It’s March 2020 and the world has been battling a new coronavirus outbreak for months. Since the first case originated in late 2019 in the city of Wuhan, China, the virus has made its way across the globe, causing economic decline, quarantines, and death. The World Health Organization has officially raised the global alert to the highest possible level. This novel coronavirus is a cause for concern because of how little we know about it and how quickly it’s spreading. What is different with this virus, which is both good and bad, is that it’s much less severe than SARs. But it also means that a lot of people remain undetected because it looks a bit like a normal common cold. They don’t develop very severe symptoms, and by the looks of it, people are already shedding the virus while they’re still quite healthy. Now, firstly, the novel coronavirus has been named SARS-Cov2, while the disease it causes is called COVID-19—short for coronavirus disease 2019. In just a few months, this coronavirus has caused over 97,000 cases of confirmed infection and has claimed over 3,000 lives, globally. These numbers continue to increase as it makes its way across the world and as we get better at identifying it. Now, as of March 3rd 2020, the WHO estimates that the death rate from COVID-19 is around a preliminary 3.4%, which is higher than the flu. But SARS-Cov2 has so far infected less than the flu has at its highest season, and estimations between the two will most likely continue to change as time moves on. No matter the comparison though, it’s still evident that lives are at stake from COVID-19. Which is why scientists are working rigorously on understanding its transmission, behavior, and how they can stop it. Since this viruses global debut, what have we learned about it and how fearful should we be? Coronaviruses are named for their structural elements, so they have this very prominent protein on their surface which is called a spike protein. We see them very prominently on the outer ring—and that looks a bit like a crown, or like the sun’s corona when we have a solar eclipse. And that gives them their name. In most cases, coronaviruses are respiratory RNA viruses that infect animals, such as bats, cats, and birds. But when they make the jump to humans, these viruses are known as zoonotic. There are seven known coronaviruses that will infect humans, causing diseases like the ones we’re familiar with: COVID-19, SARS, and MERS. SARS and MERS are previous outbreaks from the last few decades. In 2002, there was SARS, meaning Severe Acute Respiratory Syndrome. And in 2012, there was MERS, meaning Middle East Respiratory Syndrome. They each took less than 1,000 lives. But both are known to cause a severe case of pneumonia and lung injury, and death rates from these infections are higher than COVID-19: from 11% to more than 30%. So, what we see with this virus is that it’s definitely much milder than SARs, within the known SARS, within the known SARS cases. What contributes to the virus being so much milder than SARs are many, many contributing factors and we definitely don’t know the details of it yet from a virus perspective, but it appears to be where the virus infects. So more lungs alone rather than what we call systemic disease, when the virus attacks our internal organs—our intestines as well— so that makes the virus much milder than what we saw with SARS. In fact, mortality rates from COVID-19 vary on the age and previous health of the patient. Since it’s usually not the coronavirus itself, but how your immune system responds. So, for any virus to cause a human disease, they need to get into human cells. Different viruses like to grow in different cells of the body. This new coronavirus likes to grow in the lung cells. When they get into a cell, they require a surface receptor. So, the spike protein, that very prominent protein that we see, is basically the key-lock interaction that tells the cell to take up this virus so that it can eventually hijack the cellular machinery and use it to make more of itself. This virus uses a protein called ACE2, as a receptor. The virus has to bind with the receptor to be able to get inside the cells. ACE2 is found throughout the respiratory tract and SARS-Cov2 seems to have a liking to cells in both the upper and lower part of our respiratory system. The lower respiratory tract includes the trachea, bronchi, bronchioles, and alveoli. The upper respiratory tract includes the nostrils, nasal cavity, mouth, throat, and voice box. When we have an infection in our lungs, then we have a lot of immune cells that come to help clear that virus, but at the same time, that’s liquid and cells which both block that thin layer of cells from taking up oxygen. And then obviously we want a physical barrier, which is mucus, to kind of wash out the virus. And that makes us cough, that brings us respiratory problems. Because of that damage, sometimes there is an accumulation of fluid in that part of the lung, and that is what we call pneumonia. Most of the patients that have died because of this coronavirus, have died because of pneumonia. Of course, like we said before, there are other factors that can make this a lethal disease. I would also like to emphasize that it seems that most of the people that have died because of this new coronavirus, so far, were either elderly, or they had an underlying disease condition. It seems that if your immune system is compromised for any reason, then you have a higher chance of getting a severe infection. To understand the origin of SARS-Cov-2 and its transmission, scientists sampled its genomes in 53 individuals back in January 2020. They converted the viruses nearly 29,000 nucleotides bases into workable DNA, which was shared with labs across the globe. Based on that DNA, they were able to distinguish that the virus was roughly 96.2% similar to a bat coronavirus and about 79.5% was similar to the coronavirus that causes SARS. So SARS-Cov-2 seems to have started in bats, but there needs to be a link between how the coronavirus lives in bats and to the slightly different kind of coronavirus found in humans. And that link is still unknown. Despite early theories that the outbreak originated in a seafood market in Wuhan, there’s evidence that may not be the case. So, what happens next? As of February 2020, teams in China and the U.S. National Institute of Allergy and Infectious Diseases are already testing an antiviral drug called Remdesivir to combat the spread. Created by a U.S.-based biotech company named Gilead, the experimental drug was shown to block the activity of a protein that helps coronaviruses make copies of themselves. Lab tests showed promise in animal models for SARS and MERS, and the treatment was also successful when used on a U.S. patient with COVID-19. While the FDA hasn’t approved this drug, clinical trials have started with 270 patients at Beijing’s China-Japan Friendship Hospital, roughly 1,000 patients spread throughout Asia, and a clinical trial in the U.S. that administer similar treatment. I think a lot of future efforts are going to be focusing on drug development, because it’s very clear right now that these viruses might continue to jump from animals to humans, so we should definitely be ready for another outbreak in future, and antiviral drug development and vaccine development are the way to go. There’s so much to discuss when it comes to COVID-19. If there’s another aspect of it that you want to see us cover, please let us know in the comments below, and make sure to subscribe to Seeker to see how we follow this news. Thanks for watching, go wash those hands, and I’ll see you next time.