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PBL 3 G9 (Importance of H9N2 as potential pandemic influenza virus…

- - - - (Allantoic fluid) Embryonated chicken egg
        
        CPE
        
        Further do HA and HI test, RT-PCR
    - - MacConkey agar
        
        Lactose positive (pink colony)
      - Tryptose blood agar
        
        colony: low convex, shiny, moist, entire, grey
        
        gamma hemolysis
  - - - RT-PCR
    - - PCR
  - - - IFA
      - HA and HI
      - Western Blot
        
        Positive: presence of desired band
        
        Negative: Band is absence
      - ELISA
      - AGID
        
        Negative: precipitin lines continue into the test sample well without bending or with a slight bend away from antigen well
        
        Positive: precipitin lines join with and form a continuous line with the line between the test serum and antigen
    - - HA
      - ELISA
      - Immunoblotting
- - - - air droplet
      - dust
      - feed
      - water
    - - Revealed that H9N2 viruses were the donors of the internal genes of the H5N1 viruses (Hong Kong in 1997) and the novel H7N9 viruses (mainland China in 2013).
    - - mild and occasional tracheal rales, cilia loss in trachea
      - excess mucous in sinus, congested trachea, thicken air sacs
      - severe lymphoplasmocytic infiltrates sub epithelium in sinus and trachea
      - mortality is high if there are other infections
      - loss of body weight; reduced egg production
      - cause infected chicken to be more susceptible to secondary bacterial infection
        
        E.Coli
      - H9N2 virus shed from tracheae and cloacae for 8 days after infection.
    - - mammals
      - avian
    - - Cause the formation of H7N9
      - Genetic contribution of H7N9 virus genes to virulence
  - - - 6 internal genes
        (directly derived from H9N2 subtype AIVs)
      - High genetic heterogeneity (classified into 27 genotypes, whereby genotype 0 predominantly circulates in poultry and humans)
      - All the internal genes of H7N9 have high genetic compatibility with those of the H9N2 virus
    - - Virus HA protein shows a binding affinity for mammalian receptors
      - Human are able to get infected
      - HA genes in H7N9 avian influenza viruses contain several mutations that may facilitate binding to human receptors (α-2,6-linked sialic acids) rather than to avian receptors (α-2,3-linked sialic acids).
    - - Infected chicken shows no clinical sign, gross lesions, and histopathological findings (asymptomatic) but causes severe diseases in human
      - H7N9 virus was shed from chicken tracheae for only 2 days after infection and from chicken cloacae for only 1 day after infection.
      - Low-pathogenicity avian influenza virus (LPAIV) as it possesses only a single basic amino acid at the HA0 cleavage site.
    - - oropharyngeal route
      - cloacal route
    - - PB2, M, and NP are the key virulence genes, together with the surface hemagglutinin (HA) and neuraminidase (NA) proteins
      - Low-pathogenicity avian influenza virus (LPAIV) but causes severe disease in humans
      - Continue to evolve for a better genetic compatibility with other gene segments and a higher infectivity
    - - Key factor for viral replication capability
      - Critical for host adaptation to avian and human cells (effectively replicate in human and avian species).
- - - - Pigs are long considered as mixing vessel for mammalian and avian influenza variants
  - - - infect nonciliated cells in human airway epithelial cell cultures
      - spread from cell to cell forming foci of infection (similar to human influenza viruses)