SUMMARY
Background: Exposure to viral antigens that share amino acid (AA) sequence similar with self-antigens might trigger autoimmune diseases in genetically predisposed individuals, and the molecular mimicry theory suggests that epitope mimicry between the virus and human proteins can activate autoimmune diseases like type 1 diabetes (T1DM). Objective: The purpose of this study is to explore the possible similarity between the AA sequences of human glutamic acid decarboxylase - 65 kDa isoform (GAD65) human insulin, and proteins of H1N1 influenza (strain (A/California/7/2009(H1N1)), using databanks of proteins and immunogenic peptides to explain the development of T1DM. Methods: AA sequences of the A/California/7/2009(H1N1) strain, GAD65 and human insulin, available in the NCBI (National Center for Biotechnology Information) database were compared using the Basic Local Alignment Search Tool (BLAST) software. Results: Similarities were found among the A/California/7/2009(H1N1) strain, GAD and the human insulin. The similarities between Influenza A virus (A/California/7/2009(H1N1)) and the GAD65 ranged from 15.0 % to 56.0%, with statistical significance (P 0.006 and P 0.017). The similarities between the Influenza A virus (A/California/7/2009(H1N1)) and insulin ranged from 38.0 % to 45.0%, but without statistical significance. Conclusion: Bioinformatics data suggest a possible pathogenic link between A/California/7/2009(H1N1) and T1DM. Through molecular mimicry is has been observed that sequences similarity between viral Polyprotein and self-proteins could induce a crossover immune response to self-antigens, with a breakdown of self-tolerance, resulting in autoimmune disease.