Resumen 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 fisiopatología 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.

Abstract 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.

Abstract Osteoarthritis (OA) is a complex disease with a multifactorial etiology. The genetic component is one of the main associated factors, resulting from interactions between genes and environmental factors. The aim of this study was to identify gene-gene interactions (epistasis) of the articular cartilage extracellular matrix (ECM) in knee OA. Ninety-two knee OA patients and 147 healthy individuals were included. Participants were genotyped in order to evaluate nine variants of eight genes associated with ECM metabolism using the OpenArray technology. Epistasis was analyzed using the multifactor dimensionality reduction (MDR) method. The MDR analysis showed significant gene-gene interactions between MMP3 (rs679620) and COL3A1 (rs1800255), and between COL3A1 (rs1800255) and VEGFA (rs699947) polymorphisms, with information gain values of 3.21% and 2.34%, respectively. Furthermore, in our study we found interactions in high-risk genotypes of the HIF1AN, MMP3 and COL3A1 genes; the most representative were [AA+CC+GA], [AA+CT+GA] and [AA+CT+GG], respectively; and low-risk genotypes [AA+CC+GG], [GG+TT+GA] and [AA+TT+GA], respectively. Knowing the interactions of these polymorphisms involved in articular cartilage ECM metabolism could provide a new tool to identify individuals at high risk of developing knee OA.