A rational approach to COVID-19
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OPINION ARTICLE
Open Access
A rational approach to COVID-19 Ruty Mehrian-Shai
Abstract It is crucial to use the wealth of information emerging from the ongoing SARS-CoV-2 pandemic and confront COVID-19 with a rational approach. There are proactive steps to prevent and fight COVID-19. Management of the disease should be according to clinical features and laboratory test markers and personalized therapeutic targets.
Background Not applicable Main text In search for a rational approach to COVID-19, one should take into account the following 4 considerations: I. Risk factors, II. Clinical features III, Genomic and Stage markers, and IV. Treatment according to stage. Risk factors
People without comorbidities should know that even healthy young people with coronavirus infection may succumb to acute respiratory distress syndrome because of the following risk factors: smoking, stress and depression, low physical activity, and high consumption of saturated fats, sugars, and refined carbohydrates [1]. In addition, underlying medical conditions in any age increase the risk for severe COVID-19 illness. According to the Centers for Disease Control and Prevention, the underlying medical conditions include cancer, chronic kidney disease, chronic obstructive pulmonary disease, heart conditions, immunocompromised state, type 2 diabetes mellitus, obesity (BMI ≥ 30 kg/m2), pregnancy, and sickle cell disease. Clinical features
Compared to non-severe pneumonia patients, the median age of severe patients is significantly older, and they are more likely to have chronic comorbidities [2]. Most Correspondence: [email protected] Department of Pediatric Hemato-Oncology, Sheba Medical Center, Ramat Gan, Israel
common symptoms in severe patients are associated with, prolonged viral carriage in COVID-19. The symptoms are high fever, anorexia and dyspnea [3], taste and smell loss [4], and diarrhea [5]. Genomics
Personalized medicine will be enhanced by the integration of advances in human genomics into host big data of genetic determinants of susceptibility and the highly variable clinical manifestations. The host genome influences both innate and adaptive immunity. For example, a genome-wide association study for COVID-19 with respiratory failure detected a susceptibility locus at a chromosome 3p21.31 gene cluster and a potential involvement of the ABO blood-group system in COVID19 [6]. In this cluster, SLC6A20 encodes the sodium– amino acid (proline) transporter 1 (SIT1) which functionally interacts with angiotensin-converting enzyme 2, the SARS-CoV-2 cell-surface receptor [7]. Interestingly, proinflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha stimulate the activity of amino acid transporter system A [8]. C-XC motif chemokine receptor 6 (CXCR6) regulates the location of lung-resident memory CD8 T cells [9]. CCR1 deficiency increases susceptibility to fatal coronavirus infection [10]. Associations of genes with severe disease were reported for apolipoprotein E, Toll-like receptor 7, and IL-1 si
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