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At the Centers for Disease Control and Prevention, Terrence Tumpey examines a reconstructed version of the Spanish flu.

An effort to recreate the Spanish flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology, the USDA ARS Southeast Poultry Research Laboratory, and Mount Sinai School of Medicine in New York City. The effort resulted in the announcement (on 5 October 2005) that the group had successfully determined the virus's genetic sequence, using historic tissue samples recovered by pathologist Johan Hultin from an Inuit female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers[232] Roscoe Vaughan and James Downs.[233][234]

On 18 January 2007, Kobasa et al. (2007) reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from cytokine storms[235] – an overreaction of the immune system. This may explain why the Spanish flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.[236]

On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hoped had helped preserve the virus.[237] The coffin was found to be split and the cadaver badly decomposed; nonetheless, samples of lung and brain tissue were taken.[226] Similarities between a reconstruction of the virus and avian viruses, combined with the human pandemic preceding the first reports of influenza in swine, led researchers to conclude the influenza virus jumped directly from birds to humans, and swine caught the disease from humans.[227][228]

Others have disagreed,[229] and more recent research has suggested the strain may have originated in a nonhuman, mammalian species.[230] An estimated date for its appearance in mammalian hosts has been put at the period 1882–1913.[231] This ancestor virus diverged about 1913–1915 into two clades (or biological groups), which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates to between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, they were suggested as the original

Others have disagreed,[229] and more recent research has suggested the strain may have originated in a nonhuman, mammalian species.[230] An estimated date for its appearance in mammalian hosts has been put at the period 1882–1913.[231] This ancestor virus diverged about 1913–1915 into two clades (or biological groups), which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates to between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, they were suggested as the original recipients of the virus, passing the virus to humans sometime between 1913 and 1918.

An effort to recreate the Spanish flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology, the USDA ARS Southeast Poultry Research Laboratory, and Mount Sinai School of Medicine in New York City. The effort resulted in the announcement (on 5 October 2005) that the group had successfully determined the virus's genetic sequence, using historic tissue samples recovered by pathologist Johan Hultin from an Inuit female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers[232] Roscoe Vaughan and James Downs.[233][234]

On 18 January 2007, Kobasa et al. (2007) reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from cytokine storms[235] – an overreaction of the immune system. This may explain why the Spanish flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.[236]

On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic

On 18 January 2007, Kobasa et al. (2007) reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from cytokine storms[235] – an overreaction of the immune system. This may explain why the Spanish flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.[236]

On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hoped had helped preserve the virus.[237] The coffin was found to be split and the cadaver badly decomposed; nonetheless, samples of lung and brain tissue were taken.[238]

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 flu virus to invade the lungs and cause pneumonia. The combination triggered similar symptoms in animal testing.[239]

In June 2010, a team at the Mount Sinai School of Medicine reported the 2009 flu pandemic vaccine provided some cross-protection against the Spanish flu pandemic strain.[240]

One of the few things known for certain about influenza in 1918 and for some years after was that it was, except in the laboratory, exclusively a disease of human beings.[241]

In 2013, the AIR Worldwide Research and Modeling Group "characterized the historic 1918 pandemic and estimated the effects of a similar pandemic occurring today using the AIR Pandemic Flu Model". In the model, "a modern-day 'Spanish flu' event would result in additional life insurance losses of between US$15.3–27.8 billion in the United States alone", with 188,000–337,000 deaths in the United States.[242]

In 2018, Michael Worobey, an evolutionary biology professor at the University of Arizona who is examining the history of the 1918 pandemic, revealed that he obtained tissue slides created by William Rolland, a physician who reported on a respiratory illness likely to be the virus while a pathologist in the British military during World War One.[243] Rolland had authored an article in the Lancet during 1917 about a respiratory illness outbreak beginning in 1916 in Étaples, France.[244][245] Worobey traced recent references to that article to family members who had retained slides that Rolland had prepared during that time. Worobey extracted tissue from the slides to potentially reveal more about the origin of the pathogen.[citation needed]

The high mortality rate of the influenza pandemic is one aspect that sets the pandemic apart from other disease outbreaks. Another factor is the higher mortality rate of men compared with women. Men with an underlying condition were at significantly more risk. Tuberculosis was one of the deadliest diseases in the 1900s, and killed more men than woman. But with the spread of influenza disease the cases of tuberculosis cases in men decreased. Many scholars have noted that tuberculosis increased the mortality rate of the influenza in males, decreasing their life expectancy. During the 1900s tuberculosis was more common in males than females, but studies show that when the influenza spread the tuberculosis mortality rate among females changed. The death rate of tuberculosis in females increased significantly and would continue to decline until post pandemic.[246]

Death rates were particular high in those aged 20–35. The only comparable disease to

Death rates were particular high in those aged 20–35. The only comparable disease to this was the black death, bubonic plague in the 1300s. As other studies have shown, tuberculosis and influenza had comorbidities and one affected the other. The ages of males dying of the flu shows that tuberculosis was a factor, and as males primarily had this disease at the time of the pandemic, they had a higher mortality rate. Life expectancy dropped in males during the pandemic but then increased two years after the pandemic [247]

One major cause of the spread of influenza was social behavior. Men had more social variation and were mobile more than women due to their work. Even though there was higher mortality rate in males, each region showed different results, due to such factors as nutritional deficiency. In Newfoundland the pandemic spread was highly variable. The influenza did not discriminate who was infected, indeed it attacked the socioeconomic status of people. Although social variability allowed the disease to move quickly geographically, it tended to spread faster and affect men more than women due to labor and social contact. Newfoundland's leading cause of death prior to the pandemic was tuberculosis and this is known to be a severe underlying condition for people and increases the |mortality rate when infected by the influenza disease. There was a diverse labor in Newfoundland, men and woman had various occupations that involved day to day interaction. But, fishing had a major role in the economy and so males were more mobile than females and had more contact with other parts of the world. The spread of the pandemic is known to have began in spring of 1918, but Newfoundland didn't see the deadly wave until June or July, which aligns with the high demand for employment in fishery. The majority of men were working along the coast during the summer and it was typical for entire families to move to Newfoundland and work. Studies show a much higher mortality rates in males compared with females. But, during the first, second and third waves of the pandemic, the mortality shifted. During the first wave men had a higher mortality rate, but the mortality rate of females increased and was higher during the second and third wave. The female population was larger in certain regions of Newfoundland and therefore had a bigger impact on the death rate.[248]

Influenza pande

Records indicate the most deaths during the first wave of the pandemic were among young men in their 20s, which reflects the age of enlistment in the war. Mobility of young men during 1918 was linked to the spread of the influenza and the biggest wave of the epidemic. In late 1917 and throughout 1918, thousands of male troops gathered at the Halifax port before heading to Europe. Any soldier that was ill and could not depart was added to the population of Halifax, which increased the case rate of influenza among men during the war. In order to determine the cause of the death during the pandemic, war scientists used the Commonwealth War Graves Commission (CWGC), which reported under 2 million men and women died during the wars, with record of those who died from 1917 to 1918. The movement of soldiers during this time and the transportation from United States between Canada likely had a significant effect on the spread of the pandemic.[249]

See also