PMID- 22523259 OWN - NLM STAT- MEDLINE DCOM- 20121107 LR - 20120712 IS - 1537-6591 (Electronic) IS - 1058-4838 (Linking) VI - 55 IP - 3 DP - 2012 Aug TI - Clinical Sindbis alphavirus infection is associated with HLA-DRB1*01 allele and production of autoantibodies. PG - 358-63 LID - 10.1093/cid/cis405 [doi] AB - BACKGROUND: Sindbis virus (SINV) is a mosquito-borne alphavirus found in Eurasia, Africa, and Oceania. Clinical SINV infection, characterized by arthropathic disease that may persist for years, is primarily reported in Northern Europe where the disease has considerable public health importance in endemic areas. The aim of this study was to investigate the role of genetic factors in the susceptibility and outcome of SINV infection and to elucidate the association between SINV infection and autoimmunity. METHODS: The study included 49 patients with serologically confirmed symptomatic SINV infection who were followed for 3 years after acute infection. Human leukocyte antigen (HLA) genes known to be associated with rheumatic and infectious diseases and complement C4 genes were determined in 35 patients. Furthermore, a set of autoantibodies was measured at the acute phase and 3 years after infection in 44 patients. RESULTS: The frequency of DRB1*01 was significantly higher among patients with SINV infection than in the reference population (odds ratio, 3.3; 95% confidence interval, 1.7-6.5; P = .003). The DRB1*01 allele was particularly frequent in patients who at 3 years postinfection experienced joint manifestations. The frequency of rheumatoid factor at 3 years postinfection was 29.5% and had increased significantly (P = .02) during the 3-year period. In addition, antinuclear and antimitochondrial antibodies were present in serum 3 years postinfection with frequencies of 15.9% and 6.8%, respectively. CONCLUSIONS: Our data show that symptomatic SINV infection is associated with the HLA system and that autoantibody titers are elevated in patients 3 years postinfection. These findings indicate that SINV-induced arthritis shares features with autoimmune diseases. FAU - Sane, Jussi AU - Sane J AD - Infection Biology Research Program, Department of Virology, Haartman Institute, Faculty of Medicine, University of Helsinki, Finland. jussi.sane@helsinki.fi FAU - Kurkela, Satu AU - Kurkela S FAU - Lokki, Marja-Liisa AU - Lokki ML FAU - Miettinen, Aaro AU - Miettinen A FAU - Helve, Tapani AU - Helve T FAU - Vaheri, Antti AU - Vaheri A FAU - Vapalahti, Olli AU - Vapalahti O LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20120420 PL - United States TA - Clin Infect Dis JT - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America JID - 9203213 RN - 0 (Autoantibodies) RN - 0 (Complement C4) RN - 0 (HLA-DRB1 Chains) SB - IM MH - Adolescent MH - Adult MH - Aged MH - Alleles MH - Alphavirus Infections/*genetics/*immunology MH - Autoantibodies/*blood MH - Child MH - Complement C4/genetics MH - Europe MH - Female MH - *Genetic Predisposition to Disease MH - HLA-DRB1 Chains/*genetics MH - Humans MH - Male MH - Middle Aged MH - Sindbis Virus/*immunology MH - Young Adult EDAT- 2012/04/24 06:00 MHDA- 2012/11/08 06:00 CRDT- 2012/04/24 06:00 PHST- 2012/04/24 06:00 [entrez] PHST- 2012/04/24 06:00 [pubmed] PHST- 2012/11/08 06:00 [medline] AID - cis405 [pii] AID - 10.1093/cid/cis405 [doi] PST - ppublish SO - Clin Infect Dis. 2012 Aug;55(3):358-63. doi: 10.1093/cid/cis405. Epub 2012 Apr 20.