Covid-19: acquired acute porphyria hypothesis

Abstract

Edited on account of feedback from Prof Read regarding the work of Liu & Li. Pandemic Covid-19 pneumonia, of SARS-CoV-2 aetiology, presents an existential threat to health care systems globally. Multiple therapeutic and prophylactic agents are currently undergoing clinical trial, including 23 clinical trials of (hydroxy)chloroquine in China. While progress towards a curative agent or vaccine is promising, the principal limiting factor in public health emergency is time, and therefore a pre-existing licensed therapeutic would offer reprieve to health care systems operating at the edge of capacity. In this brief communication, the author argues that Covid-19 has high probability of being more than a disease of pneumonia, and that critical Covid-19 patients may be experiencing a form of acquired acute porphyria. Readily available interventions exist to treat acute porphyria and the position is advanced that urinalysis of critical Covid-19 patients would diagnose this pathology.

Letter to the Editor: Boron enhances the antiviral activity of the curcumin against SARS-CoV-2

“…In the past, CD147 has been identified as a receptor for red blood cells for infection with the Plasmodium falciparum parasite (protozoan causing malaria in humans) [ 8 ]. Recent research shows that human red blood cells are strongly involved in the pathophysiology of COVID-19 [ 9 ].…”

Covid-19: acquired acute porphyria hypothesis

“…The current review advances the author's original hypothesis published as a preprint in April 2020 (Abrahams, 2020). Erythrocytes are strongly implicated in the pathophysiology of Covid-19 although their role is thought to be under-estimated.…”

SARS-CoV-2 association with hemoglobin and iron metabolism

“…However, when it is greater than 45%, there are signs of IO. When TS is >70%, a free form of iron begins to accumulate in the plasma, known as non-transferrin bound iron (NTBI) 4,6 , thereby causing IO in the parenchymal cells. Free Fe catalyzes the conversion of free radicals from oxygen.…”

“…It has previously been demonstrated that SARS-CoV-2 binds to hemoglobin through ACE2, CD147, Cd26, and other receptors that are present on the surface of erythrocytes. After this association, virus attacks the beta1 chain of hemoglobin which leads to dysfunctional hemoglobin in addition to hemolysis, thereby reducing the oxygen supply to the body, causing tissue hypoxia, a remarkable characteristic of COVID-19 3,4 .…”