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Rheumatoid arthritis (RA) is an autoimmune disease caused by genetic and environmental factors. Infection is proposed to contribute to the pathogenesis.1 Several viral and bacterial infections, including parvovirus B19, Chikungunya, hepatitis C, Epstein-Barr virus and Porphyromonas gingivalis, have been raised to be associated with RA.1 The mechanism of how infections affect RA remains undetermined, generally considered to be via molecular mimicry and cross-reactions between self-antigens and viral proteins.1 Furthermore, recent study postulates that RA may be the result of immunosenescence, meaning premature ageing of the immune system via various mechanisms including telomere shortening.2 A recent review article illustrates that the expression of human telomerase reverse transcriptase was influenced by human papillomavirus (HPV) E6/E7.3 Therefore, immunosenescence caused by telomere shortening may be another hypothetical mechanism in RA development followed by HPV infection.
HPV infections have been found to be associated with autoimmune diseases including systemic lupus erythematosus and RA.4 5 …
Handling editor Josef S Smolen
Contributors Corresponding author JCCW had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: JCCW. Acquisition, analysis or interpretation of data: JCCW and Y-HW. Drafting of the manuscript: Y-TL and M-CC. Critical revision of the manuscript for important intellectual content: JCCW, H-KT, J-YC and Y-HW.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.