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SARS-CoV-2 COVID-19 pathogenesis clinical

Explanation of pathophysiology of COVID infection as per below mentioned approach....(available on internet).....

1.-Why there is high ferritin level ?

2.-Why there is very high DDimer levels disproportionate with the severity of infection?

3.-Why ARDS in those are nearly

Not responding to high PEEP and Fio2 levels?

4.-Why all CT chest patterns are exclusively Ground glassing and associated with rapid and marked hypoxemia disproportionates with the geographical CT findings size ?

5.- Why Early Chinese protocol for Covid includes high dosing of systemic steroids which is questioned and rejected by WHO ?

6.- Why body immune response aganist Covid is not like other respiratory viruses by lymphocytosis ( Cytotoxic T cells and Natural killer cells) , insteadly body prefers to reacts against covid by phagocytosis ( monocytosis ) ?

7.- Why Covid Attacking mature red blood cell while it is one of body cells that dose not contain nucleus and DNA ?

8.-Why Critically ill Patients are responding well to anticoagulation , Hydroxycholoquine and novel antiviral Favipiravir ?

The following molecular pathogenesis is the only one for the time being that can answer all these questions .

COVID -19 may not cause pneumonia either typical or atypical or classical ARDs . It seems like we are dealing with a presumed wrong disease.

The Key pathogenic molecular step of SARS-Cov2 is to attack the 1-Beta Chain of Hemoglobin and hunting the porphyrins dissociating the iron form it and releasing iron into the circulation.

Thus Hb loses its capacity to bind with oxygen , so oxygen is not supplied to major organs. That is why we see resistant hypoxia coupled with very rapid multi-organ failures.

Moreover The free iron released into the circulation is so toxic as it causes a powerful oxidative damage to the lungs.

Free iron toxicity causes inflammation of alveolar macrophages - leads to CT scan characteristic changes.

The body tries to compensate this by elevating the rate of Hb synthesis which explains why Hb is high in those patients.

Other compensatory mechanisms to deal with such iron load is increasing ferritin production ( iron store ) which explains the very high ferritin levels observed in those patients.

Therefore the cause of monocytosis is the body needs to excess macrophages to engulf the excess iron load .

And the cause of Lymphopenia is the WBCs differentiation favoured towards monocytes line rather than lymphocytes line.

This makes ferritin a bad prognostic marker (too much iron means too much Hb lost its Oxygen carrying capacity) .

Also this iron load and increased Hb production leads to increased blood viscosity with recurrent and diffuse micro and macro circulatory thrombosis, and that is why there are high levels of DDimer in those patients and this explains the cause of sudden deterioration and death in some sporadic cases.

This disseminated thrombosis is proved by postmortem examinations of ARDS victims ( it is not a real ARDS) .

This theory could explain why we are losing patients so rapidly and why mechanical ventilation is not so much effective in treatment and using ARDS mechanical ventilation protocol is not causing any benefit. Actually it could be futile and causing more lung damage.

On the other hand, this crucially explains the very rapid and good response of those patients to full therapeutic anticoagulation.

Chloroquine as antimalarial drugs is working by protecting Hb against invasion by malaria parasites.

It is doing the same here but just protecting the Hb against invasion by the virus.

The chemical components in chloroquine phosphate compete with the porphyrin and bind to the viral protein, thereby inhibiting the viral protein's attack on heme or binding to the porphyrin.

Favipiravir is the latest anti-novel-coronavirus drug with specific therapeutic effects.

In Favipiravir, the most critical ligand is 1RP, which is 6 - fluoro - 3 - oxo - 4 - (5 - O - phosphono - beta - D - ribofuranosyl ) - 3, 4 - dihydropyrazine - 2 - carboxamide.

Favipiravir cannot bind to E2 glycoprotein and Nucleocapsid, and its binding energy to viral envelope protein, ORF7a, orf1ab is higher than that to porphyrin.

It is useful to note that the binding energy of Envelope protein and Favipiravir is more than 2700 times the binding energy of porphyrin.

The primary function of Envelope protein is to help the virus enter host cells, which shows that Favipiravir can effectively prevent the virus from infecting human cells.

* Recommendations :-

According to these clinical observations ,correlations and understandings :-

1- Hydroxychloquine , Favipiravir and early full anti coagulation therapy should be involved as early as possible in Management Protocol of Covid-19 .

* References :-

-Data is collected and interpritated from different clinical observations and reviews of many doctors and intensivists and from the postmortem examination pictures of Covid-19 victims in USA and Europe.

-Wenzhong Liu and Hualan Li2 (2020):

COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism; School of Computer Science and Engineering, Sichuan University of Science & Engineering, Zigong, 643002, China;

School of Life Science and Food Engineering, Yibin University, Yibin,644000, China; Correspondence: [email protected];

Preprint Use of product labels to investigate the treatment of Covid-...

It has been suggested that ingestion of disinfectants may be beneficial to treat patients infected with SARS-CoV-2. DO NOT DO THIS IT IS HARMFUL TO HUMAN HEALTH.

The above article may be of interest and provide some light relief.

Please have a look at the following link:

Flawed methods in “COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism”