On Tuesday morning (11/02), the number of people infected with the novel coronavirus has surpassed 43,000 worldwide, causing over 1,000 deaths. Despite its urgency, the flood of hourly updates on the outbreak has led to a stark dilution of fact versus fiction.
Yet, for us, the fundamental questions remain unanswered. What, exactly, is 2019-nCoV or COVID-19? Is it the deadliest virus at the moment? In the midst of the media hype, are we worrying for the right reasons? What should we do collectively?
Statistics might tell you a different story.
What is COVID-19?
COVID-19 is a novel strain of RNA viruses belonging to the coronavirus family (Coronaviridae).
All viruses are encapsulated particles, surrounded by specific proteins that give them their ability to infect a host. Each viral particle contains some genetic information, either DNA, or RNA, the body’s messenger for the production of proteins.
Coronaviruses, influenza, and even HIV all carry RNA and are termed RNA viruses. They are slightly different in their makeup, hence rendering them different characteristics and infectibility.
Viruses are extremely small and can only be seen by a special microscope called an electron microscope (seen below). From their observed appearance, coronaviruses get their name from their spiky encapsulated proteins, which resemble a “crown,” and in Latin, a “corona.”
Coronavirus was first discovered in the 1960s in chickens, and since, they are known to cause mild-severe respiratory diseases in humans. Two strains of coronavirus, the HCoV-229E and HCoV-OC43, cause 15% of the common cold. Other strains cause severe and lethal pneumonia-like symptoms, including SARS-CoV and MERS-CoV, both of which caused an outbreak in 2003 and 2012 respectively. Currently, there are seven strains of coronaviruses known to infect humans.
How did coronavirus spread from animals to humans?
In animals, coronaviruses cause different diseases, ranging from respiratory diseases in chickens to diarrhea in pigs and cows. In humans, they cause almost exclusively infections of the upper respiratory tracts. So how can coronaviruses jump from animals to humans?
The process of viral infection requires the delivery of viral genome to a host cell, where they use the host machinery to make new proteins. These viral proteins are then assembled into a new virus, and like parts of a car, fully engined to attack new cells.
But in order to deliver their genome, viruses need to first bind to a special protein on the surface of the host cell, called a receptor.
A receptor engages with a specific location on the viral coat, called a binding domain. A recent structural analysis on members of coronaviruses show that the COVID-19 genome is 90% identical to a bat coronavirus. However, structurally, its binding domain is most similar to SARS-CoV.
This means that COVID-19 might have used the same mechanism as SARS, ACE2, to infect human cells. Why does it matter? Because knowing how it infects humans provides a key therapeutic opportunity that blocking this receptor might actively inhibit a COVID-19 infection.
Coronaviruses rarely leap from animal to human, or “spillover.” However, RNA replication lacks proofreading capability that DNA has, so these RNA viruses can exhibit a high mutation rate. High mutation rate, plus a close proximity to humans, i.e. animal urine and feces during butchering or at a wildlife wet market, are critical catalysts for the hop from animals to humans.
Does an infection mean a death sentence?
COVID-19 is fairly infectious, with a “basic reproduction number,” or R-naught, R0, at around 2.2-3.5. This number determines that every infected person could likely spread or have spread the virus to 2.2-3.5 people. Ebola has an R0 of 2.0, and for SARS, 3.0.
While fatalities have surpassed the highly infectious SARS 2003 outbreak, COVID-19 is still far less deadly. Why is that? Scientists determine the case fatality rate (CFR) based on the number of deaths over the number of people infected.
According to the WHO, an analysis of coronavirus infections shows that 82 percent of 17,000 reported cases in mainland China are classified as mild.
In fact, less than 3 percent of reported cases in mainland China have resulted in death. In comparison, SARS kills around 10 percent of infected cases from 26 countries, and MERS, at worse, kills about 35 percent.
In Vietnam, SARS infected 63 people and caused a total of 5 deaths by April 2004 (according to WHO). For COVID-19, up to this point (11/02) only 2 deaths outside of mainland China have been recorded.
Meanwhile, like all respiratory diseases, complications contribute to higher chance of morbidity, and COVID-19 could be deadly to some populations.
Acute conditions, including organ failure and death, are more likely to occur in those with a compromised immune system or other underlying complications. However, even for this group, death rate seems to be at around 4 to 5 percent, according to physician Peng Zhiyong at the Wuhan University South Central Hospital.
As of February 11, there have been over 4,000 coronavirus recoveries worldwide. Most patients take an average of three weeks to develop all symptoms and fight the virus, so while new cases are being recorded exponentially, the number of recovery is also likely to concurrently increase in the next couple of months.
Currently, the deadliest virus is not coronaviruses. Or even HIV.
Before the 2019 coronavirus outbreak, other deadlier pandemics have occurred in human history.
Coronaviruses, which constitute seven identified strains known to infect humans, are far less deadly than avian influenza.
H1N1, the influenza subtype that caused “The Spanish Flu” between 1918-1919, single-handedly killed 50 million people and infected 500 million, equivalent to one-third of the world population at the time.
Influenza A subtype has 18 H’s and 11 N’s, both of which denote specific proteins (Hemagglutinin or “H” and Neuraminidase or “N”) on the viral coat.
Without mutation, this makes 198 possible strains of influenza. With mutation, the possibility of a novel, deadlier strain we have never encountered before is virtually endless.
The light of the tunnel, and what we should prepare ourselves for
Modern societies have constructed infrastructure to maximize efficiency, some of them at the cost of extreme centralization.
According to the United Nations, 79% of megacities are developing countries, and 70% of the world will live in urban settings by 2050. It poses serious challenges for capacitating transportation and medical resources.
Fundamentally, it leaves us a question for the future: when the next global pandemic arrives, as society, do we have enough resources and resilience to fight and recover?
Humans do not have the natural immunity to fight any novel, infectious, and potentially deadly virus. The longer we live, the more likely we would be susceptible to new infections in our lifetime.
But, in 2019, we have far more opportunities to prevent it from happening and, when it happens, far more resources to prepare ourselves than we have in the past.
When a novel virus emerges, it causes panic.
Panic is a systemic response to an event we neither expect or prepare ourselves for. But by no means does panic encourage actions. Panic numbs us, isolates us and prevents us from moving forward.
But in the midst of terror, one thing remains true. Unlike viruses, we are organisms, and on all avenues of life, “the defining characteristic of an organism is striving” (Paul Kalanithi).
We can only move forward.
Written by Evelyn Nguyen.
Evelyn is a PhD student with 5+ years research experience in immunology, cancer biology and therapeutic development. She previously held positions at Memorial-Sloan Kettering (New York), DFCI/Harvard Medical School (Boston), K National Cancer Hospital, and Vietnam’s Institute of Biotechnology.
Evelyn covers topics in biomedicine, public health, and wellness.