Hepatitis C virus (HCV) infection has been related to self-reactivity, extrahepatic manifestations and autoimmune diseases. The main goals of this work were to study the prevalence of autoantibodies and their relationship with viral titers and biochemical markers of hepatic damage in patients infected with HCV. Autoantibodies (ANA, AMA, SMA, APC, LKM, DNAds, ANCA, ATG and RF) were determined in 73 individuals with chronic HCV infection and 44 healthy volunteers. The presence of these antibodies was related to demographic variables, viral titers and biochemical parameters. A high prevalence of autoantibodies, particularly for RF, that was associated with female gender was observed in HCV-infected patients. In addition, SMA, ANA and ATG showed increased frequencies in HCV infection. Interestingly, the concurrent detection of SMA and more than one autoantibody was associated with high gGT levels. Notably, concurrent higher gGT, HCV and SMA levels were observed in male patients as compared to their female counterparts. These results indicate a relationship between HCV infection and the concurrent detection of various autoantibodies in the absence of symptoms of autoimmune diseases. They also suggest a link among the presence of a variety of autoantibodies simultaneously with SMA, increased gGT levels and HCV titers in a population of male patients.

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 between the presence of autoantibodies and biochemical markers of hepatic damage was also investigated. Detection 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 autoantigens as compared to those without autoantibodies. On the other hand, HIV infection showed broader autoantibodies 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 infected 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 recommended 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 required to determine the role of these autoantibodies in the pathogenesis associated with viral infection in children.

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