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Published online by Cambridge University Press: 20 August 2009
Induction of autoimmune responses by viral infections
Current concepts
Infections by hepatotropic viruses are suspected as triggers for autoimmune liver diseases. Evidence for this hypothesis is provided by numerous observations of the manifestation of autoimmune hepatitis (AIH) after infections with hepatotropic viruses. The list of viruses which have been suspected to have triggered AIH is long and includes hepatitis A virus, hepatitis B virus, hepatitis C virus (HCV), Epstein–Barr virus, herpes simplex virus (HSV), human herpes virus 6 and the measles virus [1]. These viruses show profound differences in replication, tissue distribution and clinical outcome of infection, yet all may cause inflammation in hepatic tissues and may activate humoral and cellular defence mechanisms. This chapter considers potential markers of the autoimmune response induced by viral infection, the detection of which employs conventional serological and genomic analysis. Several postulates have considered how infections with hepatotropic viruses may trigger autoimmune reactions and three are considered below.
Molecular mimicry
In order to minimize the risk of recognition as nonself by the immune system, it is believed that the sequences of viral proteins evolved to resemble closely domains on host proteins which are protected by tolerance. During an immune response, B cells may be generated which show cross-reactivity towards self-proteins. Also, naive T cells with a potential to bind to peripheral self-peptides presented by major histocompatibility complex (MHC) class I or MHC class II receptors may leave the thymus. Usually, these cells will become anergic by peripheral tolerance mechanisms.
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