Response to Sanver et al.

In this issue of Diabetes Care, the letter by Sanver et al. (1) reported previous studies that demonstrated evidence of a correlation among the hepatitis C virus (HCV) antigenic subtypes, prognosis of disease, autoimmune disease development, response to the interferon (IFN)-α treatment, and various immunological responses in the host. In our 70 patients, we carried out the type of HCV genotypes as published (2). The correlations between HCV genotypes and autoimmunity are reported in Table 1.

From our data, the autoimmunity varies from 37.5% in 2c to 0% in 4 HCV-genotype groups. Interestingly, all of the patients who tested positive for thyroid autoantibodies are in the 3a HCV genotype group, but it is important to consider that in our group, 29 (41.4%) patients show 3a genotype. All patients who tested positive for autoantibodies, except one, showed the positivity before IFN-α therapy. In the majority of the cases, autoantibodies increased under IFN therapy and the clinical autoimmune disease rarely appeared. It is accepted that the autoimmune diseases are correlated with a particular genetic pattern of susceptibility and that the environmental factors may act as trigger factors, but direct evidence of this phenomenon remains circumstantial. In our patients, the presence of autoimmune phenomena has not been significantly increased with respect to the normal population. These data are in conflict with the fact that HCV chronic infection may act as a trigger factor in autoimmunity. So, our data are not sufficient to confirm the hypothesis that a specific genotype may be correlated with the autoimmune response. We think that it will be necessary to carry out further studies, before and after IFN therapy in humans, to clarify the specific role of genetic HCV subtypes and the genetic susceptibility in inducing autoimmunity.