The Novel Coronavirus - SARS-CoV2

You may have heard about the novel Coronavirus that is causing a pandemic around the globe. This pandemic has disrupted the world for around 6 months so far and it is one of the fast spreading viruses to exist. If it is a virus, just like the ones that cause common cold and upper respiratory infections, what is so different about this virus to make it viable for creating a pandemic? 

History

To start with the name, Corona means a part of the body resembling or likened to a crown. Coronavirus got this name from its crown like spikes on its body. There are 7 human Coronaviruses that have been identified since the mid 1960s. Some Coronaviruses infect animals and then are transmitted to humans to become human Coronaviruses. SARS-CoV, MERS-CoV and SARS-CoV2 (the 2019 novel Coronavirus) are such viruses that are transmitted from animals to humans. Compared to other pathogens like bacteria, viruses have evolved in such a way that it is hard to kill them or treat them. That explains why out of 10 pandemic outbreaks that occurred from 165 AD until 2019, 6 of them were caused by viruses.

Coronavirus Invasion

Viruses are structured as if they are freeloading zombies, not quite alive, yet not quite dead either. So they wait for a living being “host” cell to come into contact with in order to become alive. They are also very miniscule and don’t have characteristics of living things, so it is very difficult to target them with any drug treatments. Viruses work very differently than bacteria, which takes over the body’s cells and thrives on proteins that are generated by cells. Then, antibodies are deployed to attack these cell walls to stop producing proteins so that bacteria production can be stopped. But, since viruses operate in a different way, they only attach to certain proteins of the cells to hijack the cell body. Coronaviruses in particular use their spike proteins (S proteins) to latch on to the host cell’s ACE2 receptors (blue shapes in the picture below). It will then release its RNA or ribonucleic acid into the cell. RNA has the instructions on how to replicate hundreds of copies of the virus. This process makes the cell into a factory that creates hundreds of copies of coronaviruses that in turn invade other cells that have ACE2 receptors.  ACE2 receptors are found in many cells and tissues of the body including lungs, heart, blood vessels, kidneys, liver and the gastrointestinal tract. ACE2 is a vital element that is very important in regulating processes like wound healing, blood pressure, healing and inflammation. ACE2 particularly controls many functions of a protein called angiotensin II (ANG II) that increases blood pressure, inflammation, damage to tissues, blood vessel lining. When Coronavirus attaches to ACE2 receptors, it prevents ACE2 from performing its normal functions, including controlling ANG II, which causes various types of tissue damage, increased blood pressure and inflammation to the body. Inflammation causes damage to cells especially in the lungs, which are critical to supply oxygen to the body. This results in breathing problems and shortness of oxygen.

SARS-CoV2 spread

Current studies show that the novel Coronavirus (SARS-CoV2) attaches to the ACE2 receptors more strongly than the previous Coronaviruses that caused SARS and MERS, which makes it highly contageous. SARS-CoV2’s structure and biological makeup also makes this virus to be a silent transmitter before any obvious symptoms show up. This feature gives SARS-CoV2 an advantage to spread quickly than other Coronaviruses.

Immune Response

Our human body has evolved with defense systems to protect us from such viruses and bacterial invasions through triggered immune responses. These immune responses make the host cell release a protein to halt virus replication or completely shut down the compromised cell. However, in the case of a larger virus replication, such an immune response can call for reinforcement to defeat the virus, resulting in infections and fevers. But viruses like Coronavirus are very sneaky, so they can silently invade the cells and replicate in a high number before the immune response is triggered. By then, it will be too late for the body’s immune system to fight the virus. In the worst case, our own immune system can run in overdrive mode and try to destroy everything that has the virus in it. This situation will cause pneumonia and severe infections. 

Our Way Out

Scientists around the world are studying various aspects of SARS-CoV2 to understand its molecular composition and potential immune responses to defeat the virus at its core. Researchers are finding the best way to interfere with S protein interaction with ACE2 receptors. Instead of attacking ACE2, which is critical for human body functions, they are working on antibodies or peptides that can bind and disable functions of S proteins. SARS-CoV2 contains 29 proteins. Of the 29 SARS-CoV2 proteins, 4 of them are called structural proteins, including S proteins, and they make up the structure of the virus. The rest of the 24 proteins are “Non-Structural” and “Accessory Proteins”. Non-Structural proteins (NSP) regulate the process of how the virus assembles copies of itself. They are also crucial in interfering with a host's immune response to stop fighting the virus. So, these NSPs are being researched further as viable drug targets to defeat the virus. Accessory proteins are not needed for replication of the virus, but the virus needs them to fight with host’s immune system responses. Studies are being done to understand how mutations of these accessory proteins affect SARS-CoV2’s ability to fight with host immune response. Many research labs also developed organoids (models of organs) to understand severity of the infections by inducing the virus. These studies and research are evolving around the world and a few promising drugs and vaccines are already developed that are being tested to verify their effectiveness and are being carefully administered and approved for mainstream usage. Current estimates show that if stage 3 testing is successful with FDA approval, a viable vaccine likely to be available by January 2021.