This study investigates the hypothesis that cross-reactions may occur between human cardiac proteins and influenza antigens, thus possibly representing the molecular mechanism underlying influenzaassociated sudden unexpected death (SUD). Using titin protein as a research model, data were obtained on (1) the occurrence of the titin octapeptide AELLVLLE or its mimic AELLVALE in influenza A virus hemagglutinin (HA) sequences; (2) the immunological potential of AELLVLLE and its mimic AELLVALE; (3) the possible role of the flanking amino acid aa) context of the two octapeptide determinants in eliciting cross-reactivity between the human cardiac titin protein and HA antigens.
Autoantibodies (AAbs) against von Willebrand factor (vWF)-cleaving protease ADAMTS13 causally relate to thrombotic thrombocytopenic purpura (TTP). How anti-ADAMTS13 AAbs are generated is unknown. Starting from reports according to which influenza infection can trigger TTP by the production of ADAMTS13 AAbs, this study explores influenza viruses and ADAMTS13 protein for common peptide sequences that might underlie anti-influenza immune responses able to cross-react with ADAMTS13. Results document that numerous peptides are shared between influenza A and B viruses and ADAMTS13, thus supporting the hypothesis of cross-reactivity as a mechanism driving the generation of anti-ADAMTS13 AAbs.