COVID-19

Covid-19, facts 

While we wait for the Covid-19 RNA vaccine, the medical treatment for the most severe viral stage: Acute Respiratory Distress Syndrome (ARDS), associated with high mortality rates in older adults or in people who have chronic diseases (diabetes, obesity, arterial hypertension) or immune deficiencies lacks guaranteed efficacy, which has to do with gaps regarding: I) Coronavirus and its raison d'être II) Postmortem pathological findings and body and lung-heart axis pathogenesis. III) Reasons of increasing transmissibility (R₀), of Covid-19 and, IV) Immunological characteristics of survivors and deceased due to ARDS.  Regarding the first, the biologist Laura Alche (Buenos Aires University, 2017) https://www.youtube.com/watch?v=VpaoEP-WaaM,  affirms that, when the viruses are installed  in the environment, they have not the ability to self-reproduce so, they are not alive. -If they are dead, why to carry out environmental disinfection campaigns? - For his part, the virologist Vincent Racaniello (Columbia University, 2019), https://www.youtube.com/watch?v=svlKm4S1M3Y&t=2411s, argues that when the viruses enter an organism and reproduce, using the host genome they acquire the status of living entities, through an evolutionary process, which will continue with mutations tending to settle the virus in our genomes, which currently carry 8% of transposons and others viral remains. When  benefits were mutual for viruses, animals and humans, they coexisted properly for millions of years, until  the beginning of the industrial age, when a  massive environmental disruption human-induced,  forced viruses that lived in peace with wild animals to invade human beds. For this reason, in this quarantine, many animals have temporarily recovered their properties in different parts of the world : https://www.youtube.com/watch?v=CN9-oF626Ok. Now that worldwide human viral pandemics are favored by high human population densities, we ask ourselves: What is special about lung alveoli to attract the virus and trigger poor alveolar function there? Is there a vital factor that encourages its massive replication? The reasonable thing is that viruses look for the energy contained in the porphyrins, O2 or perhaps the iron. We need to measure pyrroles and plasma iron in critically ill patients and perform autopsies or at least lung and heart biopsies from deceased patients. Although in this regard, there are 4 somewhat biased autopsies (African Americans, 2 with diabetes and high blood pressure), these matter for the exquisite nature of their performance: SE. Fox, A Akmatbekov, JL. Harbert et al. “ Pulmonary and Cardiac Pathology in Covid-19: The First Autopsy Series from New Orleans”- medRxiv preprint. https://doi.org/10.1101/2020.04.06.20050575,  being observed: Lungs:680 to  1030 g (N: 583 +/- 216), extreme right ventricular dilatation, bilateral pulmonary edema and parcel hemorrhages, pulmonary arteries free of thromboemboli, bronchi flooded by thick white mucus, absence of signs of fungal, bacterial or inflammatory infection, cardiomegaly, no thrombi in large vessels. Microscopy: extensive alveolar damage, hyaline membranes, alveolar hemorrhages, fibrin thrombi and megakaryocytes inside the capillaries. In damaged alveoli: cytopathic effects in distended pneumocytes, intracytoplasmic RNA, neutrophil degeneration, being argued   in medical journals that what was reported corresponds to overflows of a cytokine storm, taking as reference the pathogenesis of ARDS proposed by MA Matthay and RL Zeman (Annu Rev Pathol. 2011; 28; 6: 147–163). doi: 10.1146/annurev-pathol-011110-130158,  mostly referred to patients who died of pneumonia or infectious sepsis. The reflexive aspect of ARDS induced by the current coronavirus is that it settles in very quickly, as in the case of patients who, walking on the streets of Peru and Ecuador, stopped suddenly, shortly after being struck down and dying: https://www.youtube.com/watch?v=KH0f-cW0PNg, Interesting facts  in the treatment of coronavirus are  1) The worldwide use of  hydroxychloroquine (HCQ), a drug with a broad anti-inflammatory effect in Lupus Erythematosus  which   blocks the  endo and exocytosis stages (viral entry and exit from the cell). 2) A theory  held by Wenzhong Liu and Hualan Li (Sichuan University): Covid-19: Attacks the 1-Beta Chain of Hemoglobin and captures the Porphyrin to Inhibit Human Heme Metabolism, ChemRxiv. Preprint. https://doi.org/10.26434/chemrxiv.11938173.v7 which hypothesizes that the ORF8 protein and viral surface glycoproteins bind to porphyrin, while  structural viral proteins: orf1ab, ORF10 and ORF3a attack the heme in the region:  1-beta Hb, preventing the binding of He with porphyrin, promoting that  less Hb, transport  O2 and Co2, intoxicating lung cells and triggering an intense inflammatory storm causing pulmonary ground glass images with the possibility to reverse this effect with HCQ or; reports that BCG protects against TB and other viral and parasitic diseases. Biering-Sørensen S, Aaby P, Lund N, et al. Early BCG-Denmark and Neonatal Mortality Among Infants Weighing <2500 1183-1190.="" 1="" 2017="" 65="" a="" b="" clin="" controlled="" dis.="" g:="" infect="" oct="" randomized="" trial.=""> doi: 10.1093/cid/cix525.