial (AMA), Antismooth muscle (SMA), Antiparietal Cells (APC), anti-Liver-KidneyMicrosomal (LKM), anti-double strand DNA (DNAds), anti-Tyro Globulin (ATG), Rheumatoid Factor (RF)

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