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 are named for the bulbous tips that protrude from the surface of the virus and give the appearance of a crown that surrounds it.
A coronavirus infection usually occurs in two ways: as an infection of the lungs which includes certain cases of what people call the common cold, or as an infection of the intestine which causes diarrhea. COVID-19 starts in the lungs like common cold coronaviruses, but then causes havoc in 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 into significant differences in how easily a coronavirus infects people and how it makes them sick.
SARS-CoV-2 has the same genetic equipment as the original SARS-CoV, which caused a global epidemic in 2003, but with approximately 6,000 mutations scattered in the usual places where coronaviruses grow. Think of whole milk and skim milk.
Compared to other human coronaviruses such as MERS-CoV, which appeared in the Middle East in 2012, the new virus has customized versions of the same general equipment to invade cells and copy themselves. However, SARS-CoV-2 has a completely different set of genes called accessories, which give this new virus a little advantage in specific situations. For example, MERS has a special protein that prevents the cell from sounding the alarm about a viral intruder. SARS-CoV-2 has a gene unrelated to a function still unknown at this position in its genome. Think cow’s milk and almond milk.
How the virus infects
Each coronavirus infection begins with a viral particle, a spherical shell that protects a single long chain of genetic material and inserts it into a human cell. The genetic material requires the cell to make about 30 different parts of the virus, allowing the virus to reproduce. The cells that SARS-CoV-2 prefers to infect have a protein on the outside called ACE2 which is important for regulating blood pressure.
Infection begins when long-spike proteins protruding from the viral particle lock onto the cell’s ACE2 protein. From that moment, the point is transformed, unfolded and folded up using coiled spring-shaped parts which start buried at the heart of the point. The reconfigured tip clings to the cell and blocks the viral particle and the cell together. This forms a channel where the chain of viral genetic material can enter the cell without suspicion.
SARS-CoV-2 spreads from person to person through close contact. The outbreak in Shincheonji Church in South Korea in February provides a good demonstration of the speed and spread of SARS-CoV-2. One or two people with the virus appear to have been very close to uninfected people for several minutes at a time in a crowded room. In two weeks, several thousand people in the country were infected and more than half of the infections at that time were attributable to the church. The epidemic started quickly because public health officials were not aware of the potential epidemic and were not doing large-scale testing at this stage. Since then, the authorities have worked hard and the number of new cases in South Korea has continued to decrease.
How the virus makes people sick
SARS-CoV-2 grows in type II lung cells, which secrete a soap-like substance that helps air get deep into the lungs and cells lining the throat. As with SARS, most of the damage caused by COVID-19, the disease caused by the new coronavirus, is caused by the immune system defending against the scorched earth to prevent the virus from spreading. Millions of immune system cells invade infected lung tissue and cause considerable damage when the virus and infected cells are cleaned up.
Each COVID-19 lesion ranges from the size of a grape to the size of a grapefruit. The challenge for healthcare workers treating patients is to support the body and keep the blood oxygenated while the lung is repairing.
SARS-CoV-2 has a movable gravity scale. Patients under the age of 10 seem to be able to clear the virus easily, most people under the age of 40 seem to bounce back quickly, but the elderly suffer from increasingly severe COVID-19. The ACE2 protein that SARS-CoV-2 uses as a gateway into cells is also important for regulating blood pressure, and it doesn’t do its job when the virus first arrives. This is one of the reasons why COVID-19 is more serious in people with high blood pressure.
SARS-CoV-2 is more serious than seasonal flu in part because it has many more ways of preventing cells from calling the immune system for help. For example, cells try to respond to the infection by making interferon, the alarm signaling protein. SARS-CoV-2 blocks this by a combination of camouflage, cutting the protein markers on the cell that serve as distress beacons, and ultimately shredding any antiviral instructions that the cell makes before it can be used. As a result, COVID-19 can become infected for a month, causing a little bit of damage each day, while most people get over a flu case in less than a week.
Currently, the transmission rate of SARS-CoV-2 is slightly higher than that of the 2009 pandemic H1N1 flu virus, but SARS-CoV-2 is at least 10 times more fatal. COVID-19 is very similar to severe acute respiratory syndrome (SARS) in the data currently available, although it is less likely than SARS to be severe.
What we don’t know
There are still many mysteries about this virus and coronaviruses in general – the nuances of how they cause disease, how they interact with proteins inside the cell, the structure of proteins that form new viruses and how some of the basic virus copying machines work.
Another unknown is how COVID-19 will respond to seasonal changes. The flu tends to follow the cold, both in the northern and southern hemispheres. Some other human coronaviruses spread low throughout the year, but then appear to peak in the spring. But no one really knows why these viruses vary with the seasons.
What’s amazing so far in this outbreak is all the good science that has come out so quickly. The research community discovered the structures of the virus’s peak protein and the ACE2 protein with part of the peak protein attached just over a month after the genetic sequence became available. I spent my first 20 years working on coronaviruses without benefiting from one or the other. This bodes well for a better understanding, prevention and treatment of COVID-19.
Benjamin Neuman, professor of biology, Texas A&M University-Texarkana
This article is republished from The Conversation under a Creative Commons license. Read the original article.