Unusual mortality pattern of 1918 influenza A virus

The 1918 influenza pandemic was particularly lethal, not only for the very young and the very old (as observed for typical influenza), but unexpectedly also for young adults, 20 to 40 years of age (pictured). It has been suggested that the increased lethality in young adults occurred because they lacked protective immunity that would be conferred by previous infection with a related virus. Reconstruction of the origins of the 1918 influenza virus provides support for this hypothesis. Analysis of influenza virus genome sequences using a host-specific molecular clock together with seroarchaeology (analysis of stored sera for the presence of antibodies to influenza virus) indicates that the 1918 H1N1 virus arose ~1915 by reassortment of an avian influenza virus with an H1 virus that had previously emerged around 1907. The 1918 virus acquired the HA gene from the 1907 virus, and the NA gene and internal protein genes from an avian virus. This 1918 virus also infected pigs, in which descendants continue to circulate; however the human 1918 virus was displaced in 1922 by a reassortant with a distinct HA gene. Seroarchaeology and mortality data indicate that an influenza pandemic in 1889-1893 was caused by an influenza H3N8 virus. This virus appears to have circulated until 1900, when it was replaced by a H1N8 virus (the N8 gene originating from the previously circulating H3N8 virus). How do these events explain the unusual mortality pattern of the 1918 influenza A virus? High mo...
Source: virology blog - Category: Virology Authors: Tags: Basic virology Information 1918 pandemic H1N1 H2N2 H3N8 HA influenza seroarchaeology vaccine viral virus Source Type: blogs