COVID-19: How does it stack up in the ring?
In March of 2020, our world stood still. The nightmare situation flooded this globalized, interconnected world. Humanity’s highest prides and symbols of innovation over the past century seemed to have turned against us: our ease of transportation, globalized infrastructure, international interdependence proved to be a significant burden towards attempting to corral a pandemic, especially a virus as elusive and contagious as COVID-19. To better understand the possible future trajectories of the disease, as well as to pinpoint where everything went wrong, it is vital for us to look back at our history. COVID-19 has been the most impactful pandemic of the 21st century, leaving many to scramble in frenzy for answers. The most important question we must ask ourselves is how did we let this happen? We may not know the full answer for decades, but we do possess a vital tool that can assist us in the search: the global history of pandemics.
A basic understanding of the SARS-CoV-2 morphology is essential to understand how the virus was able to wreak such devastating havoc all around the world. Coronaviruses are non-segmented, enveloped viruses with single-stranded RNA (ssRNA) ranging between 26 to 32 kb in length. The coronavirus genome is the longest among RNA viruses. Electron microscopy (EM) revealed a spherical shape, with diameters ranging from 60–140 nm and an outer surface studded with 9 to 12-nm long spikes that gave virions the appearance of a solar corona, hence their derived name of the Coronavirus family. Coronaviruses use an RNA-dependent RNA polymerase (RdRp) complex for replication transcription. Phylogenetic-based analysis of genomes suggest that SARS-CoV-2 is closer to SARS-like bat coronaviruses than to SARS-CoVs. It was also noted that the SARS-CoV-2 (106-sequence) genome has a much lower mutation rate and genetic diversity than SARS-CoV (39 sequences) [1].
The 2002-2004 SARS epidemic provides us the most important historical contrast with COVID due to their morphological similarities. Most of the time, human coronaviruses such as SARS cause mild respiratory illnesses like the common cold. In fact, four types of human coronaviruses cause 10 to 30 percent of upper respiratory tract infections in adults. The initial animal host and transmission of SARS was also believed to be bats. Both SARS and COVID are remarkable in their droplet transmission and stability when suspended in the air. In fact, the two virions share 86% of their genomes.
However, COVID has spread much faster. In 2003, 8,098 SARS cases, with 774 deaths occurred within 8 months. By contrast, within 2 months of the start of the SARS-CoV-2 outbreak, the novel coronavirus tallied over 82,000 infections, resulting in more than 2,800 deaths.
Furthermore, COVID-19 has been especially notorious for its rapid transmission. This is partly a result of its long incubation period, allowing infected but symptom-free people to continue spreading the disease before they are aware of their need to quarantine. However, there are other molecular reasons for this contrast. This is partially due to a new spike protein that recognizes and becomes activated by an enzyme called furin. This enzyme resides in the liver, lungs, and small intestines, allowing the virus to attack several organs at once. The spike protein needs to bind to a receptor on human cells called angiotensin-converting enzyme 2 (ACE2), which SARS-CoV-2 binds to ACE2 with higher affinity than other coronaviruses. This highlights the reasons why SARS-CoV-2 binds 10 times more tightly to host cells than SARS-CoV [2].
Ultimately, there were other factors in addition to what we can observe under a microscope that affected the trajectories of these pandemics. The SARS genome was sequenced in less than a year, and the CDC was largely successful in containing the spread of the virus. Although cases were reported in five continents and 29 countries, it is nothing like the scale we are observing now.
Swine flu was detected first in the US and then spread across the country and eventually around the globe, and it contained a blend of flu genes that previously had not been observed in animals or people. This novel influenza A (H1N1) virus emerged in the spring of 2009, and was the last major pandemic we had before COVID-19 according to Amesh A. Adalja, MD, senior scholar at the Johns Hopkins Center for Health Security [3].
This pandemic is similar in that a novel strain arose within an animal vector, ultimately leading to many deaths. H1N1 led to an estimated 274,304 hospitalizations, and approximately 12,500 deaths over the course of 2009. The symptoms from H1N1 were actually quite similar to COVID, including respiratory symptoms such as coughing, as well as aches and malaise.
The crucial comparison we can draw between swine flu and the current coronavirus pandemic is within the highly politicized US-government responses. Barack Obama was criticized at the time for failing to heed advice in providing PPE needs, as well as the vaccine development and delivery processes. As the swine flu pandemic progressed, public leaders and officials ultimately realized that the virus did not present the cataclysmic problem that they had feared. Measures such as closing schools would not have to be enacted for prolonged periods of time. This is a stark contrast to the deadly COVID-19 pandemic, which has been earmarked by mistakes from President Trump and other public officials, within the United States and abroad. These included failing to take the deadly illness seriously, slashing funding for critical public safety nets, and significantly lagging in testing during the first weeks and months of the pandemic.
Of course, it is also important to provide context in a broader history. The Bubonic Plague wiped out as much as 50% of the European population in the 14th century. The disease was originally introduced into Europe through the Sicilian port of Messina, where an early form of biological warfare conducted by the Genghis Khan led Mongols killed most of the sailors within the ships that entered the port. The Black Death is a zoonotic infection within domestic and wild animals, primarily transmitted through rodent bites. COVID-19, on the other hand, originated in an animal reservoir, but broke the species barrier and now spreads through human respiratory droplets and close contact. If the plague is not treated quickly, the bacteria can spread to other parts of the body and result in more serious illnesses such as meningitis, pneumonia, and septicemic plague (which almost certainly led to mortality) [4].
These two pandemics can primarily be compared due to their global scale. As of today, the Bubonic Plague has not been eradicated. Approximately 1,000 cases of the Bubonic Plague are still reported every year today, although it is primarily a significant issue in developing countries. In 2020, a case of Bubonic Plague was reported in California, as a man believed to have contracted the disease from a flea bite during a dog walk. Overall, the bacteria that causes the Bubonic Plague can be treated by a course of antibiotics, so it does not present a significant issue in the 21st century. Crucially, the Bubonic Plague was most prominent in an era where germ theory had not even existed. People turned towards the clergy and religious guides for counsel. The most striking example would be the flagellants, a group who whipped themselves as they believed the plague was a form of retribution on behalf of God. The people were struck by a phenomenon they had no understanding of. At first glance, the technological innovation and advancement over 600 years means our society is a stark contrast from this era, but the more we think about it, the harder it is to shake the feeling that we were placed in a similar situation in the beginning stages of the COVID-19 pandemic.
So what can we learn from this history? Well, it is evident that within the discourses of pandemics, both of the distant past and the modern era, there were lessons that we unfortunately failed to learn from. As we progress into an even more technologically-connected and mechanized future, it becomes even more imperative that we make the necessary preparations for another apocalyptic pandemic like COVID-19 has been. We have valuable guides and information hidden within our history. The most important tool we have towards controlling a pandemic (as well as public health issues as a whole) is education of the public. We must understand how these things work, and truly comprehend their mechanisms.
References
[1] Mittal, A., Manjunath, K., Ranjan, R. K., Kaushik, S., Kumar, S., & Verma, V. (2020). COVID-19 pandemic: Insights into structure, function, and hACE2 receptor recognition by SARS-CoV-2. PLoS pathogens, 16(8), e1008762. https://doi.org/10.1371/journal.ppat.1008762
[2] Hui D. S. (2013). Severe acute respiratory syndrome (SARS): lessons learnt in Hong Kong. Journal of thoracic disease, 5 Suppl 2(Suppl 2), S122–S126. https://doi.org/10.3978/j.issn.2072-1439.2013.06.18
[3] Dandagi, G. L., & Byahatti, S. M. (2011). An insight into the swine-influenza A (H1N1) virus infection in humans. Lung India : official organ of Indian Chest Society, 28(1), 34–38. https://doi.org/10.4103/0970-2113.76299
[4] Duncan, C J, and S Scott. “What Caused the Black Death?” Postgraduate Medical Journal, The Fellowship of Postgraduate Medicine, 1 May 2005, https://pmj.bmj.com/content/81/955/315