"? COVID-19 CURE
There is a mention about the influence of genes on disease resistance. I will save the response for another day. Let us go this route for now. Viruses mutate, and there is cross-resistance, meaning an antibody developed against a certain virus might as well protect us from closely related viruses or viral strains. Coronaviruses group have been with us for long and it mostly causes mild symptoms. Indeed the current Sars-CoV-2 only drastically affects 20% of those infected. And of those who have severe symptoms, only 4-5% of them die.
Current medical intervention (in the First World) might ensure that that only 2% of the 4-5% succumb to the illness as fatalities. How do we arrive at such figures? The pathophysiology of the disease is slowly getting obvious; people drown in their own secretions and the lungs are unable to ensure adequate oxygenation due to fibrosis. How do we heal by fibrosis? Yes, in immunological terms it is called healing by “secondary intention”. Can we delay such healing and thereby circumvent fibrosis?
Let me throw in novel remedial treatments here! Yes, pn(x) and h******se(y) are novel in this area. X is locally available from _______! What do they do? And how can they be administered, and through what route? These are reserved for critically ill patients and are to be preferably administered through aerosol! We break them into microparticles and inhale it. X diminishes speed of scar formation, Y increases cell membrane (alveoli) permeability. The combination of the two ensures continued gaseous exchange thus mitigating on hypoxemia. I could explain it further but save that for another page. These two are reserved for very severe cases and must be accompanied with ventilation.
Remember fluid collection within the lungs creates a potential for infection, and that is when we throw in azithromycin or a similar acting antibiotic. What of chloroqune and hydrochloroquine? These work at preceding levels and reduce viral penetrance and virulence. Some clinicians have also thought of drugs like losartan to be co-administered in select Sars-Cov-2 infection. Losartan is an ACE2 blocker. ACE2 receptors are in lungs, kidneys, amongst other locations. So how does it help in Covid-2? It alleviates symptoms associated with impeding heart failure due to inevitable co-pulmonale, nothing more. It also helps in persons with poor cardio and persons with a co-morbidity like high blood pressure.
So, do we need to worry so much about Covid-2 impending mortalities? Yes. We must still prioritize prevention, even when there is acure. The cure or supportive treatment results into astronomical expenditure, that is largely avoidable if we could only break the chain of infection.
Now, where are my sources, and who am I referencing? Save that for later, since this is pro-bono, as usual. How about plasma transfusion from persons who recover? Yes, that helps since it might be a ready source of antibodies. However such antibodies have a short longevity. Our bodies must produce their own antibodies in order to fight diseases in the long term.
What of use of zinc, vitamic C and the like? There is a lot of literature on that. It is thought that they prevent people from getting sick and also reduce the duration of illness. These are never strategies that in themselves stand in the way of any disease!
We have not included any antivirals in this strategy, eg. abacavir, lopinavir, remdesivir. There is none of them that has been proven to work on Sars-Cov-2. It is worth trying various combinations with modified doses. There is no harm in creating cohorts that would later act as reference points for future research. It is time for use judicious judgment in the ad hoc use of antivirals especially for patients that we would otherwise lose to the disease!"
Finally, despite all the above, the main approach is prevention, prevention, prevention…