In contrast, none of the healthy controls had antibodies to p105, only 23% had a single band to p60, and 3% had a positive response to the p86 peptide. Significant antibodies were noted among the other specified peptides in both HCV and HBV but not in the controls.
We confirmed that chronic HCV and HBV patients demonstrate the presence of autoantibodies to peptides which are not usually found in the healthy individual. Although HCV is an RNA virus in the flavivirus family and HBV is a DNA virus in the Hepadnaviridae family, both chronic infectious states appear to induce an autoimmune component. Neither the viral induction of autoimmune responses 4 nor the clinical evidence of autoimmunity in these infections is new. 5 Abuaf et al. 6 reported that 18% of chronic HCV patients had positive anti-nuclear antibodies compared with 3% among a normal blood donor population. However, the presence of significant autoantibodies may be misleading in diagnosis as many of these antibodies are thought to be found only in specific rheumatic or autoimmune diseases. The irregular patterns and the inconsistent findings among the patients suggest that the development of these autoantibodies are probably an epiphenomenon which is caused by tissue destruction and by the availability of protected proteins that are not normally seen by the individual' s immune system. However, in recent studies in which microbial infections triggered autoimmunity, the theory of molecular mimicry is suggested where some molecules of the microorganisms resemble those of the host. 7 As the host mounts a defense against the infectious agent, it inadvertently activates immune responses against the host' s own molecules. Segal et al. 7 further suggest that the production of interleukin (IL)-12 arouses the self-reactive immune cells. As Cassani et al. 1 stated, further studies are needed to assess the relevance of autoimmune response development and symptoms and as well as infectious disease progression.