Interferon–ribavirin therapy induces serum antibodies determining 'rods and rings' pattern in hepatitis C patients. Issue 12 (14th July 2014)

• Record Type: Journal Article
• Authors: Novembrino, Cristina; Aghemo, Alessio; Ferraris Fusarini, Chiara; Maiavacca, Rita; Matinato, Caterina; Lunghi, Giovanna; Torresani, Erminio; Ronchi, Mariangela; Garlaschi, Maria Cristina; Ramondetta, Miriam; Colombo, Massimo
• Is Part Of: Journal of viral hepatitis. Volume 21:Issue 12(2014)
• Page Start: 944
• Page End: 949
• Publication Date: 2014-07-14
• Subjects: Hepatitis, Viral -- Periodicals; Hepatitis, Viral, Animal; Hepatitis, Viral, Human; 616.3623
• DOI: 10.1111/jvh.12281
• Languages: English
• ISSNs: 1352-0504

Abstract

<abstract abstract-type="main" id="jvh12281-abs-0001"> <title>Summary</title> <p>A cytoplasmic antigen associated to inosine‐5'‐monophosphatedehydrogenase 2 eliciting specific antibodies (antirods and rings, RR) has been identified in patients with chronic hepatitis C who were exposed to pegylated interferon (PI) and ribavirin (RBV). The significance of anti‐RR in these patients merits to be investigated. Sera from 88 chronic hepatitis C virus (HCV)‐infected patients undergoing PI‐RBV therapy were analysed for the presence of RR pattern by indirect immunofluorescence on HEp‐2 substrate (Inova Diagnostics, San Diego, CA, USA). Anti‐RR antibodies developed <italic>de novo</italic> in 32 patients independently of any demographic and virological feature, but with a significant association with cumulative exposure to PI‐RBV (<italic>P</italic> = 0.0089; chi‐square test). RR pattern was significantly more frequent in relapsers than in patients achieving sustained virological response (56% <italic>vs</italic> 30%; <italic>P</italic> = 0.0282, chi‐square test). Anti‐RR titre ranged from 1:80 to 1:1280, but significantly declined following treatment cessation. Anti‐RR develop de novo in a substantial proportion of patients exposed to PI‐RBV in relation to the duration of treatment exposure. Further investigations are necessary to unravel the mechanisms leading to the formation of these autoantibodies.</p> </abstract>