Download igotmadhopz4anazn The Deadly Spanish Influenza The 1918

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The Deadly Spanish Influenza
The 1918 outbreak of the Spanish Influenza killed over 40 to 100 million people
worldwide (Olson, 2004). It is a virus thought to have originated from Europe during World War
I and could easily kill a person within three days. However, it quickly disappeared and during the
summer of 1918, it returned with even more lethal characteristics. A virus is a small particle that
hijacks another cell, called the host cell. Viruses are bound to mutate, or change in its genetic
structure. Due to its constant mutations(changes in genetic structure) and changes that viruses go
through each year, the human immune system cannot always defend the human body against
these influenzas. One of the mutations was the hemagluttin protein, a protein that causes blood to
clot, which was found in new Spanish flu strains (Gibbs, 2001). New research has shown that the
Spanish Influenza strain of 1918 has similar characteristics to early swine flu strains
(Taubenerger, 1997). This 1918 strain holds many different characteristics that severely
impacted the human population.
The Spanish influenza of 1918 has the neuraminidase on the surface of this virus. One
of these characteristics is the neuraminidase gene, an enzyme on the surface of the virus that is
targeted by the human immune system(the system that protects the human from viruses). First,
the virus particle attaches onto a particular cell which becomes its host cell. Then, the virus
particle will inject its genetic material into the cell and hijack it, gaining complete control over
all functions of the cell (movement, introduction, etc.). The virus starts to make copies of itself
inside the cell. It makes copies until it bursts out and kills the host cell. The neuraminidase
enzyme allows the virus to be released from the host cell enabling it to spread to other cells., The
neuraminidase enzyme is potentially dangerous because antibodies, things that protect the cell
through the immune system, do not prevent initial infection (Reid, 2000). In other words, the
antibodies in the human body are unable to stop the viruses with this enzyme from infecting the
cells. This is a predicament for weak infants who cannot fight off this disease because of their
immune system hasn’t been fully developed. The neuraminidase mutations prevent antibody
recognition, preventing your antibodies from recognizing the new virus. This is due to the
globular head of the enzyme (Reid, 2000). A globular head is a spherical shape. Structure
denotes function in all living things, which means that the form of something will determine how
it works, much like how the form of a boat will allow it to float on water. The globular head of
the neuraminidase enzyme has at least two antigenic sites. An antigen is something that will
combine with the antibodies of our body and the antigenic site is where the combining occurs.
These sites will allow the virus to escape previous immunity by combining with the antibodies.
(Reid, 2000) In other words, someone encountered this virus already, under normal
circumstances, one’s body would be able to simply refight it off; however, with the
neuraminidase enzyme, one’s bodys resistance to the disease is prevented from happening.
Another mutation that may have been found is the virus becoming more avian(bird-like)
(Enserink, 2007). This is important because it could possibly shows how viruses change which
allows them to spread to other mammals: from bird to pig, etc. and eventually to humans.
A second gene of the Spanish Flu is the Hemagluttin Gene, or HA gene for short. The
HA gene is something that prevents blood from clotting. There are two theories that explain why
the gene mutated. The first is recombination or the process where a new allelic (a form of a gene)
combination in offspring is formed. Thirty Hemagluttin 1- subtypes (something that is related to
the original) complete Hemagluttin genes were analyzed by Mark J. Gibbs in an experiment. In
September of 2001, his team found every combination of nucleotides sequences from the set
which was examined by the sister-scanning method (a method which helps identify nuclotides).
The sister-scanning method will send signals to indicate the nucleotides. Four sequences were
identified. The different regions that these genes came from contained conflicting signals of
nucleotides when compared with several other signal combinations of HA sequences from pigs
and humans. There are many similar phylogenetic (related evolution among organisms over a
period of time) signals in the sequence. This shows an evolutionary change in the HA gene. The
only time this occurred was when there was a swine and a human lineage(a descendant)
compared with it. (Gibbs, 2001). The events that further suggest recombination is the avian
influenza HA gene. It seems to have diverged(split) into two different strains before 1918 which
can be seen in the phylogenic tree that Taubenberger created in 1997. A phylogenic tree is a
diagrammatic presentation that shows evolutionary changes. Therefore, this shows the avian HA
gene produced the 1918 recombined HA gene in a mixed infection because there were no other
viruses that split into this strain (Gibbs, 2001). This changed gene was one of the factors of this
overwhelming disease.
All flu’s are extremely dangerous due to their ability to mutate. These mutations give
these flus new characteristics which strengthen them. The Spanish flu of 1918 was only one
particular example. Currently, the world is battling the new swine flu outbreak. This swine flu
was from a mutation in one of the early 1918 strains (Taubenberger, 1997). As one can see, due
to the similarities in the different flu strains, studying past flus will medically aid our world.
Basler, F.C., & Crowe Jr., J. (2008). Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors. Nature, 455, 532-536.
Gibbs , J.M., Armstrong S. J., & Gibbs J. A. (2001). Recombination in the Hemaglutinin Gene of the 1918
Spanish Flu. Science, 293, 1842-1845.
Taubenberger, K. J., Reid H. A., Krafft E. A., Bijwaard E. K., & Fanning G. T. (1997). Initial Genetic
Characterization of the 1918 Spanish Influenza Virus. Science, 275, 1793- 1796.
Enserink, M. (2007). From Two Mutations, an Important Clue about the Spanish Flu. Science, 314, 582.
Pickrell, J. (2001). Killer Flu with a Human-Pig Pedigree?. Science, 292, 1041.
Edelson, P. J., Morse, S. S., Olson, D. R., & Simonsen, L. (2005)
Holmes, E. C. (2004). 1918 and All That. Science, 303, 1787 – 1788.