The COVID-19 pandemic: a global health crisis
| Autor: | Michael P. Morran, Andrea L. Nestor-Kalinoski, Casey Pollard |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male ARDS Physiology Disease Comorbidity 030204 cardiovascular system & hematology medicine.disease_cause Global Health 0302 clinical medicine Pulmonary fibrosis genetics Child Coronavirus Aged 80 and over education.field_of_study Respiratory Distress Syndrome Transmission (medicine) Vaccination Mini-Review Middle Aged Cardiovascular Diseases Child Preschool Female Adult Adolescent Population Biology Antiviral Agents Sepsis 03 medical and health sciences Young Adult medicine Humans Genetic Predisposition to Disease education COVID-19 Serotherapy Aged GTPases pulmonary fibrosis SARS-CoV-2 Immunization Passive Infant Newborn COVID-19 Infant Viral Vaccines medicine.disease United States COVID-19 Drug Treatment 030104 developmental biology Immunology Cytokine storm |
| Zdroj: | Physiological Genomics |
| ISSN: | 1531-2267 1094-8341 |
| Popis: | The novel coronavirus SARS-CoV-2 was identified as the causative agent for a series of atypical respiratory diseases in the Hubei Province of Wuhan, China in December of 2019. The disease SARS-CoV-2, termed COVID-19, was officially declared a pandemic by the World Health Organization on March 11, 2020. SARS-CoV-2 contains a single-stranded, positive-sense RNA genome surrounded by an extracellular membrane containing a series of spike glycoproteins resembling a crown. COVID-19 infection results in diverse symptoms and morbidity depending on individual genetics, ethnicity, age, and geographic location. In severe cases, COVID-19 pathophysiology includes destruction of lung epithelial cells, thrombosis, hypercoagulation, and vascular leak leading to sepsis. These events lead to acute respiratory distress syndrome (ARDS) and subsequent pulmonary fibrosis in patients. COVID-19 risk factors include cardiovascular disease, hypertension, and diabetes, which are highly prevalent in the United States. This population has upregulation of the angiotensin converting enzyme-2 (ACE2) receptor, which is exploited by COVID-19 as the route of entry and infection. Viral envelope proteins bind to and degrade ACE2 receptors, thus preventing normal ACE2 function. COVID-19 infection causes imbalances in ACE2 and induces an inflammatory immune response, known as a cytokine storm, both of which amplify comorbidities within the host. Herein, we discuss the genetics, pathogenesis, and possible therapeutics of COVID-19 infection along with secondary complications associated with disease progression, including ARDS and pulmonary fibrosis. Understanding the mechanisms of COVID-19 infection will allow the development of vaccines or other novel therapeutic approaches to prevent transmission or reduce the severity of infection. |
| Databáze: | OpenAIRE |
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