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Cytokine Growth Factor Rev ; 58: 82-91, 2021 04.
Article in English | MEDLINE | ID: covidwho-1081152


SARS-COV-2 infection represents the greatest pandemic of the world, counting daily increasing number of subjects positive to the virus and, sadly, increasing number of deaths. Current studies reported that the cytokine/chemokine network is crucial in the onset and maintenance of the "cytokine storm", the event occurring in those patients in whom the progression of COVID-19 will progress, in most cases, to a very severe and potentially threatening disease. Detecting a possible "immune signature" in patients, as assessed by chemokines status in patients with COVID-19, could be helpful for individual risk stratification for developing a more or less severe clinical course of the disease. The present review is specifically aimed at overviewing current evidences provided by in vitro and in vivo studies addressing the issue of which chemokines seems to be involved, at least at present, in COVID-19. Currently available experimental and clinical studies regarding those chemokines more deeply studied in COVID-19, with a specific focus on their role in the cytokine storm and ultimately with their ability to predict the clinical course of the disease, will be taken into account. Moreover, similarities and differences between chemokines and cytokines, which both contribute to the onset of the pro-inflammatory loop characterizing SARS-COV-2 infection, will be briefly discussed. Future studies will rapidly accumulate in the next months and their results will hopefully provide more insights as to the complex physiopathology of COVID-19-related cytokine storm. This will likely make the present review somehow "dated" in a short time, but still the present review provides an overview of the scenario of the current knowledge on this topic.

COVID-19/complications , COVID-19/immunology , Chemokines/physiology , Cytokine Release Syndrome/etiology , SARS-CoV-2/pathogenicity , Chemokines/metabolism , Cytokine Release Syndrome/immunology , Cytokines/metabolism , Cytokines/physiology , Humans , SARS-CoV-2/immunology
Med Hypotheses ; 143: 110125, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-665482


The novel coronavirus (SARS-CoV-2) is primarily a respiratory pathogen and its clinical manifestations are dominated by respiratory symptoms, the most severe of which is acute respiratory distress syndrome (ARDS). However, COVID-19 is increasingly recognized to cause an overwhelming inflammatory response and cytokine storm leading to end organ damage. End organ damage to heart is one of the most severe complications of COVID-19 that increases the risk of death. We proposed a two-fold mechanism responsible for causing acute coronary events in patients with COVID-19 infection: Cytokine storm leading to rapid onset formation of new coronary plaques along with destabilization of pre-existing plaques and direct myocardial injury secondary to acute systemic viral infection. A well-coordinated immune response is the first line innate immunity against a viral infection. However, an uncoordinated response and hypersecretion of cytokines and chemokines lead to immune related damage to the human body. Human Coronavirus (HCoV) infection causes infiltration of inflammatory cells that cause excessive production of cytokines, proteases, coagulation factors, oxygen radicals and vasoactive molecules causing endothelial damage, disruption of fibrous cap and initiation of formation of thrombus. Systemic viral infections also cause vasoconstriction leading to narrowing of vascular lumen and stimulation of platelet activation via shear stress. The resultant cytokine storm causes secretion of hypercoagulable tissue factor without consequential increase in counter-regulatory pathways such as AT-III, activated protein C and plasminogen activator type 1. Lastly, influx of CD4+ T-cells in cardiac vasculature results in an increased production of cytokines that stimulate smooth muscle cells to migrate into the intima and generate collagen and other fibrous products leading to advancement of fatty streaks to advanced atherosclerotic lesions. Direct myocardial damage and cytokine storm leading to destabilization of pre-existing plaques and accelerated formation of new plaques are the two instigating mechanisms for acute coronary syndromes in COVID-19.

Acute Coronary Syndrome/etiology , Betacoronavirus , Coronavirus Infections/complications , Models, Cardiovascular , Pandemics , Pneumonia, Viral/complications , Acute Coronary Syndrome/physiopathology , CD4-Positive T-Lymphocytes/immunology , COVID-19 , Chemokines/physiology , Coronary Artery Disease/etiology , Coronary Artery Disease/physiopathology , Coronary Vessels/metabolism , Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Cytokines/physiology , Humans , Immunity, Innate , Plaque, Atherosclerotic/etiology , Plaque, Atherosclerotic/physiopathology , Platelet Activation , Pneumonia, Viral/immunology , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Vasoconstriction , Virus Diseases/complications , Virus Diseases/immunology