It’s hard to believe that viruses can take over the world. Though we can’t see these invaders with our own eyes, they have the scary ability to hijack our cells and use them for their own evil purposes! However, this may be slightly inaccurate - viruses aren’t actually alive, so they don’t have an evil agenda to destroy us. In actuality, viruses just want to continue their line and make more copies of themselves. Viruses are known as obligate intracellular parasites which is just a fancy way of saying viruses lack the tools for replication on their own, so they rely on infecting cells to get the job done. In today’s Bite-Sized Science post, we’ll be doing an overview and deep dive into the replication cycle of the virus that has been at the forefront of our concerns this year: COVID-19.
Not all coronaviruses are the same. In fact, most just cause common colds or don’t even infect humans! However, the SARS-CoV-2 strain turned out particularly virulent and capable of causing severe disease. To clarify, SARS-CoV-2 stands for severe acute respiratory syndrome coronavirus 2, and it is the name of the virus. SARS-CoV-2 causes the disease known as coronavirus disease 19, which is shortened to COVID-19.
In general, coronaviruses are identifiable by their spiky, crown-like appearance, thanks to the aptly named “spike proteins.” Spike proteins are one of the 3 structural proteins located on the outer shell, and they play an important role in helping the virus enter a cell. The other two proteins are the membrane and envelope proteins, which help the virus assemble later on when it wants to infect new cells. All the genetic information of coronaviruses are contained in strands of RNA; RNA is like a code for protein synthesis, or you can think of it as the recipe that cells follow to make proteins.
So how does the virus actually infect a person? Let’s take a look at the general life cycle of a virus to answer this question.
Step 1: Virus enters a cell
All viruses need to enter a person before they can start infecting cells. Step 1 involves the virus finding a way into the body, and then into a cell. With SARS-CoV-2, the route of entry is the nose or mouth. This is one reason why wearing a face covering is so important! To enter a cell, the virus attaches itself to a receptor on the surface of a cell. Think of receptors as the receptionists for your doctor’s office, but instead of an office, it’s a cell. When you have an appointment and the receptionist correctly identifies who you are, they let you go past them and into an examination room. Receptors wait for the correct molecule to come along so they can let it enter, but when they see a virus,
they make a mistake, and let it go into the cell even though it shouldn’t be able to! In this case, SARS-CoV-2 fools the angiotensin converting enzyme II (ACE2) receptor, and uses it to enter. This name sounds long and complex, and part of the reason is because ACE2 is actually meant for a different system in the body. Though we won’t go into the specifics here, maybe in the future we’ll explore the role of angiotensin on Bite-Sized Science! Now, remember the spike proteins we mentioned earlier? Spike proteins work together to attach the outer shell of the virus to the cell membrane, resulting in RNA release into the cell. To attach to the cell, proteases such as TMPRSS2 and furin are needed. Proteases are basically molecules that cut proteins. Fun fact: Furin is found all around the body, and one reason scientists think SARS-CoV-2 is so easily spread is because furin is available everywhere to help the virus enter cells.
Step 2: Virus replicates in the cell
So now, the virus is in the cell. What’s Step 2? Well, the main goal of a virus is to keep its own kind going, so now that it has access to the cell, it will use the cell’s “machinery” to start replicating itself. The virus brings some of its own tools to read the RNA, and then it uses the welcoming environment of the cell to churn out many more copies of itself. The cell is turned into a virus-making factory!
Step 3: Virus starts infecting more cells
This finally brings us to Step 3: the RNA is packaged in various cell pathways with the help of envelope and membrane proteins, and then it is released. In addition to this normal method of viral spread, SARS-CoV-2 can also form syncytia with the help of proteases. Syncytia are essentially cells that are fused together. Instead of going through the whole process of finding another cell with the right receptor, the virus can now hide from our immune system and simply merge itself with another cell to infect it.
Hopefully, this blog post hasn’t been too much to swallow. The viral life cycle is complex and still under discovery. However, knowing what the coronavirus does in our body is important for drug discovery and treatment, which was previously covered in the first blog post of our COVID-19 series. Stay tuned for COVID-19 mythbusters next week!
References
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