New virions are then
assembled in the cell membrane in a process called budding. During
the process, part of the cell membrane is wrapped around virions to
form lipid viral envelopes. Finally, neuraminidase (NA) on the surface
of new budding viruses cleaves terminal sialic acid (SA) residues from
hemagglutinin (HA) and new viruses are released to start a new cycle
of infection and replication. All of these steps in the life cycle of
influenza A virus are essential for its virulence, replication, and
transmission. Development of small molecule based inhibitors that
block any of these steps can generate potential efficient strategies to
treat or prevent influenza A infections. In the following sections, we
will go through new strategies currently being used or proposed for
overcoming the resistance of influenza A virus to current M2 ion
channel blocker drugs (amantadine and rimantadine) and NA inhibitor
drugs (e.g. oseltamivir)