tetano
Editor, Senior Moderator
J Transl Autoimmun
. 2022;5:100154.
doi: 10.1016/j.jtauto.2022.100154. Epub 2022 Apr 12.
SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
Regina Larionova[SUP] 1 2 [/SUP], K Byvaltsev[SUP] 3 [/SUP], Оlga Kravtsova[SUP] 2 [/SUP], Elena Takha[SUP] 1 [/SUP], Sergei Petrov[SUP] 1 4 [/SUP], Gevorg Kazarian[SUP] 1 [/SUP], Anna Valeeva[SUP] 1 [/SUP], Eduard Shuralev[SUP] 1 4 5 [/SUP], Malik Mukminov[SUP] 1 4 [/SUP], Yves Renaudineau[SUP] 1 6 [/SUP], Marina Arleevskaya[SUP] 1 2 [/SUP]
Affiliations
Abstract
The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN-I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development.
Keywords: ACE2, angiotensin converting enzyme 2; ACPA, anti-cyclic citrullinated peptide autoAb; ANA, antinuclear autoAb; AutoAb, autoantibodies; BAFF/BlySS, B-cell-activating factor/B lymphocyte stimulator; CCL, chemokine ligand; COVID-19, coronavirus disease 2019; DMARDs, disease-modifying anti-rheumatic drugs; E, envelope; HEp-2, human epithelioma cell line 2; IFN-I, interferon type I; IFNAR, IFN-alpha receptors; IL, interleukin; IRF, interferon regulatory factor; ISGs, IFN-stimulated genes; ITP, immune-thrombocytopenic purpura; Ig, immunoglobulin; Infection; Inflammation; Jak, Janus kinase; LDH, lactate dehydrogenase; M, membrane; MDA-5, melanoma differentiation-associated protein; MERS-Cov, Middle East respiratory syndrome coronavirus; MIS-C, multisystem inflammatory syndrome in children; N, nucleocapsid; NET, nuclear extracellular traps; NF-κB, nuclear factor-kappa B; NK, natural killer; NLRP3, NOD-like receptor family; Rheumatoid arthritis; Risk factors; SARS-Cov2; Systemic lupus erythematosus; T cell receptor, TLR; Toll-like receptor, TMPRSS2; aPL, antiphospholipid; mAb, monoclonal Ab; open reading frame, PACS; pathogen-associated molecular patterns, pDC; pattern recognition receptors, RA; peptidylarginine deiminase 4, PAMPs; plasmacytoid dendritic cells, PMN; polymorphonuclear leukocytes, PRRs; post-active COVID-19 syndrome, PAD-4; primary Sjögren's syndrome, SLE; pyrin domain containing 3, ORF; reactive oxygen species, rt-PCR; receptor binding domain, RF; regulatory T cells, VDJ; retinoic acid-inducible gene I, ROS; reverse transcription polymerase chain reaction, S; rheumatoid arthritis, RBD; rheumatoid factor, RIG-I; severe acute respiratory coronavirus 2, SjS; signal transducer and activator of transcription, TCR; single-stranded ribonucleic acid, STAT; spike, SAD; systemic autoimmune disease, SARS-Cov2; systemic lupus erythematosus, SSc; systemic sclerosis, ssRNA; transmembrane serine protease 2, TNF; tumor necrosis factor, Treg; variable, diversity and joining Ig genes.
. 2022;5:100154.
doi: 10.1016/j.jtauto.2022.100154. Epub 2022 Apr 12.
SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases
Regina Larionova[SUP] 1 2 [/SUP], K Byvaltsev[SUP] 3 [/SUP], Оlga Kravtsova[SUP] 2 [/SUP], Elena Takha[SUP] 1 [/SUP], Sergei Petrov[SUP] 1 4 [/SUP], Gevorg Kazarian[SUP] 1 [/SUP], Anna Valeeva[SUP] 1 [/SUP], Eduard Shuralev[SUP] 1 4 5 [/SUP], Malik Mukminov[SUP] 1 4 [/SUP], Yves Renaudineau[SUP] 1 6 [/SUP], Marina Arleevskaya[SUP] 1 2 [/SUP]
Affiliations
- PMID: 35434592
- PMCID: PMC9005220
- DOI: 10.1016/j.jtauto.2022.100154
Abstract
The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN-I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development.
Keywords: ACE2, angiotensin converting enzyme 2; ACPA, anti-cyclic citrullinated peptide autoAb; ANA, antinuclear autoAb; AutoAb, autoantibodies; BAFF/BlySS, B-cell-activating factor/B lymphocyte stimulator; CCL, chemokine ligand; COVID-19, coronavirus disease 2019; DMARDs, disease-modifying anti-rheumatic drugs; E, envelope; HEp-2, human epithelioma cell line 2; IFN-I, interferon type I; IFNAR, IFN-alpha receptors; IL, interleukin; IRF, interferon regulatory factor; ISGs, IFN-stimulated genes; ITP, immune-thrombocytopenic purpura; Ig, immunoglobulin; Infection; Inflammation; Jak, Janus kinase; LDH, lactate dehydrogenase; M, membrane; MDA-5, melanoma differentiation-associated protein; MERS-Cov, Middle East respiratory syndrome coronavirus; MIS-C, multisystem inflammatory syndrome in children; N, nucleocapsid; NET, nuclear extracellular traps; NF-κB, nuclear factor-kappa B; NK, natural killer; NLRP3, NOD-like receptor family; Rheumatoid arthritis; Risk factors; SARS-Cov2; Systemic lupus erythematosus; T cell receptor, TLR; Toll-like receptor, TMPRSS2; aPL, antiphospholipid; mAb, monoclonal Ab; open reading frame, PACS; pathogen-associated molecular patterns, pDC; pattern recognition receptors, RA; peptidylarginine deiminase 4, PAMPs; plasmacytoid dendritic cells, PMN; polymorphonuclear leukocytes, PRRs; post-active COVID-19 syndrome, PAD-4; primary Sjögren's syndrome, SLE; pyrin domain containing 3, ORF; reactive oxygen species, rt-PCR; receptor binding domain, RF; regulatory T cells, VDJ; retinoic acid-inducible gene I, ROS; reverse transcription polymerase chain reaction, S; rheumatoid arthritis, RBD; rheumatoid factor, RIG-I; severe acute respiratory coronavirus 2, SjS; signal transducer and activator of transcription, TCR; single-stranded ribonucleic acid, STAT; spike, SAD; systemic autoimmune disease, SARS-Cov2; systemic lupus erythematosus, SSc; systemic sclerosis, ssRNA; transmembrane serine protease 2, TNF; tumor necrosis factor, Treg; variable, diversity and joining Ig genes.
