Virology half-understood, pseudoscience and and maybe a little hope:
Coronaviruses are interesting. They have the biggest genome of any RNA viruses in their nucleocapsid (the envelope with the RNA in). There are three proteins – S- or spike protein which makes up the spikey part on the outside, M protein which makes up the outer membrane and N protein which encloses the nucleocapsid inside.
The virus spreads in two ways. It can force replication of its own RNA and the new virus particles exit the cell emerging into the extracellular space to infect other cells. The other way it moves to new cells is by syncytial spread – moving through cell membranes into adjacent cells. The ‘clever’ part about that is that it can spread along a mucosal (lining membrane) surface without ever being exposed to the extracellular environment where antibodies (IgG and IgM) can neutralise it, or extracellular toxins (like drugs) can affect it.
The virus has an affinity for a particular site on human cell membranes called angiotensin converting enzyme-2 or ACE-2 receptors. That receptor is common and present on many cells in the body. The purpose of ACE is to increase levels of angiotensin which is important in the renin/angiotensin mechanism (which keeps your blood pressure up). This renin angiotensin pathway raises blood pressure by causing vasoconstriction. Inhibitors of ACE can occupy these receptors on cells and work by causing smooth muscle relaxation and lowering of blood pressure.
The Coronavirus spike protein latches onto that receptor site and changes shape to allow passage of the nucleocapsid into the cytoplasm of the infected cell, where is latches onto the Golgi apparatus and creates replicas of its own RNA. Unfortunately giving ACE inhibitors doesn’t prevent viral attachment because the spike protein can change the morphology of the receptor site to adapt.
Potentially the only way to affect the virus is during replication or to block the exiting particles.
Chloroquine affects the developing malaria parasite by blocking one locus on the protein necessary for it to exit the red blood cell it infects. Since Coronaviruses have a large complex RNA chain and require certain proteins to burst out of the host cell there must be some logic in using Chloroquine to damage those proteins.
Similarly, bacteriostatic antibiotics (Doxycycline, Azithromycin) inhibit protein manufacture by acting on a different locus on mycoplasma proteins (the antibiotics of choice for Chlamydia) and prevent the infected cell from letting out the infecting organism.
So, my feeling is to treat the infection as early as possible with those two drugs, so the extent of the infection is reduced and hopefully the second phase of the illness won’t occur. This is unproven but there was one small study, poorly controlled and much criticized which did show that patients on these two drugs did better than patients who did not take them, albeit in a different hospital but otherwise age and illness matched.
I think that if/when I get this virus, I want early treatment with those 2 drugs!