RESUMO
SARS-CoV-2, a virus belonging to the large family of coronavirus, aroused great interest following the outbreak of this new strain reported in 2019, in Wuhan China. Its clinical spectrum is highly variable, ranging from a self-limited disease to an acute respiratory distress syndrome with systemic clinical manifestations (COVID-19), in which the immune system plays a key role in the pathophysiology of this disease and in its severity; several studies show the prevalence of some autoimmune markers suggesting that they may lead to autoimmune states. The most important strategy worldwide to protect the population was the development of vaccines to induce immunity to severe COVID-19; however, vaccines have also been shown to have the ability to produce autoimmune states in a small percentage of the world's population; nevertheless, the best strategy remains vaccination. The aim of this review is to show the current overview of the mechanisms of SARS-CoV-2-induced autoimmunity and post-vaccination for a better understanding and identification of these in the population. Publications from 2019 to 2022 were reviewed in PubMed as the primary search source.
El SARS-CoV-2, un virus perteneciente a la gran familia de los coronavirus despertó gran interés después del brote de la nueva cepa reportada en 2019, en Wuhan, China. Las manifestaciones clínicas son variables: desde enfermedad con curación espontánea hasta síndrome de dificultad respiratoria aguda, con alteraciones clínicas sistémicas (COVID-19), donde el sistema inmunitario tiene participación importante en la fi-siopatología de la enfermedad y su gravedad. Diversos estudios demuestran la prevalencia de algunos marcadores autoinmunes, lo que sugiere que pueden conducir a estados de autoinmunidad. La estrategia más importante a nivel mundial para proteger a la población fue el desarrollo de vacunas para inducir inmunidad frente al COVID-19 grave; sin embargo, se ha demostrado que tienen la capacidad de producir estados autoinmunitarios en un pequeño porcentaje de la población; no obstante, siguen siendo la mejor estrategia de tratamiento. El objetivo de esta revisión es mostrar el panorama actual de los mecanismos de autoinmunidad inducidos por SARS-CoV-2 y la post-vacunación, para una mejor comprensión e identificación en la población. Se revisaron las publicaciones de 2019 a 2022 en PubMed como fuente principal de búsqueda.
Assuntos
Doenças Autoimunes , COVID-19 , Humanos , SARS-CoV-2 , COVID-19/prevenção & controle , Autoimunidade , Doenças Autoimunes/etiologia , VacinaçãoRESUMO
BACKGROUND: Ankylosing spondylitis (AS) is an autoimmune disease that affects the enthesis and synovial membrane of the spine, the sacroiliac vertebrae and peripheral joints. Genetic susceptibility to AS is mainly due to the presence of the HLA-B*27 (B27) allele, and endoplasmic reticulum aminopeptidase-1 (ERAP-1) plays a key role in antigen processing and presentation to HLA class I molecules. Tobacco consumption is one of the main environmental factors involved in the pathogenesis of various diseases, including AS. The objective of the present study was to evaluate the association and the interactive effects of variants of the ERAP1 gene with smoking in modulating the risk of AS. METHODS AND RESULTS: A case-control study in the Mexican population. The association of two functional variants of the ERAP1 gene (rs30187 and rs27044) in patients with AS was analyzed by the allelic discrimination method using TaqMan probes. B27 was typified by PCR-SSP. The interaction between the variants of ERAP1 and B27 and smoking was assessed using the multifactorial dimensionality reduction (MDR) method. There was no significant association of the two variants of ERAP1 in the cases compared with the controls (P > 0.05); however, a strong interaction between the variants and smoking could be demonstrated, with entropy values of 4.97% for rs30187 and 5.13% for rs27044. In addition, these interaction effects were increased in patients carrying the B27 allele. CONCLUSIONS: The rs30187 and rs27044 variants of the ERAP1 gene appear to potentiate the effect of smoking in patients with AS carrying the B27 allele.