Explainer: Why is the coronavirus so deadly?
New and ongoing studies show that COVID-19 attacks multiple organs and puts almost the entire body of the patient at risk.
TAIPEI — COVID-19 is an airborne disease that spreads in tiny droplets that contain the new coronavirus, known as SARS-CoV-2. When people inhale contaminated droplets, the virus enters into the nose and the throat.
COVID-19 infection usually begins in the nose and throat, because the mucous membranes of these sites contain epithelial cells that are rich in ACE2 cell surface receptors. The virus needs to exploit ACE2 to get into human cells.
The coronavirus's outer coating is covered in spike proteins that give the virus its crown-like appearance. The spike protein possesses receptor binding domains, or RBDs, that the virus uses to pry open receptors before penetrating the cellular membrane.
The ACE2 receptor normally regulates blood pressure. But the coronavirus's downward RBD can bind with this receptor and allow the virus to enter, and then hijack, the host cell.
Once the virus enters the human cell, its coating dissolves and frees viral RNA to hijack the host cell's apparatuses. The cell's endoplasmic reticulum produces viral RNA and proteins, while its Golgi body packages them into whole new viruses.
As the virus multiplies, the infected person may develop early symptoms, such as a sore throat and dry cough, while spreading plentiful amounts of the virus to others.
Other symptoms for the first week of infection include fever; a loss of smell and taste; and muscle aches.
The lungs contain air sacs called alveoli that keep us alive by exchanging carbon dioxide for oxygen.
If the virus moves down the lungs, it attacks the alveoli, which are lined with vulnerable, ACE2 receptor-rich cells.
To fight off infections, white blood cells release cytokines to summon more immune cells. Pneumonic COVID-19 may trigger cytokine storm syndrome, a phenomenon where the body scrambles too many immune cells.
As the virus attacks the lungs, the cytokine storm floods the lungs with white blood cells that destroy both healthy and infected cells.
This fills the air sacs with liquids, mucous and the detritus of dead cells.
Pneumonic COVID-19 disrupts the exchange of oxygen and damages the lungs extensively, which leads to dangerously low oxygen levels that may become fatal.
When the virus gets into the heart, it strikes blood vessel cells that are rich in ACE2 receptors. Clinical studies suggest the viral onslaught causes blood clots that obstruct the artilleries and trigger heart attacks.
Intestinal cells that are responsible for absorbing nutrition called enterocytes also express the RNA for ACE2 and a related enzyme that the virus also exploits, which makes the intestines vulnerable.
A clinical study from the Chinese city of Wuhan found more than a third of COVID-19 patients suffered neurological complications.
According to the neurological study, as many as 35 percent of patients had neurological complications including impaired cognition, stroke and muscle damage. Blood clots that travelled to the brain could be the cause of the strokes.
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