When an infected person expels virus-laden droplets and another person inhales them, the SARS-CoV-2 coronavirus gets into the nose and throat. The cells there are rich in a cell surface receptor called angiotensin-converting enzyme 2 (ACE2) . Throughout the body, the presence of ACE2, which normally helps regulate blood pressure, marks the tissues most vulnerable to infection, because the virus requires this enzyme to enter the cell. Once inside, the virus ‘hijacks’ the cell’s machinery, forcing it to make copies of itself and invading new cells.
As the virus multiplies, an infected person can shed large amounts of the virus, while symptoms may be absent. The new victim of the virus may develop fever, dry cough, loss of smell and taste, or headaches and body aches.
Normally, the immune system clears the infection on its own after a few days, but some patients, especially people with a depressed immune system, the elderly, and other illnesses, are unable to cope with the infection, and it worsens.
What happens in severe cases?
If the immune system does not counteract SARS-CoV-2 during this initial phase, the virus travels down the windpipe to attack the lungs. The ends of the branches of the lungs end in small air sacs called alveoli, each lined by a layer of cells rich in ACE2 receptors.
Normally, oxygen crosses the alveoli into the capillaries, small blood vessels that lie next to the air sacs; and so oxygen is transported to the rest of the body. But as the immune system fights off the invader, this battle disrupts a healthy oxygen transfer.
As described in a comprehensive report published by Science Magazine , white blood cells release inflammatory molecules called chemokines. These, in turn, summon more immune cells that attack and kill the coronavirus-infected cells, leaving a trail of pus and dead cells behind. This is the pathology underlying pneumonia, with its corresponding symptoms: cough; fever; and rapid, shallow breathing. Many COVID-19 patients recover, at times, with no other support than inhaled oxygen through respirators.
But other patients deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS) . Their blood oxygen levels plummet and they struggle more and more to breathe. Many of these patients die. Autopsies show that their alveoli filled with fluid, white blood cells, mucus, and debris from destroyed lung cells.
A cytokine storm, under suspicion
Some doctors suspect that what happens to many seriously ill patients is a disastrous overreaction of the immune system known as a ‘cytokine storm’ , which is known to trigger other viral infections.
Cytokines are chemical signaling molecules that guide a healthy immune response; But in a cytokine storm, the levels of certain cytokines rise far beyond what is needed, and immune cells begin to attack healthy tissues.
Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients, leading many scientists to believe that this inflammation is the true reason for the virus’s mortality. But some others don’t think there is convincing data on this , and addressing a cytokine suppression pathway could have counterproductive effects on the patient, such as suppressing their natural immune response.
