Abstract
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.
Highlights
Exposure to viral antigens that share amino acid (AA) sequences 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 disease.Type 1diabetes (T1DM) is a heterogeneous disorder characterized by destruction of pancreatic beta cells, resulting in the loss of insulin secretion
The pathogenesis of T1DM is predicated on two factors: genetic predisposition and the presence of autoantibodies against islet cells, insulin, tyrosine phosphatase, and glutamic acid decarboxylase-65 kDa isoform (GAD65).(1) In the past decades, the incidence of T1DM has increased of 2-5% annually worldwide
(2) Studies in humans and animal models indicate that various viruses are clearly able to modulate the development of T1DM by different mechanisms, including direct beta-cell lysis, bystander activation of autoreactive T cells, loss of regulatory T cells and molecular mimicry.[3]. Recent studies suggest an association between T1D and viral infections including enteroviruses, rubella, mumps, rotavirus, parvovirus, cytomegalovirus and H1N1 influenza.[2,3] Influenza A virus causes systemic and most commonly non-systemic infection, and it can replicate only in the presence of trypsin-like enzymes.[4]
Summary
Exposure to viral antigens that share amino acid (AA) sequences 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 disease.Type 1diabetes (T1DM) is a heterogeneous disorder characterized by destruction of pancreatic beta cells, resulting in the loss of insulin secretion. Exposure to viral antigens that share amino acid (AA) sequences 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 disease. 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.
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