The influenza pandemic of 1918-1919 had a profound global impact,
affecting approximately 500 million people, which represented about one-fifth
of the world's population. This devastating outbreak led to the loss of 20 to
100 million lives, with the United States alone witnessing the death of around
675,000 individuals. Notably, this death toll surpassed the number of
casualties from battle-related injuries during World War I, which had recently
concluded at that time.
The same viral culprit responsible for the Spanish flu, identified
as the H1N1 strain, resurfaced seven decades later as swine flu. This
resurgence infected nearly 20% of the world's population and resulted in
200,000 to 300,000 fatalities between 2009 and 2010. It's crucial to underscore
that the H1N1 strain differs from the typical seasonal flu virus.
Viruses exhibit a strong affinity for living organisms, including
humans, as they lack the ability to replicate independently and rely on host
cells for multiplication. Viruses attach their proteins to the host cell's
surface, introduce genetic material (DNA or RNA), and take control of the
host's cellular machinery to produce more viruses. Subsequently, the virus
moves on to infect another host cell.
In response to a previous infection by a particular virus, the
host's immune system generates antibodies that prevent the virus from adhering
to the host cell's surface. However, viruses can undergo mutations, altering
their surface proteins, which challenges the host's immune system in
recognizing and combating them. Consequently, antibodies produced after a prior
flu infection are ineffective against new and distinct strains, necessitating
the development of a new flu vaccine each season.
While some viruses, like smallpox, employ DNA for replication and
meticulously inspect for errors during genetic code duplication, RNA viruses
such as influenza do not exhibit such caution. This rapid replication process
allows RNA viruses to mutate swiftly, outpacing the host's immune response and
leading to the emergence of novel viral strains.
The influenza virus possesses the ability to combine genetic
elements from avian, swine, and human sources. Pigs can readily acquire the
virus from birds and humans, serving as intermediaries for transmission. While
pigs can host mutated viruses without falling ill, humans are not as fortunate.
The H1N1 Spanish flu and swine flu serve as examples of such mutated strains
that significantly differed from previous ones, leaving humans vulnerable due
to their lack of immunity.
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