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In December 2008, research by Yoshihiro Kawaoka of the University of Wisconsin linked the presence of three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from Spanish flu samples to the ability of the 1918 flu virus to invade the lungs and cause pneumonia. These genes were inserted into a modern H1N1 strain and triggered ...
The sequences of the polymerase proteins (PA, PB1, and PB2) of the 1918 virus and subsequent human viruses differ by only 10 amino acids from the avian influenza viruses. Viruses with 7 of the 10 amino acids in the human influenza locations have already been identified in currently circulating H5N1 .
Axon terminals (also called terminal boutons, synaptic boutons, end-feet, or presynaptic terminals) are distal terminations of the branches of an axon. An axon, also called a nerve fiber, is a long, slender projection of a nerve cell that conducts electrical impulses called action potentials away from the neuron's cell body to transmit those ...
The events of the synaptic vesicle cycle can be divided into a few key steps: [10] 1. Trafficking to the synapse. Synaptic vesicle components in the presynaptic neuron are initially trafficked to the synapse using members of the kinesin motor family. In C. elegans the major motor for synaptic vesicles is UNC-104. [11]
That is exactly what happened with the 2009 H1N1 swine flu and the Spanish flu of 1918 pandemics. Influenza A subtypes. Influenza A (but not B) also has subtypes labeled H and N. These refer to ...
Flu: The Story of the Great Influenza Pandemic of 1918 and the Search for the Virus That Caused It. New York: Farrar Straus Giroux. ISBN 0-333-75105-1. Closing in on a Killer: Scientists Unlock Clues to the Spanish Influenza Virus Archived 2014-03-10 at the Wayback Machine (exhibit at National Museum of Health and Medicine, 1996)
The 1918 flu pandemic, commonly referred to as the Spanish flu, was a category 5 influenza pandemic caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1. The difference between the influenza mortality age-distributions of the 1918 epidemic and normal epidemics.
In ideal circumstances, influenza virus neuraminidase (NA) should act on the same type of receptor the virus hemagglutinin (HA) binds to, a phenomenon that does not always happen. It is not quite clear how the virus manages to function when there is no close match between the specificities of NA and HA. [citation needed]