Abstract
The influenza virus infects host cells via the collective interaction (polyvalence) between many hemagglutinin (HA) sites, which are glycoproteins found on the viral envelope, and sialic acid (SA) residues found on the membrane of the host cell. Therefore, a proposed antiviral targeting influenza would have to also react polyvalently for optimal performance, for which we propose the Q-Beta virus as a bacteriophage scaffold. We have introduced mutations that should allow for the introduction of unnatural amino acids that will serve as sites for the attachment of sugars that will alter protein expression, causing the Q-Beta virus to bind and inhibit influenza.
