Evidence for Functional Protein Fragment Homology in Viral Genome Types

In this paper evidence is presented that supports the hypothesis that amino acid usage bias is a fundamental property of viral genome types. Clues to the biological basis for the observed differences in viral amino acid usage are examined. Capsid proteins are analyzed to evaluate the hypothesis that replication mechanism is exclusively responsible for observed amino acid usage profile bias. DSSP secondary structure characterization data is examined to evaluate the competing hypothesis that genome types universally use different sets of functionally equivalent amino acid fragments as building blocks.