“The Spanish flu resulted in high mortality rates for those born between the years 1878 and 1898, which coincides almost perfectly with the circulation of a putative H3N8 virus in the population between 1880 and 1900”
Raggie Jessy Rithaudeen
#تتفچوۏيد19: ڤنموان بارو بنتو جلسكن سبب چورق جڠكيتن چوۏيد-19 بربيذا انتارا نڬارا
#TTFCovid19
A team of researchers from the University of Arizona Department of Ecology and Evolutionary Biology believes it has uncovered the mystery behind the Spanish Flu pandemic that killed over 50 and 100 million people between the years 1918 and 1919.
According to a study led by a Professor Michael Worobey, the pandemic virus arose shortly before 1918 when a human H1 virus, which they infer had already been circulating in the human population since about 1900, picked up genetic material from a bird flu virus.
While the Human influenza A virus (H1 to H18 subtypes) typically sees higher mortality rates for infants and the elderly, the Spanish flu pandemic caused extensive deaths in people aged 20 to 40, primarily from secondary bacterial infections, especially pneumonia.
Put differently, the Spanish flu resulted in high mortality rates for those born between the years 1878 and 1898, which coincides almost perfectly with the circulation of a putative H3N8 virus in the population between 1880 and 1900.
The surface proteins of the H3N8 virus was far different from the 1918 virus.
Due to its prevalence, the immune systems of those born between 1880 and 1900 would have been busy fighting the H3N8 strain and would have developed the necessary antibodies for the purpose.
However, individuals born before or after said period were exposed to a virus variant similar to the 1918 virus, meaning, they would have developed antibodies that could have resisted the 1918 Spanish flu to a certain degree.
If the theory holds, it probably explains why the Spanish flu hit healthy young adults (those born between 1878 and 1898) the hardest, apart from the elderly, whose weaker immune systems and (or) other pre-existing conditions would probably have made them extremely vulnerable as well.
“You can picture the flu virus as a tiny soccer ball studded with lollipops,” Worobey explained.
“The candy part of the lollipop is by far the most potent part of the flu virus, against which our immune system can make antibodies.
“If antibodies cover all the lollipop heads, the virus can’t even infect you.’
“For example, a person exposed to a flu strain studded with blue candy lollipops would have antibodies protecting it from future infections with that flu virus.
“However, if faced with a different strain containing red candy, that same person would get sick because the “anti-blue” antibodies would not recognize the red lollipops, allowing the virus to slip through the body’s immune defenses unscathed.
Based on the research, and the way I see it, we need to breakdown the histories of virus infections worldwide for a reasonable number of years and categorise them according to country.
Once done, we could proceed to study the virus strain prevalent in a given country within a given timespan and discover if its protein layer bears any degree of resemblance to the strain responsible for Covid-19 infections.
Repeating this for all possible time periods, we can then proceed to discover if:
1. the history of virus infections in a given country correlates with the severity of Covid-19 infections and mortality trends between one age group and another, and
2. if differences in the history of virus infections from one country to another contribute to differences in Covid-19 infection trends and mortality to infection ratios between these countries.
