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1.
Rev Med Virol ; 31(6): e2221, 2021 11.
Article in English | MEDLINE | ID: covidwho-1575100

ABSTRACT

The current pandemic caused by SARS-CoV-2 virus infection is known as Covid-19 (coronavirus disease 2019). This disease can be asymptomatic or can affect multiple organ systems. Damage induced by the virus is related to dysfunctional activity of the immune system, but the activity of molecules such as C-reactive protein (CRP) as a factor capable of inducing an inflammatory status that may be involved in the severe evolution of the disease, has not been extensively evaluated. A systematic review was performed using the NCBI-PubMed database to find articles related to Covid-19 immunity, inflammatory response, and CRP published from December 2019 to December 2020. High levels of CRP were found in patients with severe evolution of Covid-19 in which several organ systems were affected and in patients who died. CRP activates complement, induces the production of pro-inflammatory cytokines and induces apoptosis which, together with the inflammatory status during the disease, can lead to a severe outcome. Several drugs can decrease the level or block the effect of CRP and might be useful in the treatment of Covid-19. From this review it is reasonable to conclude that CRP is a factor that can contribute to severe evolution of Covid-19 and that the use of drugs able to lower CRP levels or block its activity should be evaluated in randomized controlled clinical trials.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , C-Reactive Protein/antagonists & inhibitors , COVID-19/drug therapy , Complement System Proteins/immunology , Cytokine Release Syndrome/drug therapy , SARS-CoV-2/pathogenicity , ADAM17 Protein/antagonists & inhibitors , ADAM17 Protein/genetics , ADAM17 Protein/immunology , Angiotensin-Converting Enzyme 2/antagonists & inhibitors , Angiotensin-Converting Enzyme 2/genetics , Angiotensin-Converting Enzyme 2/immunology , Biomarkers/blood , C-Reactive Protein/genetics , C-Reactive Protein/immunology , COVID-19/immunology , COVID-19/pathology , COVID-19/virology , Celecoxib/therapeutic use , Complement System Proteins/genetics , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/pathology , Cytokine Release Syndrome/virology , Cytokines/antagonists & inhibitors , Cytokines/genetics , Cytokines/immunology , Disease Progression , Doxycycline/therapeutic use , Gene Expression Regulation , Humans , Randomized Controlled Trials as Topic , Severity of Illness Index , Survival Analysis
2.
Adv Biol Regul ; 81: 100820, 2021 08.
Article in English | MEDLINE | ID: covidwho-1351735

ABSTRACT

The article describes the possible pathophysiological origin of COVID-19 and the crucial role of renin-angiotensin system (RAS), providing several "converging" evidence in support of this hypothesis. SARS-CoV-2 has been shown to initially upregulate ACE2 systemic activity (early phase), which can subsequently induce compensatory responses leading to upregulation of both arms of the RAS (late phase) and consequently to critical, advanced and untreatable stages of COVID-19 disease. The main and initial actors of the process are ACE2 and ADAM17 zinc-metalloproteases, which, initially triggered by SARS-CoV-2 spike proteins, work together in increasing circulating Ang 1-7 and Ang 1-9 peptides and downstream (Mas and Angiotensin type 2 receptors) pathways with anti-inflammatory, hypotensive and antithrombotic activities. During the late phase of severe COVID-19, compensatory secretion of renin and ACE enzymes are subsequently upregulated, leading to inflammation, hypertension and thrombosis, which further sustain ACE2 and ADAM17 upregulation. Based on this hypothesis, COVID-19-phase-specific inhibition of different RAS enzymes is proposed as a pharmacological strategy against COVID-19 and vaccine-induced adverse effects. The aim is to prevent the establishment of positive feedback-loops, which can sustain hyperactivity of both arms of the RAS independently of viral trigger and, in some cases, may lead to Long-COVID syndrome.


Subject(s)
ADAM17 Protein/biosynthesis , Angiotensin-Converting Enzyme 2/biosynthesis , COVID-19/metabolism , Renin-Angiotensin System , SARS-CoV-2/metabolism , Spike Glycoprotein, Coronavirus/metabolism , ADAM17 Protein/antagonists & inhibitors , Angiotensin I/metabolism , Angiotensin-Converting Enzyme 2/antagonists & inhibitors , COVID-19/drug therapy , Gene Expression Regulation, Enzymologic , Humans , Peptide Fragments/metabolism , Spike Glycoprotein, Coronavirus/antagonists & inhibitors , Up-Regulation
3.
Basic Res Cardiol ; 115(3): 31, 2020 04 09.
Article in English | MEDLINE | ID: covidwho-46686

ABSTRACT

From January 2020, coronavirus disease (COVID-19) originated in China has spread around the world. The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The presence of myocarditis, cardiac arrest, and acute heart failure in COVID-19 patients suggests the existence of a relationship between SARS-CoV-2 infection and cardiac disease. The Notch signalling is a major regulator of cardiovascular function and it is also implicated in several biological processes mediating viral infections. In this report we discuss the possibility to target Notch signalling to prevent SARS-CoV-2 infection and interfere with the progression of COVID-19- associated heart and lungs disease.


Subject(s)
Betacoronavirus/pathogenicity , Coronavirus Infections/drug therapy , Coronavirus Infections/physiopathology , Heart Diseases/drug therapy , Heart Diseases/etiology , Lung Diseases/drug therapy , Lung Diseases/etiology , Pneumonia, Viral/drug therapy , Pneumonia, Viral/physiopathology , Receptors, Notch/antagonists & inhibitors , ADAM17 Protein/antagonists & inhibitors , Angiotensin-Converting Enzyme 2 , Betacoronavirus/drug effects , COVID-19 , China , Coronavirus Infections/pathology , Coronavirus Infections/virology , Disease Progression , Furin/metabolism , Heart Arrest/etiology , Heart Arrest/pathology , Heart Diseases/pathology , Heart Diseases/physiopathology , Heart Failure/etiology , Heart Failure/pathology , Humans , Interleukin-6/immunology , Lung Diseases/pathology , Lung Diseases/physiopathology , Myocarditis/etiology , Myocarditis/pathology , Pandemics , Peptidyl-Dipeptidase A/deficiency , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/pathology , Pneumonia, Viral/virology , Receptors, Notch/metabolism , SARS-CoV-2 , Signal Transduction/drug effects
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