Kishor R Danao, Vijayshri V Rokde, Ujwala N Mahajan
{"title":"The Severity of COVID-19 in Systemic Lupus Erythematosus Patient.","authors":"Kishor R Danao, Vijayshri V Rokde, Ujwala N Mahajan","doi":"10.2174/0118715265326851241115072224","DOIUrl":null,"url":null,"abstract":"<p><p>As of early October 2020, the COVID-19 pandemic, caused by the novel coronavirus SARS-CoV-2, resulted in approximately 35 million cases and one million fatalities worldwide. Systemic lupus erythematosus (SLE) is an autoimmune disease marked by the generation of pathogenic autoantibodies and a lack of tolerance to nuclear self-antigens. Hypocomple-mentemia, or an abnormal blood complement deficit, is a reliable predictor of infection in SLE patients. Moreover, it has been found that immunoglobulin (Ig), particularly IgG and IgM, is lowered in SLE patients, which may be a factor in their heightened susceptibility to infection. Bloodstream autoantibodies, lymphopenia, aberrant T cells, proinflammatory cytokines, and impaired regulatory systems all lead to an immune response that is aberrant in lupus patients. SLE patients exhibit impaired CD8 T cell responses, including abnormal phagocytosis and chemotaxis. Recent study has shown that COVID-19 infections significantly boost type I inter-feron responses. Patients with SLE and Covid-19 infection typically get immune-suppressing drugs viz corticosteroids, Janus kinase inhibitors (JAK), and tocilizumab, which improve their immune systems and diminution susceptible to Covid-19 infections.</p>","PeriodicalId":101326,"journal":{"name":"Infectious disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infectious disorders drug targets","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/0118715265326851241115072224","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
As of early October 2020, the COVID-19 pandemic, caused by the novel coronavirus SARS-CoV-2, resulted in approximately 35 million cases and one million fatalities worldwide. Systemic lupus erythematosus (SLE) is an autoimmune disease marked by the generation of pathogenic autoantibodies and a lack of tolerance to nuclear self-antigens. Hypocomple-mentemia, or an abnormal blood complement deficit, is a reliable predictor of infection in SLE patients. Moreover, it has been found that immunoglobulin (Ig), particularly IgG and IgM, is lowered in SLE patients, which may be a factor in their heightened susceptibility to infection. Bloodstream autoantibodies, lymphopenia, aberrant T cells, proinflammatory cytokines, and impaired regulatory systems all lead to an immune response that is aberrant in lupus patients. SLE patients exhibit impaired CD8 T cell responses, including abnormal phagocytosis and chemotaxis. Recent study has shown that COVID-19 infections significantly boost type I inter-feron responses. Patients with SLE and Covid-19 infection typically get immune-suppressing drugs viz corticosteroids, Janus kinase inhibitors (JAK), and tocilizumab, which improve their immune systems and diminution susceptible to Covid-19 infections.