What is the pathophysiology of avian influenza?

Updated: Feb 12, 2020
  • Author: Nicholas John Bennett, MBBCh, PhD, MA(Cantab), FAAP; Chief Editor: Michael Stuart Bronze, MD  more...
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Answer

The pathophysiology of avian influenza differs from that of normal influenza. Avian influenza is still primarily a respiratory infection but involves more of the lower airways than human influenza typically does. This is likely due to differences in the hemagglutinin protein and the types of sialic acid residues to which the protein binds. Avian viruses tend to prefer sialic acid alpha(2-3) galactose, which, in humans, is found in the terminal bronchi and alveoli. Conversely, human viruses prefer sialic acid alpha(2-6) galactose, which is found on epithelial cells in the upper respiratory tract. One group has reported that ex vivo cultures of human tonsillar, adenoidal, and nasopharyngeal tissues can support replication of H5N1 avian influenza. [8]

Although this results in a more severe respiratory infection, it probably explains why few, if any, definite human-to-human transmissions of avian influenza have been reported; infection of the upper airways is probably required for efficient spread via coughing and sneezing. Many are concerned that subtle mutation of the hemagglutinin protein through antigenic drift will result in a virus capable of binding to upper and lower respiratory epithelium. The 1918 pandemic strain was so lethal partially because the receptor utilization of the hemagglutinin differed from that of other strains, and H5N1 has that potential to acquire that same biology through mutation.

Differences in the PA, NP, M1, NS1, and PB2 genes tend to correlate with human strains of influenza, including human infections with avian influenza. [9] The functional role of these genetic markers has yet to be determined but likely involves replication enhancement and immune suppression.

Unlike with human influenza, most deaths associated with avian influenza have been due to primary viral pneumonia, with no evidence of secondary bacterial infection.


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