INTRODUCTION
The COVID-19 pandemic has profoundly impacted global society, resulting in a significant loss of life and widespread social, political, and economic disruption. In the wake of this unprecedented event, many have naturally sought to understand its severity by drawing comparisons to past pandemics, most notably the 1918 Spanish Flu. Understanding how these global health crises compares in spanish, or in any language for that matter, is crucial for grasping the nuances of our current situation and preparing for future challenges. This article delves into a detailed comparison between COVID-19 and the 1918 Spanish Flu, aiming to provide a comprehensive overview of their similarities and differences, offering insights valuable for navigating the ongoing pandemic and beyond. We acknowledge the foundational work of Andrew Price Smith, whose analysis of the 1918 influenza, particularly his research into Austrian archives highlighting the virus’s impact on Axis troops, significantly contributed to our understanding of that historical pandemic’s global impact.
HISTORICAL CONTEXT: THE 1918 SPANISH FLU
The 1918 Spanish Flu, caused by an H1N1 influenza A virus believed to have originated in avian species, swept across the globe between 1918 and 1920. This pandemic unfolded in four distinct waves. The first wave emerged around February 15, 1918, and subsided by June 1, 1918. A more devastating second wave followed from August 1 to December 2, 1918. The third wave occurred 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 approximately 500 million people, representing about one-third of the global population at the time, and caused an estimated 50 million deaths, including 675,000 in the United States alone. The pandemic’s moniker, “Spanish Flu,” arose from early media reports in Madrid, notably in the ABC newspaper on May 22, 1918, which first publicly acknowledged the epidemic. Despite its name, the actual origin of the virus remains uncertain, with many epidemiologists and virologists suggesting potential origins in the USA or France. By May 28, 1918, even Spain’s King Alfonso XIII and his Prime Minister had fallen ill, underscoring the rapid spread. The widespread illness caused significant disruption, forcing temporary closures of essential services like postal, telegraph, and banking operations across affected regions.
A DETAILED COMPARISON: COVID-19 VERSUS 1918 INFLUENZA
Several key factors differentiate COVID-19 and the 1918 influenza, starting with the demographics most affected. The 1918 influenza disproportionately claimed the lives of young adults aged 25-40, whereas COVID-19 primarily impacts individuals over 65, particularly those with pre-existing health conditions. Specifically, the 1918 influenza exhibited a strikingly high mortality rate among younger demographics, reaching 8%-10% in the 25-40 age group, compared to an overall mortality rate of 2.5%. In stark contrast, COVID-19 presents a much lower mortality rate of 0.2% for the same 25-40 age bracket against an overall mortality rate of 2.4%. Notably, 40% of deaths during the 1918 pandemic were among those aged 25-40, whereas the 18-44 age group accounts for only 3.9% of COVID-19 deaths. Geographically, the reach of the pandemics also differed. While the 1918 pandemic spared more countries, notably smaller Pacific Islands like the Solomon Islands and Vanuatu remain among the few places untouched by COVID-19. Another critical difference lies in the impact on pregnant women. The Spanish Flu carried a staggering 23%-37% mortality rate for pregnant women, and 26% of survivors experienced the loss of their child. The mortality rate for pregnant women with COVID-19 is still being studied, but initial data suggests a different profile. In terms of overall impact, the Spanish Flu caused acute illness in 25%-30% of the global population, resulting in over 50 million deaths. COVID-19, as of November 16, 2020, had infected nearly 55 million people globally, with 1.3 million deaths. In the United States alone, COVID-19 cases surpassed 11 million by November 16, 2020, marking a nearly 40% increase from the preceding month.
Furthermore, the mechanisms of death differ significantly between the two diseases. Spanish Flu fatalities were primarily attributed to secondary bacterial pneumonia, while COVID-19 deaths are often linked to an overactive immune response leading to multiple organ failure. Acute Respiratory Distress Syndrome (ARDS), a severe lung condition, can occur as a complication in both infections. However, ARDS resulting from the Spanish Flu had a near 100% fatality rate, 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 suggesting a $5.76-$6.17 trillion reduction in the US Gross Domestic Product (GDP). Economic data from the 1918 pandemic era is less readily available, but it is documented that Mexico alone suffered a $9 billion loss at the time.
Diagnostic tools, treatments, and vaccine development faced delays in both pandemics. In the early stages of COVID-19, the US experienced difficulties with its initial diagnostic tests from the Centers for Disease Control and Prevention (CDC), leading individual states to develop their own testing protocols. Currently, no COVID-19 treatments are officially approved by the Food and Drug Administration, although antivirals like remdesivir, antibody therapies, and interleukin 33 blockers are under active investigation. Vaccine development is also progressing rapidly. In 1918, medical understanding was limited, and treatments were rudimentary. Bleeding was initially used as a treatment for influenza, even recommended by the renowned physician William Osler to alleviate symptoms, highlighting the limited progress against pneumonia at the time. However, in 1917-1918, a significant advancement occurred when Dr. Rufus Cole, Dr. Oswald Avery, Dr. Alphonse Dochez, and their team at the Rockefeller Institute developed and tested a vaccine targeting pneumonia caused by types I, II, and III pneumococci. In March 1918, this vaccine was administered to 12,000 troops on Long Island, and none of the vaccinated soldiers developed pneumonia from these specific strains, compared to 101 cases among 19,000 unvaccinated soldiers serving as controls.
Despite this vaccine progress against bacterial pneumonia, neither a direct influenza vaccine nor antibiotics to combat secondary bacterial infections were available during the 1918 pandemic. Consequently, containment efforts relied heavily on isolation and quarantine measures, mirroring current strategies employed against COVID-19.
The origins and duration of both pandemics are subjects of ongoing discussion. The 1918 influenza pandemic lasted approximately 25 months, and its origin remains debated, with theories pointing to Spain, France, or the USA. COVID-19 emerged in Wuhan, China, around December 31, 2019, with its precise origin still under investigation, focusing on possibilities including a wet market or the Wuhan Institute of Virology. A notable scientific advancement in the context of COVID-19 is the ability to use DNA sequencing to predict disease progression, identifying a single base change (11 083G>T) that can indicate whether an infected individual will be symptomatic or asymptomatic.
CONCLUSIONS
Both the COVID-19 pandemic and the 1918 influenza pandemic have inflicted significant negative impacts on the global economy, strained international relations, and faced delays in diagnosis, treatment, and vaccine development. However, key differences exist, particularly in the populations most at risk and the mechanisms of mortality. The 1918 influenza affected fewer countries and disproportionately impacted healthy young adults aged 25-40, whereas COVID-19 has spread to nearly all countries, posing the greatest risk to older adults over 65 with comorbidities. The primary cause of death in the 1918 influenza was secondary bacterial pneumonia, while COVID-19 fatalities are often linked to an overactive immune response and subsequent organ failure. Table 1 summarizes these critical distinctions.
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 comparative analyses are vital for understanding and anticipating the long-term consequences of the ongoing COVID-19 pandemic. The comparatively lower death toll of COVID-19 might reflect advancements in modern medicine, including improved diagnostic capabilities and technologies like extracorporeal membrane oxygenation machines.
Looking ahead, synthetic biology offers potential solutions for enhancing pandemic preparedness and response. Full genome sequencing of COVID-19 strains, facilitated by synthetic biology, can improve diagnostics and reveal viral diversity. Furthermore, analyzing patient genotypes can provide insights into viral expression and disease severity. Synthetic biology also holds promise for vaccine development, enabling the rapid production of vaccines in unlimited quantities using nanotechnology, potentially surpassing traditional methods that rely on fertilized chicken eggs. Future vaccines could be tailored to specific viral strains, incorporating unique sensors on monoclonal antibodies for efficient and targeted vaccination strategies.
Deciphering the complexities of the COVID-19 virus remains a critical endeavor. Detailed study of each base of its positive-sense messenger RNA to determine its individual function can improve patient prognosis and treatment strategies. Currently, intensive care unit outcomes for COVID-19 patients are often poor, marked by high mortality rates and the risk of lasting lung damage.
As our understanding of COVID-19’s functional phenotypic expression deepens, we can improve our ability to predict viral mRNA expression and initiate earlier interventions. The ongoing battle against this 21st-century virus is a race against time, leveraging the most advanced synthetic biology tools of our era, a century removed from the limited resources available during the 1918 influenza pandemic. Harnessing synthetic biology, alongside public health measures like social distancing, offers the best path towards achieving victory in this ongoing global health challenge.
Table 1 effectively highlights the key distinctions between COVID-19 and the 1918 influenza.
Footnotes
Contributors: STTL, LTL and JMR made substantial contributions to the conception or design of the work, the acquisition, analysis and interpretation of data for the work; drafting and revising the paper; final approval of the version to be published; and were accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. JMR lead the ideation and STTL did the majority of the data analysis and writing.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
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.
