Rachel Parise, S. Ramesh, Jun Ren, Manoj Govindarajulu, Rishi M. Nadar, Suhrud Pathak, Timothy Moore, M. Dhanasekaran
{"title":"A scientific perspective of how and why Omicron is less severe than SARS-CoV-2","authors":"Rachel Parise, S. Ramesh, Jun Ren, Manoj Govindarajulu, Rishi M. Nadar, Suhrud Pathak, Timothy Moore, M. Dhanasekaran","doi":"10.1097/EC9.0000000000000092","DOIUrl":null,"url":null,"abstract":"Abstract Omicron is currently the dominant variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus responsible for the coronavirus disease 2019 (COVID-19) pandemic. Omicron is associated with mild symptoms, although it can cause harmful effects in high-risk patient populations. Omicron and COVID-19 affect multiple organ systems, including the respiratory system, gastrointestinal tract, cardiovascular system, central nervous system, ophthalmic system, genitourinary tract, and musculoskeletal system. COVID-19 infects additional organ systems, including the hematological system, hepatobiliary system, renal system, and dermatologic system. The viral-induced complications were compared to discuss the effects of Omicron versus the authentic SARS-CoV-2 virus, revealing less detrimental outcomes for Omicron. Moreover, COVID-19 is more likely to infect older adults, males, and obesity with mild to severe symptoms. Omicron causes mild symptoms in younger populations and overweight females. Data were acquired using PubMed, Centers for Disease Prevention and Control, and the World Health Organization. COVID-19 and Omicron mechanisms causing organ system-related complications are likely because of the natural immune response to the active infection, the uncontrollable release of cytokines causing cytokine release syndrome, and direct viral damage through angiotensin-converting enzyme 2/transmembrane serine protease 2 receptor binding and entrance to the host cell for infection.","PeriodicalId":72895,"journal":{"name":"Emergency and critical care medicine","volume":"3 1","pages":"115 - 121"},"PeriodicalIF":0.0000,"publicationDate":"2023-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Emergency and critical care medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/EC9.0000000000000092","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Abstract Omicron is currently the dominant variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus responsible for the coronavirus disease 2019 (COVID-19) pandemic. Omicron is associated with mild symptoms, although it can cause harmful effects in high-risk patient populations. Omicron and COVID-19 affect multiple organ systems, including the respiratory system, gastrointestinal tract, cardiovascular system, central nervous system, ophthalmic system, genitourinary tract, and musculoskeletal system. COVID-19 infects additional organ systems, including the hematological system, hepatobiliary system, renal system, and dermatologic system. The viral-induced complications were compared to discuss the effects of Omicron versus the authentic SARS-CoV-2 virus, revealing less detrimental outcomes for Omicron. Moreover, COVID-19 is more likely to infect older adults, males, and obesity with mild to severe symptoms. Omicron causes mild symptoms in younger populations and overweight females. Data were acquired using PubMed, Centers for Disease Prevention and Control, and the World Health Organization. COVID-19 and Omicron mechanisms causing organ system-related complications are likely because of the natural immune response to the active infection, the uncontrollable release of cytokines causing cytokine release syndrome, and direct viral damage through angiotensin-converting enzyme 2/transmembrane serine protease 2 receptor binding and entrance to the host cell for infection.