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Erratum to: Infectious Aspects and the Etiopathogenesis of Rheumatoid Arthritis

Authors:
Michal Kasher Meron at Meir Medical Center
Michal Kasher Meron
Howard Amital at Sheba Medical Center
Howard Amital
Daniel Shepshelovich at Tel Aviv University
Daniel Shepshelovich
Ori Barzilai at Memorial Sloan Kettering Cancer Center
Ori Barzilai
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Abstract

Infections are believed to contribute to the maturation of the immune system from the innate to the adaptive phases and therefore may take part in the induction of autoimmune conditions. In the current study, we present an extensive analysis conducted on sera samples of patients with rheumatoid arthritis in order to seek evidence of previous or coexisting infectious processes using the Bio-Rad BioPlex immunoassay analyzer. We detected higher rates of serological evidence of infections with Epstein-Barr virus and cytomegalovirus viruses. Our findings may indicate a role of these viruses in the pathogenesis of RA.
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ERRATUM
Erratum to: Infectious Aspects and the Etiopathogenesis
of Rheumatoid Arthritis
Michal Kasher Meron &Howard Amital &Daniel Shepshelovich &Ori Barzilai &
Maya Ram &Juan-Manuel Anaya &Roberto Gerli &Nicola Bizzaro &Yehuda Shoenfeld
Published online: 1 February 2014
#Springer Science+Business Media New York 2014
Erratum to: Clinic Rev Allerg Immunol (2010) 38:287–291
DOI 10.1007/s12016-009-8158-6
The original version of this article unfortunately contained a
mistake. Professor Nicola Bizzaro’s name appears as “Bizzaro
Nicola”instead of “Nicola Bizzaro”.
The correct name is shown in the author group and affili-
ation section.
The online version of the original article can be found at http://dx.doi.org/
10.1007/s12016-009-8158-6.
M. K. Meron :H. Amital
Department of Medicine ‘D’,
Meir Medical Center affiliated with Tel Aviv University Sackler
Faculty of Medicine,
Kfar-Saba, Israel
D. Shepshelovich :O. Barz ilai :M. Ram :Y. Shoenfeld (*)
Department of Internal Medicine B,
Center for Autoimmune Diseases affiliated with Tel Aviv
University Sackler Faculty of Medicine, Sheba Medical Center,
Tel Hashomer 52621, Israel
e-mail: shoenfel@post.tau.ac.il
J.<M. Anaya
Cellular Biology and Immunogenetics Unit,
Corporación para Investigaciones Biológicas,
Universidad del Rosario,
Medellin, Colombia
R. Gerli
Rheumatology Unit,
Department of Clinical and Experimental Medicine,
University of Perugia,
Perugia, Italy
N. Bizzaro
Laboratorio di Patologia Clinica,
Ospedale Civile,
30027 S Donà di Piave, Venice, Italy
Y. Shoenfeld
Laura Schwarz-Kipp, Tel Aviv University,
Tel Av iv, Is rae l
Clinic Rev Allerg Immunol (2014) 47:110
DOI 10.1007/s12016-014-8410-6
... Genetic and environmental factors are the main ones involved in the pathogenesis of ADs. Infections and exposure to pathogens or opportunistic organisms are among the major environmental factors that may induce the initiation or exacerbation of ADs, including RA [1,2]. ...
... I i,b and I i,a were the indicator variables that took on the value of 1 when the i-th individual was an incident case of inflammatory arthritis and the diagnosis was before/after COVID-19 respectively, and 0 otherwise. Notice that according to (1) and ( Then, both the incidence rate (IR) of inflammatory arthritis and RArelated diagnosis given that there was a COVID-19 episode prior to the inflammatory arthritis diagnosis (IR RA|SARS− CoV− 2 ) and the IR of inflammatory arthritis given that there was not a COVID-19 episode prior to the inflammatory arthritis diagnosis (IR IA|¬SARS− CoV− 2 ) were defined as follows [11]: ...
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An increase in the incidence of inflammatory arthritis after COVID-19 has been reported. Since many diseases exhibit population-specific causal effect sizes, we aimed to evaluate the incidence trends of inflammatory arthritis, including rheumatoid arthritis (RA), after COVID-19 in a large admixed Colombian population. Data analysis for this retrospective, population-based cohort study was carried out using the COOSALUD EPS registry. The following codes were selected for analyses: M059, seropositive RA, M069, unspecified RA, M060 seronegative RA, and other RA-related diagnoses: M064, M139, M068, M058, M130 and M053. The study period was limited to January 01, 2018, through December 31, 2022. Incidence rates (IRs) and incidence rate ratios (IRRs) were assessed. A Cox survival model was built to evaluate the influence of age, gender, and COVID-19 vaccination status on the development of inflammatory arthritis. A bioinformatic analysis was performed to evaluate the homology between SARS-CoV-2 and autoantigen peptides related to RA. The entire population study comprised 3,335,084 individuals. During the pandemic period (2020-2022) the total IIR for seropositive and unspecified RA were 1.60 (95% CI, 1.16-2.22) and 2.93 (95% CI, 2.04-4.19), respectively, and the IIR for overall RA-related diagnosis was 2.01 (95% CI 1.59-2.53). The age groups hazard ratios (HRs) were increased until the age group of 51-60 years (HR: 9.16; 95% CI, 7.24-11.59) and then decreased slightly in the age group 61 years or older (HR: 5.364; 95% CI, 4.24-6.78) compared to those within 18-30 years. Men were less at risk than women to develop inflammatory arthritis (HR: 0.21; 95% CI, 0.18-0.24). The greater time since COVID-19 diagnosis was associated with a lower likelihood of developing inflammatory arthritis (HR: 0.99; 95% CI:0.998-0.999). Vaccination (all types of COVID-19 vaccines included) did not prevent the development of inflammatory arthritis after COVID-19. Low identity was found between the SARS-CoV-2 ORF1ab antigen and the human antigens Poly ADP-ribose polymerase 14 and Protein mono-ADP-ribosyltransferase PARP9 isoform D (39% and 29%, respectively). In conclusion, our study confirms increased incidence of inflammatory arthritis, including RA, after COVID-19, with the greatest increase occurring before the first year post-covid. Women in their fifties were more susceptible. Further research is required to examine the effectiveness of vaccination in preventing post-COVID inflammatory arthritis and the mechanisms implicated in the development of RA after COVID-19.
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... In fact, studies on this topic revealed a similar prevalence between rheumatoid arthritis patients and healthy controls [223]. The eradication effect on rheumatoid arthritis evolution also remains debatable since both positive [128,129] and null [130,131] findings were reported. The risk of rheumatoid arthritis and lupus erythematosus in the setting of H. pylori infection might be related to the virulence features of this bacterium [123]. ...
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... p-value: 0.19), and the authors concluded that H. pylori infection had no significant effect on RA pathogenesis [29]. Meron et al. [71] found no significant differences in the rates of antibodies against H. pylori between RA patients and healthy controls. ...
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