Announcement

Collapse
No announcement yet.

Comparison of the Pathology Caused by H1N1, H5N1, and H3N2 Influenza Viruses

Collapse
X
 
  • Filter
  • Time
  • Show
Clear All
new posts

  • Comparison of the Pathology Caused by H1N1, H5N1, and H3N2 Influenza Viruses

    Archives of Medical Research
    Volume 40, Issue 8, Pages 655-661 (November 2009)



    Comparison of the Pathology Caused by H1N1, H5N1, and H3N2 Influenza Viruses

    Jeannette GuarneraCorresponding Author Informationemail address, Reynaldo Falc?n-Escobedob

    Received 8 September 2009; accepted 21 September 2009. published online 07 January 2010.

    The spectrum of morbidity and mortality of H1N1, H5N1, and H3N2 influenza A viruses relates to the pathology they produce. In this review, we describe and compare the pathology of these viruses in human cases and animal models. The 1918 H1N1, the novel 2009 H1N1 pandemic virus, and H5N1 show inflammation, congestion, and epithelial necrosis of the larger airways (trachea, bronchi and bronchioles) with extension into the alveoli causing diffuse alveolar damage. Seasonal influenza A viruses (H3N2 and H1N1) have primarily caused inflammation, congestion and epithelial necrosis of the larger airways with lesser extension of the inflammatory process to alveoli. Localization of the inflammation and cellular damage relate to the presence of virus in different cell types. Infections with 1918 H1N1, the novel 2009 H1N1 pandemic virus, and H5N1 show virus in mucosal epithelial cells of the airways (from the nasopharynx to the bronchioles), alveolar macrophages, and pneumocytes, whereas infections with seasonal influenza viruses show viral antigens primarily in mucosal epithelial cells of the larger airways. The increased morbidity that has been encountered with the 2009 H1N1 virus is related to infection of cells in the upper and lower airways. The 2009 H1N1 virus shows similar pathology to that encountered with other highly virulent influenza A viruses such as the 1918 H1N1 and H5N1 viruses.

Working...
X