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The Biology Behind COVID-19 - A Case Study for Students

For students studying advanced biology, the COVID-19 virus is a perfect case study for various different yet connected biology topics. The case study is divided into sections by topic:

  • Viruses

  • Genetics

  • Immune system

  • Cell to Cell Communication and Receptors

First, let’s clarify the terms. COVID-19 refers to the disease, while SARS-CoV-2 refers to the name of the virus. SARS stands for severe acute respiratory syndrome. The virus does not yet have a formal scientific name with the binomial nomenclature because we don’t know enough about the virus’s evolutionary lineage yet. The general name of this virus family, coronaviruses, comes from the crown-like spikes that are on the virus’s surface (“Corona” means crown).

How the Virus Works

Alveoli, the air sacs in our lungs
Alveoli, the air sacs in our lungs

SARS-CoV-2 can lodge and infect humans either in the throat or lungs. They destroy human cells in those locations and multiply rapidly. Infection in the throat can be stopped early on. Tiny hairs called cilia in the throat help prevent the viral invaders. However, infection in the lungs is much more lethal. The lungs have delicate air sacs called alveoli. When the virus attacks the lungs, they destroy the cells that make up the alveoli, ultimately blocking the air passage and collapsing the alveoli.

SARS-CoV-2 is especially contagious compared to its virus relatives because it can start leaving behind viral parts early on in the infection. Even when the virus has just entered and is still in the throat, it can start leaving the viral parts This allows for easy transfer from the human host to other people nearby. After all, it is much easier to cough up viruses from the throat than to expel viruses from the lungs or other internal organs.

Bad Genes

Mutations can either be advantageous or disadvantageous so on one hand, viruses want to prevent mutations from happening, but on the other hand, they need to increase their genetic variation somehow. SARS-CoV-2 is an RNA virus that can very effectively prevent deleterious mutations from arising with its robust proofreading abilities. Normally, RNA viruses do not have tools for proofreading, and that makes them more susceptible to drugs that can induce mutations in the viral genome and suppress the viral infection.

SARS-CoV-2 is also able to “trade” and combine small segments of RNA with other viruses within the family. That allows for incredible genetic variation. More importantly, this random recombining of genes leads to a higher probability of multiple dangerous genes ending up all in one particular viral strain. SARS-CoV-2 is exhibit A of this. This is also the reason that animal hosts such as bats tend to be carriers of the most virulent viruses -- they can host over 50 different viruses simultaneously! This creates the perfect opportunity for viruses to swap genetic segments with each other.

Immune System Overreaction

How the immune system reacts to invading viruses
Antibodies and cytokines in action. Image by pikisuperstar

Our own immune system also plays a significant role in COVID-19 and further exacerbates the condition. In some patients, SARS-CoV-2 can trigger an overreaction from the host’s immune system, called a cytokine storm. This response is a wave of cytokines (a diverse group of cell signaling proteins that can circulate in the blood) that are released rapidly and creates excessive inflammation in the affected area. The inflammation can then lead to severe tissue damage in the internal organs of the patient.

Cell to Cell Communication and Receptors

So what are those crown-like spikes on the surface of coronaviruses? They are actually proteins called receptor-binding domains. They are highly species-specific, and the SARS-CoV-2 can bind extremely well to human cells. They bind to a particular receptor called ACE2. This receptor is found on the surface of human cells that line blood vessels. One of the reasons the lungs are especially susceptible to the virus is that the alveoli are covered with blood vessels. This means they are covered in cells with ACE2, which is the virus’s target for binding.

Unlike less lethal viruses, the receptor-binding domain on SARS-CoV-2 can snap in half once it binds to the host cell. This cleavage causes special peptide chains to help fuse the virus membrane with the human host’s cell membrane. This is where it gets dangerous, because the fusion allows the viral DNA to enter the host cell and mass-produce more viruses.

The combination of all these different biological factors makes SARS-CoV-2 a particularly interesting and comprehensive case study. There are studies currently being done across the globe in an effort to better understand the virus structure and detailed mechanisms of infection. Understanding these aspects will help scientists develop more accurate testing methods, effective and safe vaccines, and treatments for infected patients.

Much of the information presented here is based on a fascinating and scientifically sound article that dives deeper into the biology and evolution of SARS-CoV-2.

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