INTRODUCTION
This analysis is dedicated to Andrew Price Smith, acknowledging his profound work on the 1918 influenza pandemic, particularly his groundbreaking research within the Austrian Spanish Influenza Archives. Smith’s investigations revealed the virus’s earlier impact on Axis troops, a crucial factor influencing Kaiser’s decision to pursue peace during World War I.
The global COVID-19 pandemic has profoundly impacted lives worldwide, resulting in a significant loss of life and widespread social, political, and economic disruption. A natural question arises: how does this contemporary crisis compare to seasonal influenza and historical pandemics? Examining past pandemics, notably the 1918 Spanish flu, offers valuable context for understanding and navigating the current health emergency. To effectively Compare In Spanish or any language, requires a deep understanding of historical events and their parallels to today’s challenges. This comparative approach provides critical insights for public health strategies and pandemic preparedness.
A BRIEF LOOK AT THE 1918 SPANISH FLU
The 1918 Spanish flu was caused by an H1N1 influenza A virus, believed to have originated from avian sources. This devastating pandemic spanned from 1918 to 1920, unfolding in four distinct waves. The initial wave occurred from approximately February 15, 1918, to June 1, 1918, followed by a more lethal second wave from August 1, 1918, to December 2, 1918. The third wave extended from December 3, 1918, to April 30, 1919, and the final, fourth wave lasted from December 1, 1919, to April 30, 1920. It is estimated that the Spanish flu infected around 500 million people globally – roughly one-third of the world’s population at the time – and caused approximately 50 million deaths, including 675,000 in the United States alone.
Interestingly, the pandemic gained its moniker “Spanish flu” because the first public reports of the epidemic emerged in Madrid on May 22, 1918, in the ABC newspaper. However, the actual origin remains uncertain, with most epidemiologists and virologists suggesting either the USA or France as potential starting points. Just a week later, on May 28, 1918, even King Alfonso XIII of Spain, along with the Prime Minister and some cabinet members, fell ill. As the influenza rapidly spread, essential services, including postal, telegraph, and banking, were forced to temporarily shut down, highlighting the societal disruption caused by the pandemic.
COVID-19 VERSUS 1918 INFLUENZA: A COMPARATIVE ANALYSIS
Several key differences and similarities emerge when we compare in Spanish – or any language – the characteristics of COVID-19 and the 1918 influenza.
Firstly, the affected populations differ significantly. The 1918 influenza disproportionately impacted young adults aged 25–40, whereas COVID-19 primarily affects individuals over 65, particularly those with pre-existing health conditions. Notably, the mortality rate for the Spanish flu surged to 8%–10% in younger demographics, compared to an overall mortality of 2.5%. In contrast, the mortality rate for the 25–40 age group with COVID-19 is considerably lower at around 0.2%, against an overall mortality rate of 2.4%. Young adults in the 25–40 age range accounted for a staggering 40% of deaths during the 1918 influenza pandemic, whereas the 18–44-year-old range represents only 3.9% of COVID-19 related deaths. Geographically, the 1918 pandemic, while devastating, spared more countries than COVID-19, with only a few smaller Pacific Islands like the Solomon Islands and Vanuatu remaining COVID-19 free. Another stark contrast is seen in pregnant women; the Spanish flu had a mortality rate of 23%–37% for pregnant women, and 26% of survivors lost their child, while the mortality rate for pregnant women with COVID-19 is still being studied. The Spanish flu caused acute illness in 25%–30% of the global population, resulting in over 50 million deaths. As of November 16, 2020, COVID-19 had infected nearly 55 million people globally, with 1.3 million deaths, and in the USA alone, cases exceeded 11 million, marking a near 40% increase from the previous month.
Secondly, the mechanisms of death differ between the two diseases. Spanish flu fatalities were primarily due to secondary bacterial pneumonia, whereas COVID-19 deaths often result from an overactive immune response leading to multiple organ failure. Acute Respiratory Distress Syndrome (ARDS) can develop in both infections. However, ARDS as a complication of influenza had a near 100% fatality rate in 1918, compared to a 53.4% mortality rate when associated with COVID-19.
The economic repercussions of COVID-19 are projected to be substantial, with estimates of a $5.76–$6.17 trillion decrease in the US Gross Domestic Product (GDP). Historical economic data from the 1918 pandemic is limited, but it is documented that Mexico experienced a $9 billion loss at the time.
Diagnosis, treatment, and vaccine development faced delays in both pandemics. During the COVID-19 pandemic, the initial diagnostic test from the Centers for Disease Control and Prevention (CDC) encountered issues, leading states to develop their own tests. Currently, while there are no FDA-approved COVID-19 treatments, antivirals like remdesivir, antibody therapies, and interleukin 33 blockers are under investigation, and vaccines are in development. In 1918, medical practices were rudimentary; bleeding was initially used as a treatment for influenza symptoms, even recommended by the renowned physician William Osler. However, in 1917, Dr. Rufus Cole, Dr. Oswald Avery, and Dr. Alphonse Dochez, along with Rockefeller researchers, developed and tested a vaccine against pneumonia caused by pneumococci types I, II, and III. In March 1918, this vaccine was administered to 12,000 troops on Long Island, and none developed pneumonia from these strains, compared to 101 cases among 19,000 unvaccinated control soldiers.
Despite these advances in pneumonia prevention, neither a flu vaccine nor antibiotics for secondary bacterial infections were available during the 1918 pandemic. Consequently, containment strategies heavily relied on isolation and quarantine, mirroring current measures against COVID-19.
Regarding duration and origin, both pandemics are shrouded in some uncertainty. The 1918 influenza lasted approximately 25 months, with its origin debated as potentially Spain, France, or the USA. COVID-19 emerged in Wuhan, China, on December 31, 2019, with ongoing debate about its origin in a wet market or the Wuhan Institute of Virology. A significant advancement in the COVID-19 era is DNA sequencing, which can predict symptomatic versus asymptomatic infections based on a single base change (11 083G>T), a capability unavailable during the 1918 pandemic.
CONCLUSIONS
Both the COVID-19 and 1918 influenza pandemics have inflicted significant negative impacts on the global economy and international relations, and both faced initial delays in diagnosis, treatment, and vaccine development. Key differences lie in the most vulnerable populations and the mechanisms of mortality. The 1918 influenza affected fewer countries and primarily targeted healthy young adults aged 25–40, whereas COVID-19 has reached nearly every country, with the most vulnerable being adults over 65 with comorbidities. The 1918 influenza primarily caused death through secondary bacterial pneumonia, while COVID-19 mortality is often linked to an overactive immune response leading to organ failure. Table 1 summarizes the major distinctions between these two pandemics.
Table 1.
Summary of major differences: COVID-19 versus 1918 influenza
| COVID-19 | 1918 influenza |
|---|---|
| Viral aetiology | SARS-CoV-2 |
| Mortality rate | 2.40% |
| Number of deaths | 2.2 million |
| Highest risk population | 65+ with comorbidities |
| Cause of death | Overactive immune system leading to end organ failure |
| Place of origin | Wuhan (either in a wet market or Wuhan Institute of Virology) |
| Virus type | Coronavirus |
| Economic impact | $5.76 trillion–$6.17 trillion decrease in Gross Domestic Product (GDP) |
These historical comparisons are essential for understanding and anticipating the long-term consequences of the COVID-19 pandemic. The comparatively lower death toll in the current pandemic may reflect advancements in modern medicine, including diagnostic tools and extracorporeal membrane oxygenation (ECMO) machines.
Synthetic biology offers promising avenues for improved diagnostics through full COVID-19 strain sequencing, enabling the identification of numerous strains and potentially revealing patient genotype impacts on viral expression. Furthermore, synthetic biology and nanotechnology can revolutionize vaccine development, allowing for mass production of strain-specific vaccines with unique sensors for rapid strain identification and targeted vaccination.
Unraveling the complexities of the COVID-19 virus through in-depth study of its positive-sense messenger RNA and individual base function can enhance patient prognosis prediction and treatment strategies. Currently, intensive care unit prognosis remains poor, with high mortality and the risk of lasting lung damage.
A deeper understanding of COVID-19’s functional phenotypic expression is crucial for predicting viral mRNA expression and initiating earlier interventions. The current situation is a race to leverage 21st-century synthetic biology against a 21st-century virus. While we have advanced significantly in medical science since 1918, the duration of this battle remains uncertain. However, by combining synthetic biology with public health measures like social distancing, we can strive for victory against this pandemic.
Table 1 underscores the critical differences between COVID-19 and the 1918 influenza, providing valuable lessons for navigating the ongoing pandemic and future public health challenges.
Footnotes
Contributors: STTL, LTL, and JMR made substantial contributions to the conception, design, data acquisition, analysis, and interpretation; drafted and revised the paper; approved the final version; and are accountable for the work’s integrity. JMR led the ideation, and STTL primarily conducted data analysis and writing.
Funding: No specific grant was declared for this research.
Competing interests: None declared.
Patient consent for publication: Not required.
Provenance and peer review: Not commissioned; externally peer-reviewed.
Contributor Information
Shu Ting Liang, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA; Department of Plastic Surgery, Geisel School of Medicine, Dartmouth College, Hanover, New Hampshire, USA.
Lin Ting Liang, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA.
Joseph M Rosen, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA; Department of Plastic Surgery, Geisel School of Medicine, Dartmouth College, Hanover, New Hampshire, USA.
