The biology of why coronavirus is so deadly
COVID-19 is caused by a coronavirus called SARS-CoV-2. Coronaviruses belong to a group of viruses that infect animals, from peacocks to whales. They’re named for the bulb-tipped spikes that project from the virus’s surface and give the appearance of a corona surrounding it.
A coronavirus infection usually plays out one of two ways: as an infection in the lungs that includes some cases of what people would call the common cold, or as an infection in the gut that causes diarrhoea. COVID-19 starts out in the lungs like the common cold coronaviruses, but then causes havoc with the immune system that can lead to long-term lung damage or death.
SARS-CoV-2 is genetically very similar to other human respiratory coronaviruses, including SARS-CoV and MERS-CoV. However, the subtle genetic differences translate to significant differences in how readily a coronavirus infects people and how it makes them sick. SARS-CoV-2 has all the same genetic equipment as the original SARS-CoV, which caused a global outbreak in 2003, but with around 6,000 mutations sprinkled around in the usual places where coronaviruses change. Think whole milk versus skim milk.
Compared to other human coronaviruses like MERS-CoV, which emerged in the Middle East in 2012, the new virus has customized versions of the same general equipment for invading cells and copying itself. However, SARS-CoV-2 has a totally different set of genes called accessories, which give this new virus a little advantage in specific situations. For example, MERS has a particular protein that shuts down a cell’s ability to sound the alarm about a viral intruder. SARS-CoV-2 has an unrelated gene with an as-yet unknown function in that position in its genome. Think cow milk versus almond milk.
How the virus infects
Every coronavirus infection starts with a virus particle, a spherical shell that protects a single long string of genetic material and inserts it into a human cell. The genetic material instructs the cell to make around 30 different parts of the virus, allowing the virus to reproduce. The cells that SARS-CoV-2 prefers to infect have a protein called ACE2 on the outside that is important for regulating blood pressure.
The infection begins when the long spike proteins that protrude from the virus particle latch on to the cell’s ACE2 protein. From that point, the spike transforms, unfolding and refolding itself using coiled spring-like parts that start out buried at the core of the spike. The reconfigured spike hooks into the cell and crashes the virus particle and cell together. This forms a channel where the string of viral genetic material can snake its way into the unsuspecting cell.
SARS-CoV-2 spreads from person to person by close contact. The Shincheonji Church outbreak in South Korea in February provides a good demonstration of how and how quickly SARS-CoV-2 spreads. It seems one or two people with the virus sat face to face very close to uninfected people for several minutes at a time in a crowded room. Within two weeks, several thousand people in the country were infected, and more than half of the infections at that point were attributable to the church. The outbreaks got to a fast start because public health authorities were unaware of the potential outbreak and were not testing widely at that stage. Since then, authorities have worked hard and the number of new cases in South Korea has been falling steadily.