After inhalation, the virus is deposited onto the respiratory tract epithelium, where it attaches to ciliated columnar epithelial cells via its surface hemagglutinin. Local host defenses, such as mucociliary clearance, or secretion of specific secretory IgA antibodies can remove some of the virus particles. However, if mucociliary clearance is impaired (as in smokers [21] or older patients [22] ) or secretory antiinfluenza IgA antibodies are absent (as in no antecedent exposure to the virus), infection continues unabated [23] . Respiratory epithelial cells are invaded, and viral replication occurs. Newer viruses then infect larger numbers of epithelial cells, shut off the synthesis of critical proteins, and ultimately lead to host cell death [24] .