How COVID-19 kills:
A Pathophysiological discussion in lay terms.
The Lungs consist of a network of air conduits which subdivide into a finer network of air passages which terminate into air sacs called 'alveoli'.
The alveoli are the membranes where O2 & CO2 are exchanged

CO2 waste from the body tissues diffuses into the air sac from the capillaries (blue) as O2 needed for metabolism diffuses into the capillary (red) so it may be returned to the heart & pumped to the tissues. The Alveolus is formed of 2 predominate cell types; I & II pneumocytes

Type I cells exchange O2 & CO2. Type II cells secrete a surfactant, a fatty substance which keeps the alveoli from collapsing at rest by regulating surface tension. The virus (SARS-COV-2) binds to a specific surface protein on Type II cells, called the ACE-2 receptor.

ACE, which may sound familiar, is the same receptor responsive to ACE-receptor blockers (eg losartan) used to treat high Blood Pressure. Binding by the virus permits entry into Type II cells, which allows release of the viral RNA into the cell, where it is converted into DNA

RNA conversion to DNA is a process called "Reverse transcription". RNA viruses (retroviruses) use this mechanism to incorporate their info into the the host cell DNA. Once integrated, viral DNA directs the host cell to replicates multiple viral copies until the cell dies.

The new virus particles affect (infect) neighboring Type cells and the process of overtaking the host, replication & cell death continue in a cascade. Eventually, the body's immune surveillance notices & starts an inflammatory response to stop it. 'Cytokines' are released.

Cytokines are a group of chemical mediators [interleukins(IL), interferons (IFs), Tumor necrosis Factors (TNFs)] produced by specific immune cells to produce a response, namely to kill affected cells and to protect to the host.
In COVID, the mediators are Il-1, Il-6 & TNF-alpha

The effect of the "Cytokine Storm" is to cause an inflammatory reaction which attacks the lungs, fills the alveoli with fluid & pus/exudate, ie Pneumonia. This impairs O2/CO2, lung compliance and leads to respiratory distress.

The clinical syndrome that some will develop as a consequence of the viral pneumonia is A.R.D.S (Acute Respiratory Distress Syndrome) which is frequently fatal. Only about 50% of ARDS patients who are placed on a ventilator will survive. This is how COVID patients die.

How do you treat ARDS?
1) Oxygen
2) Mechanical Ventilation
3) Steroids to quell/suppress the cytokine storm
4) Diuretics to manage fluid in lungs
5) Treat the precipitant. Unfortunately, no drug 'cures' COVID.
6) Supportive measures- ie Blood Clot Prophylaxis, positioning

How do I know this? I am a PhD Biochemist & A retired Surgeon, who unfortunately developed ARDS a few years ago. I was hospitalized for 42 day, including a week on the vent. I was one of the 50% that survived. My lungs are permanently scarred. Recovery was a bitch.