Background
We previously reported that a Human Ro52 gene sequence (TRIM21) produced a significant stretch of protein sequence homologous to T. cruzi Antigen 36 (Ag 36) protein sequence, when Ag 36 was translated in the second reading frame. Comparison of their respective DNA sequences demonstrated a 114 nucleotide region of both genes having ~ 70 percent partial homology. After Ro52 was shown to be an E3 Ubiquitin dependent Type I ligase for transcription factors for Interferon genes, we proposed that the Ag 36 gene, which contains a repetitive motif within it, may function to repress Ro52 in the human heart through RNA interference, or other unknown mechanism, giving rise to autoimmunity found in Chronic Chagas Cardiomyopathy (CCC).
Results
To test that hypothesis, we compared various mammalian TRIM genes to the T. cruzi Ag 36 DNA sequence using the Needleman-Wunsch algorithm in the http:\\usegalaxy.eu bioinformatics tool base. In addition to human and chimpanzee, TRIM21 comparable gene regions from canine, shrew, ferret, bat, feline, and armadillo, and aardvark showed homology to the gene for Ag 36 ranging from 68 to 30 percent. However, mouse and eight other mammalian species showed no significant homology. Since mice have been shown to have severe cardiac cardiomyopathy after infection, but their TRIM21 was not homologous to Ag 36 in this study, we conclude that the gene homology has no causative link to CCC.
Conclusions
In addition to human TRIM21, eight mammalian species showed partial gene homology to T. cruzi Ag 36, and some of these have been demonstrated to have CCC. However, rats and mice TRIM21 showed no partial homology to Ag 36. Since these species have been demonstrated to have CCC, the partial gene homology between Ag36 and TRIM 21 may not be causative or associated with CCC, as was originally hypothesized.