The war against the SARS-CoV2 infection: Is it better to fight or mitigate it?

Fabrizio Dal Moro; Igor Vendramin; Ugolino Livi

doi:10.1016/j.mehy.2020.110129

The war against the SARS-CoV2 infection: Is it better to fight or mitigate it?

Med Hypotheses. 2020 Oct:143:110129. doi: 10.1016/j.mehy.2020.110129. Epub 2020 Jul 22.

Authors

Fabrizio Dal Moro¹, Igor Vendramin², Ugolino Livi²

Affiliations

¹ Department of Urology, Department of Medical Area (DAME), University of Udine, Udine, Italy; Department of Surgery, Oncology and Gastroenterology - Urology, University of Padova, Padova, Italy. Electronic address: fabrizio.dalmoro@uniud.it.
² Cardiothoracic Department, Department of Medical Area (DAME), University of Udine, Udine, Italy.

Abstract

In trying to understand the biochemical mechanism involved in the recent pandemic COVID-19, there is currently growing interest in angiotensin-converting enzyme II (ACE2). Nevertheless, the attempts to counteract COVID-19 interference with this enzymatic cascade are frustrating, and the results have thus far been inconclusive. Let's start again by considering the involved factors in an alternative way: we could postulate that COVID-19 could be more aggressive/fatal due to a high level of "basal" inflammation with low Nitric Oxide (NO) levels in hypertensive, diabetic and obese patients. Interestingly, the "protective" effects of several factors (such as estrogens) may play a role by increasing the formation of endogenous NO. From a therapeutic point of view, phosphodiesterase type 5 inhibitors such as oral Tadalafil, could be used in order to increase the basal NO levels. In this way, we don't fight the virus, but we may be able to mitigate its effects.

Keywords: ACE2; COVID-19; Hypertension; Interleukins; Nitric oxide; Phosphodiesterase type 5 inhibitors; SARS-CoV2.

Publication types

Letter

MeSH terms

Angiotensin-Converting Enzyme 2
Animals
Betacoronavirus / drug effects
Betacoronavirus / physiology*
COVID-19
Coronavirus Infections / complications
Coronavirus Infections / drug therapy*
Cytokine Release Syndrome / etiology
Cytokine Release Syndrome / physiopathology
Estrogens / physiology
Humans
Hypertension / complications
Hypertension / physiopathology
Inflammation
Interleukins / physiology
Models, Animal
Models, Biological
Nitric Oxide / metabolism*
Nitric Oxide / therapeutic use
Obesity / complications
Obesity / physiopathology
Off-Label Use
Pandemics*
Peptidyl-Dipeptidase A / drug effects
Peptidyl-Dipeptidase A / physiology
Phosphodiesterase 5 Inhibitors / pharmacology
Phosphodiesterase 5 Inhibitors / therapeutic use
Pneumonia, Viral / complications
Pneumonia, Viral / drug therapy*
Receptors, Virus / drug effects
Receptors, Virus / physiology
SARS-CoV-2
Sildenafil Citrate / pharmacology
Sildenafil Citrate / therapeutic use
Tadalafil / pharmacology
Tadalafil / therapeutic use

Substances

Estrogens
Interleukins
Phosphodiesterase 5 Inhibitors
Receptors, Virus
Nitric Oxide
Tadalafil
Sildenafil Citrate
Peptidyl-Dipeptidase A
ACE2 protein, human
Angiotensin-Converting Enzyme 2