OBJECTIVE: To evaluate the role of parvovirus B19 (B19), varicella zoster virus (VZV), and human herpes virus 6 (HHV-6) in the aetiopathology of giant cell arteritis (GCA). METHODS: Temporal artery biopsy specimens from 57 patients with GCA and 56 controls were investigated. DNA was obtained by biopsy, and quantitative real time polymerase chain reaction assay performed to establish the prevalence and viral load of B19, VZV, and HHV-6. Amplification of the human beta-globin gene was used as internal positive control. RESULTS: (a) B19 was detected in 31/57 (54%) patients (median viral load 45.2 (25th-75th centiles 0-180.2) copies/microg DNA) v 21/56 (38%) controls (median viral load 0 (0-66.7) copies/microg of DNA; p = 0.07 for DNA prevalence, p = 0.007 for viral load. Among 31 B19 positive samples, 21 (68%) patients with biopsy proven GCA had >10(2) B19 copies/microg of DNA v 5/21 (24%) controls; p = 0.001. (b) No significant difference was found for VZV (p = 0.94 for DNA prevalence; p = 0.76 for viral load) and HHV-6 (p = 0.89 for DNA prevalence; p = 0.64 for viral load) in the GCA group compared with controls. CONCLUSION: B19 may have a role in the aetiopathology of GCA, particularly in those patients with high viral load; no evidence was found for VZV and HHV-6.
OBJECTIVE: To evaluate the role of parvovirus B19 (B19), varicella zoster virus (VZV), and human herpes virus 6 (HHV-6) in the aetiopathology of giant cell arteritis (GCA). METHODS: Temporal artery biopsy specimens from 57 patients with GCA and 56 controls were investigated. DNA was obtained by biopsy, and quantitative real time polymerase chain reaction assay performed to establish the prevalence and viral load of B19, VZV, and HHV-6. Amplification of the human beta-globin gene was used as internal positive control. RESULTS: (a) B19 was detected in 31/57 (54%) patients (median viral load 45.2 (25th-75th centiles 0-180.2) copies/microg DNA) v 21/56 (38%) controls (median viral load 0 (0-66.7) copies/microg of DNA; p = 0.07 for DNA prevalence, p = 0.007 for viral load. Among 31 B19 positive samples, 21 (68%) patients with biopsy proven GCA had >10(2) B19 copies/microg of DNA v 5/21 (24%) controls; p = 0.001. (b) No significant difference was found for VZV (p = 0.94 for DNA prevalence; p = 0.76 for viral load) and HHV-6 (p = 0.89 for DNA prevalence; p = 0.64 for viral load) in the GCA group compared with controls. CONCLUSION:B19 may have a role in the aetiopathology of GCA, particularly in those patients with high viral load; no evidence was found for VZV and HHV-6.
Authors: Z Sachetto; S C B Costa; P D Andrade; R A Conde; E M I Amstalden; A M Samara; S R M Fernandes Journal: Ann Rheum Dis Date: 2006-03 Impact factor: 19.103
Authors: Maria A Nagel; Andrew N Russman; Howard Feit; Igor Traktinskiy; Nelly Khmeleva; D Scott Schmid; Barry Skarf; Don Gilden Journal: Neurology Date: 2012-12-19 Impact factor: 9.910
Authors: Don Gilden; Teresa White; Nelly Khmeleva; Anna Heintzman; Alexander Choe; Philip J Boyer; Charles Grose; John E Carpenter; April Rempel; Nathan Bos; Balasubramaniyam Kandasamy; Kelly Lear-Kaul; Dawn B Holmes; Jeffrey L Bennett; Randall J Cohrs; Ravi Mahalingam; Naresh Mandava; Charles G Eberhart; Brian Bockelman; Robert J Poppiti; Madhura A Tamhankar; Franz Fogt; Malena Amato; Edward Wood; Vikram Durairaj; Steve Rasmussen; Vigdis Petursdottir; Lea Pollak; Sonia Mendlovic; Denis Chatelain; Kathy Keyvani; Wolfgang Brueck; Maria A Nagel Journal: Neurology Date: 2015-02-18 Impact factor: 9.910