Reply to Cimolai: Post-COVID syndrome and autoimmunity

Yeny Acosta-Ampudia; Juan Manuel Anaya

doi:10.1093/infdis/jiac106

Reply to Cimolai: Post-COVID syndrome and autoimmunity

Yeny Acosta-Ampudia, Juan Manuel Anaya

Producción científica: Contribución a una revista › Editorial › revisión exhaustiva

3 Citas (Scopus)

Resumen

Al editor-La correspondencia de Cimolai sugiere que la activación de células B policlonales inespecíficas podría ser responsable de la presencia de autoanticuerpos tras la infección por coronavirus 2 del síndrome respiratorio agudo grave (SARS-CoV-2). Las infecciones víricas inducen respuestas autoinmunes transitorias con títulos bajos de autoanticuerpos. Sin embargo, en múltiples infecciones se ha descrito la progresión de este estado inmunitario a una enfermedad autoinmune establecida con producción de autoanticuerpos específicos de órganos o tejidos [1].
Se ha demostrado que algunas infecciones víricas desencadenan autoinmunidad debido a mecanismos como la propagación de epítopos, la activación de transeúntes, el mimetismo molecular y los epítopos crípticos [1]. El SARS-CoV-2 comparte características de otros virus asociados con el desarrollo de autoinmunidad, entre las que se incluyen las siguientes:
Actividad superantígena. La proteína S del SARS-CoV-2 contiene motivos de secuencia y estructura similares a los de un superantígeno bacteriano y puede unirse directamente al receptor de células T. De hecho, los pacientes con COVID-19 grave muestran un sesgo del receptor de células T consistente con la activación del superantígeno [2].

Idioma original	Inglés estadounidense
Páginas (desde-hasta)	753-754
Número de páginas	2
Publicación	The Journal of infectious diseases
Volumen	226
N.º	4
DOI	https://doi.org/10.1093/infdis/jiac106
Estado	Publicada - sep. 4 2022

Áreas temáticas de ASJC Scopus

Inmulogía y alergología
Enfermedades infecciosas

ODS de las Naciones Unidas

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title = "Reply to Cimolai: Post-COVID syndrome and autoimmunity",

abstract = "To the Editor—The correspondence by Cimolai suggests that the activation of nonspecific polyclonal B cells could be responsible for the presence of autoantibodies after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Viral infections induce transient autoimmune responses with low titers of autoantibodies. However, progression of this immune state to an established autoimmune disease with production of organ- or tissue-specific autoantibodies has been described in multiple infections [1].Some viral infections have been shown to trigger autoimmunity due to mechanisms such as epitope spreading, bystander activation, molecular mimicry, and cryptic epitopes [1]. SARS-CoV-2 shares characteristics of other viruses associated with the development of autoimmunity; these include the following:Superantigen activity. The S protein of SARS-CoV-2 contains sequence and structure motifs similar to those of a bacterial superantigen and can bind directly to the T-cell receptor. Indeed, patients with severe COVID-19 exhibit a T-cell receptor skewing consistent with superantigen activation [2].Molecular mimicry. Accumulating evidence demonstrates that the virus has structural similarity to host-derived components. In addition, SARS-CoV-2 has the ability to induce hyperstimulation of the immune system, leading to the synthesis of multiple autoantibodies in patients with severe coronavirus disease 2019 (COVID-19) [3]. Latent autoimmunity has been described in post–COVID-19 syndrome (PCS) and correlates with humoral response to SARS-CoV-2 [4].",

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N2 - To the Editor—The correspondence by Cimolai suggests that the activation of nonspecific polyclonal B cells could be responsible for the presence of autoantibodies after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Viral infections induce transient autoimmune responses with low titers of autoantibodies. However, progression of this immune state to an established autoimmune disease with production of organ- or tissue-specific autoantibodies has been described in multiple infections [1].Some viral infections have been shown to trigger autoimmunity due to mechanisms such as epitope spreading, bystander activation, molecular mimicry, and cryptic epitopes [1]. SARS-CoV-2 shares characteristics of other viruses associated with the development of autoimmunity; these include the following:Superantigen activity. The S protein of SARS-CoV-2 contains sequence and structure motifs similar to those of a bacterial superantigen and can bind directly to the T-cell receptor. Indeed, patients with severe COVID-19 exhibit a T-cell receptor skewing consistent with superantigen activation [2].Molecular mimicry. Accumulating evidence demonstrates that the virus has structural similarity to host-derived components. In addition, SARS-CoV-2 has the ability to induce hyperstimulation of the immune system, leading to the synthesis of multiple autoantibodies in patients with severe coronavirus disease 2019 (COVID-19) [3]. Latent autoimmunity has been described in post–COVID-19 syndrome (PCS) and correlates with humoral response to SARS-CoV-2 [4].

AB - To the Editor—The correspondence by Cimolai suggests that the activation of nonspecific polyclonal B cells could be responsible for the presence of autoantibodies after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Viral infections induce transient autoimmune responses with low titers of autoantibodies. However, progression of this immune state to an established autoimmune disease with production of organ- or tissue-specific autoantibodies has been described in multiple infections [1].Some viral infections have been shown to trigger autoimmunity due to mechanisms such as epitope spreading, bystander activation, molecular mimicry, and cryptic epitopes [1]. SARS-CoV-2 shares characteristics of other viruses associated with the development of autoimmunity; these include the following:Superantigen activity. The S protein of SARS-CoV-2 contains sequence and structure motifs similar to those of a bacterial superantigen and can bind directly to the T-cell receptor. Indeed, patients with severe COVID-19 exhibit a T-cell receptor skewing consistent with superantigen activation [2].Molecular mimicry. Accumulating evidence demonstrates that the virus has structural similarity to host-derived components. In addition, SARS-CoV-2 has the ability to induce hyperstimulation of the immune system, leading to the synthesis of multiple autoantibodies in patients with severe coronavirus disease 2019 (COVID-19) [3]. Latent autoimmunity has been described in post–COVID-19 syndrome (PCS) and correlates with humoral response to SARS-CoV-2 [4].

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