Influenza viruses bind to the respiratory tract epithelium.
Viral hemagglutinin (H) binds sialic acid residues (neuraminic acid derivatives) on the host cell membrane → virus fusion with the membrane → entry into the cell
The virus replicates in the nucleus of the cell.
The new virus particles travel to the cell membrane → formation of a membrane bud around the virus particles (budding).
Viral neuraminidase (N) cleaves the neuraminic acid → virions exit the cell.
Host cell dies → cellular breakdown triggers a strong immune response
Subtypes are differentiated by cell surface antigens hemagglutinin and neuraminidase (e.g., H1N1 is “swine flu”)
Hemagglutinin (H): promotes viral entry by binding to sialic acid residues
Neuraminidase (N): promotes the release of virion progeny from host cells by cleaving terminal sialic acid residues
Genetic mutations
Antigenic shift
Two subtypes of viruses (e.g., human and swine influenza) infect the same cell and exchange genetic segments (reassortment) to create new subtypes (e.g., H3N1 → H2N1).
Causes pandemics
Antigenic drift
Minor changes in antigenic structure (hemagglutinin and/or neuraminidase) via random point mutation
Causes epidemics (limited to a specific population or region)
Etiology: Common causative pathogens include S. pneumoniae, S. aureus (including MRSA), S. pyogenes, and H. influenzae.
Pathophysiology
Influenza virus attacks the tracheobronchial epithelium and results in decreased cell size and a loss of cilia, which promotes bacterial colonization.
The influenza surface protein neuraminidase also cleaves sialic acid off host glycoproteins, leading to an increased amount of free sugar in the respiratory tract, which fosters bacterial growth.
Clinical features
Development of a purulent, productive cough ∼ 4–14 days after an initial period of improvement
