Published in

MDPI, Viruses, 4(14), p. 694, 2022

DOI: 10.3390/v14040694

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Epidemiology of the Epstein–Barr Virus in Autoimmune Inflammatory Rheumatic Diseases in Northern Brazil

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

Abstract

The present study aimed to describe the seroprevalence infection, Epstein-Barr virus (EBV) genotypes, relate the infection’s profile with the epidemiological and corticotherapy data of patients with Autoimmune inflammatory rheumatic diseases (AIRD). A cross-sectional study was carried out with 139 individuals, 92 with systemic lupus erythematosus (SLE), 27 with rheumatoid arthritis (RA) and 20 with other autoimmune diseases, who were undergoing clinical follow-up in Brazil. Serological tests for the detection of EBV anti-VCA IgM and IgG antibodies, as well as the amplification of a segment of the EBV EBNA-3c gene by conventional PCR were performed to identify the infection and the viral subtype. The Epstein–Barr nuclear antigen 3 (EBNA3C) gene participates of maintenance of viral latency and infected B-lymphocytes immortalization by unclear signaling cascades. The association of active/latent EBV infection with EBV infection profile was assessed by Fisher’s exact test and multiple logistic regression. The seroprevalence of EBV anti-VCA IgG was 100%, while that of anti-VCA IgM was 1.43% (2/139). Active-phase infection was confirmed by the presence of EBV DNA in 40.29% of the population evaluated (56/139), with 45.65% (42/92) in SLE, 25.92% (7/27) in the RA and in 35% (7/20) in other autoimmune diseases. It was observed that individuals with SLE had a higher prevalence of active/lytic EBV infection and that oral corticosteroid therapy at a dose lower than 20 mg/day increased the risk of EBV activity by up to 11 times. Only the presence of EBV-1 was identified. Thus, EBV lytic infection was higher in individuals with SLE when compared to other autoimmune diseases with rheumatologic involvement and the lytic activity of the virus precedes corticosteroid-induced immunosuppression.