The Coronavirus — Everything You Need To Know
What Is It? How Does It Infect The Body? How Does It Spread? What Are Scientists Doing To Combat It? All your questions answered.
Coronavirus. It’s all everyone has been talking about for about a couple of months now. From schools being shut down in countries like Canada, to complete nationwide lockdown in countries including Italy and India, it has caused complete chaos in civilizations across the globe. It’s spurred consumers to overspend on commodities like sanitizer, masks, and toilet paper (still not quite sure about that one. Why??). But for something that has made such a huge impact around the world, fairly little is known about what it is, how it spreads, how it affects the body, and what scientists and medical professionals are doing to stop it.
So, here’s just a little summary of everything you need to know about coronavirus.
What The Heck Is It?
Essentially, coronavirus, formally known as SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), is a RNA virus, which causes the disease/slew of symptoms known as COVID-19. As far as we know, the virus was transferred into humans via consumption of a bat infected with the coronavirus, after which it mutated to adapt to its new host.
For the non-biology nerds out there, a virus is an infectious agent that consists only of a shell made of protein, envelope proteins on this shell, and some genetic information (usually DNA) on the inside. That’s usually it. Most viruses have nothing else. That’s why they’re not even considered to be living.
Because they lack any cellular machinery, viruses also depend on infecting cells and hijacking their cellular machinery to replicate its own genome and produce the protein shells (called capsids).
RNA viruses operate in the same way, but instead of housing DNA in the capsids, they hold RNA strands. Since most cells do not have the cellular machinery to replicate RNA, the viruses must encode their own proteins that do so. Many notorious viruses, including the influenza virus, and viruses that cause hemorrhagic disorders like Ebola, dengue, and yellow fever, are RNA viruses.
The coronavirus, specifically, contains a positive-sense RNA-based genome. This means that the host cell can identify the virus’ RNA as an mRNA strand, allowing for immediate translation into the capsid proteins. On the other hand, negative-sense RNA strands require the virus to store an enzyme that usually turns the RNA into DNA, which is then incorporated into the host’s genome.
Another thing most of you might not know about the coronavirus… it’s not the first one. In fact, coronavirus, or coronaviridae, is just the name of a class of viruses.
There have been previous coronavirus outbreaks, with the most notable being the SARS outbreak (SARS-CoV virus) from 2002–2004 and the MERS (Middle Eastern Respiratory Syndrome) outbreak that started in 2015 and continues in the region. All of these viral strains are classified under the broader category of coronaviruses because of their similar characteristics, including their structure, methods of infection, and general effects on the body.
One of the most distinctive characteristics shared across all coronavirus strains is the club-shaped S (spike) glycoproteins on the capsid. These proteins give a crown-like or halo-like appearance to the virus, which is why they are named coronaviruses in the first place (“corona-” means crown in Latin). The virus also has other proteins that contribute to its ability to infect our body. Envelope (E) glycoproteins are crucial for controlling the assembly, release, and infectivity of mature viruses. Nucleocapsid (N) proteins knit a characteristic shell of identical subunits, like the panes of a greenhouse, that binds and packages the RNA genome. These proteins also serve as a cloaking device, hiding the virus from the immune system. The Membrane (M) glycoprotein lies beneath the spikes and shapes mature viral particles and binds the inner layers.
As far as we know, the virus spreads from person to person via droplet infections when people cough, or by touching your face after coming into contact with an infected person. Next, the virus usually enters the body through the respiratory tract, where it makes its way into the lungs.
Once there, the virus targets the epithelial cells that line and protect your lungs. The S proteins attach to receptors on the cell surface (specifically, ACE2 receptors) that allow the virus to inject its genome into the host cell. Once this happens, things are about to start getting really bad.
The cell, oblivious to what’s happening, accepts the RNA from the virus, and starts replicating the genome, and assembling the protein capsids. Soon, the cell is filled with hundreds of assembled copies of the coronavirus just waiting to be released.
Once the cell reaches a critical point, the viruses make one final lethal blow. They cause the cell to release chemicals that cause its cell membrane to lyse, or rupture, releasing the cytoplasmic content, including hundreds of coronaviruses, into the surroundings. These viruses infect more cells, which produce more viruses, and the process continues. The number of infected cells in the lungs grows exponentially and after only about 10 days, millions of epithelial cells are infected.
But the worst is yet to come.
As these viruses are released into the surroundings, some of them begin to infect your immune cells.
Your immune system consists of many different types of immune cells that all have the function of keeping your body safe from foreign invaders, including viruses. All of these cells communicate with one another using signalling molecules known as cytokines, which signal the immune system to react to a specific invader.
With the coronavirus, infected immune cells overreact and release an excessive amount of cytokines, causing your immune system to overreact.
As the immune cells arrive at the site of infection, two specific types of cells take action. The first, neutrophils, release tons of enzymes that cause the death of both healthy and infected cells. The second, known as killer T cells, normally instruct infected cells to commit suicide, preventing viral reproduction. But, because of the excessive number of killer T cells that arrive on the scene, they begin to give the same instruction to healthy cells. Overall, the immune overreaction causes the death of hundreds or thousands of epithelial cells.
In younger individuals with stronger immune systems, the disease rarely progresses to this stage, since the immune system is able to handle the virus and return to normal before the extreme reaction. Younger patients will only really experience flu-like symptoms. In particularly bad cases where the disease does progress this far, it can cause permanent scarring that can lead to severe disorders and complications later in life, and may even require hospitalization.
But for seniors and patients with compromised immune systems, it’s about to get a whole lot worse.
One of the most important functions of the epithelial cells is to protect the body from foreign invaders including bacteria. With most of the epithelial protection degraded in immunosuppressed (individuals with weak immune systems, either because of age, some disorder, or side effects from medical treatments like chemotherapy) individuals, the lungs are vulnerable to thousands of bacteria that were harmless to the body before. The alveoli (air sacs in your lungs) are stormed by these bacteria, causing patients to develop pneumonia and become dependent on ventilators to survive. The immune system, which had been fighting full force for weeks before, becomes overwhelmed as the bacteria very quickly overrun the body, in a condition known as sepsis, making death imminent. This is the reason why the elderly and immunocompromised have the highest death rate amongst coronavirus patients.
How Does It Spread?
Another reason the coronavirus is so severe is the fact that it spreads so fast.
As mentioned above, the virus spreads mainly through salivary droplets that are released into the air when someone sneezes or coughs. According to a study conducted in China, the virus can remain in the air for 30 minutes. If an individual happens to inhale these droplets, or they come into contact with a surface that has the viruses, they themselves can become infected.
But the biggest problem contributing to the spread is the lack of symptoms in patients for the first stage of infection. Other diseases with a similar method of transmission present symptoms very quickly, which often prevents patients from interacting with large groups of people. Patients that have been infected by the coronavirus, however, tend to not experience any symptoms for about two weeks. The viruses can, however, begin shedding (released into the environment) within two days of the infection and can continue to do so for up to 20 days after recovery. This means that even individuals that seem healthy could be spreading the virus among their peers, family, and the public.
That’s why there is a huge focus on social distancing. If individuals remain at home and avoid gatherings and interactions with large groups of individuals, they can reduce their chances of getting and distributing the virus exponentially.
Is There A Solution?
As we don’t have a fully FDA tested drug or vaccine developed yet, healthcare centres have been using a slew of antiviral medications to help facilitate the reduction of the symptoms of COVID-19. On the other hand, researchers are working to develop new targeted drugs and repurpose old ones. For the latter option of repurposing effective drugs from similar conditions, researchers found that two compounds that were previously used as antimalarial drugs — chloroquine and hydroxychloroquine — showed great potential in reducing the viral load seen in patients.
Recent research also indicates that other antibiotics such as azithromycin (used to disrupt the growth of mycobacterial infections) which was thought to prevent excess growth of the respiratory tract infections caused by COVID-19, and remdesivir (a medication used to treat Ebola) were similarly effective in the process of treating COVID-19, and in fact reinforced the efficacy of hydroxychloroquine when used in combination. According to trials conducted by a joint group from France and Vietnam, the synergetic use of hydroxychloroquine and azithromycin over 6 days resulted in a 100% virological cure rate (p<0.001), whereas the hydroxychloroquine-integrated group displayed 57.1%, which could be compared to a control of 12.5%:
When a disease is virologically cured, it indicates that after a set period of time the virus levels in the body are either zero or at a similarly negligible rate. In the case of COVID-19, viral levels are usually tested using PCR (polymerase chain reaction), which allows researchers to “scale-up” extremely low concentrations of viral DNA from nasopharyngeal swab samples (upper part of the throat) allowing it to replicate itself billions of times into detectable concentrations. Researchers can then use specific genetic sequences that they know to be part of the coronavirus genome to see if the genome samples generated through PCR contain those sequences.
In terms of developing a vaccine; however, progress is much slower despite the urgency put forth by health organizations such as the WHO, and because of the inherently slow nature of this process relative to adopting repurposed versions of older drugs. Nevertheless, the genetic similarity between COVID-19 (SARS-CoV-2 ) and SARS-CoV (Severe Acute Respiratory Syndrome) allows researchers to repurpose and modify the viruses present in old vaccines.
The mechanism of action for most vaccines is quite simple — by creating “weaker” or less potent versions of a given virus and introducing it to the body, the immune system eradicates the foreign substance and generates memory B cells in the process. These cells are responsible for the formation and constant updating of their immune “database”, which ensures that in the case of the same viruses being introduced at full potency and strength, the memory B cells initiate a “secondary immune response” to fight it. This is the reason why humans are almost never infected twice with diseases such as chickenpox or measles.
In this case, however, researchers are testing a different approach to providing vaccination. Instead of introducing weakened versions of the virus, they actually introduce a small piece of mRNA that had been extracted from the virus and expanded in the lab. This mRNA codes for the spike proteins crucial for the virus to enter human cells. The researchers hope that the immune system can learn to recognize the spike proteins should the individual get infected with coronavirus, and kill the viruses before they can damage the body. Testing of the vaccine has already begun in Seattle, and researchers are just waiting for results.
The only challenges that researchers face during the creation and testing of drugs and vaccine candidates would be to ensure their precision. This is because most antiviral and antibacterial drugs can attack a considerable portion of healthy cells along with the virus, which can lead to a series of side-effects that can be potentially fatal, especially for the elderly population.
Moreover, drugs need to be developed with properly tested dosages, and this dosage may need to be tailored to the person being treated, as research showed that several dosages of drugs (especially in combinations) was less effective, and in studies, that the given measure of the drug (0.46μg/ml hydroxychloroquine serum)in the trial would have a varied effect on different patients.
At this point, researchers are in the process of finding and testing current candidates for vaccines to COVID-19, and the majority of these candidates are based on SARS-CoV vaccine contents. While researchers develop these candidates, it is our duty as citizens of our respective countries to continue to slow its spread through the practice of social distancing, proper handwashing techniques, and self-isolation when necessary so that humanity can eradicate COVID-19 as fast as possible.