Comparing our results for Aβ1–42 monomersand fibrils with earlier work, we find a common theme: FI10 and otherSARS-CoV-2 protein fragments can indeed increase amyloid formationof human proteins such as αS, SAA, and amylin.,,, As such small viral protein fragments are likely present in vivo following cleavage during infection-caused inflammation,amyloid diseases may be triggered in this way by SARS-CoV-2 and likelyalso other viral infections. This evidence concerns the gene IAPP and viral infectious disease.