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Abstract: No evidence of parvovirus B19, Chlamydia pneumoniae or human herpes virus infection in temporal artery biopsies in patients with giant cell arteritis

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www.ProHealth.com • April 18, 2002




Original Papers

J. Helweg-Larsen, B. Tarp1, N. Obel1 and B. Baslund2
Department of Infectious Diseases, Hvidovre University Hospital,

1 Department of Infectious Diseases, Marselisborg Hospital, Aarhus University Hospital and

2 Department of Rheumatology, Rigshospitalet, Copenhagen, Denmark


Objectives. Recent studies have suggested that infective agents may be involved in the pathogenesis of giant cell arteritis (GCA), in particular Chlamydia pneumoniae and parvovirus B19. We investigated temporal arteries from patients with GCA for these infections as well as human herpes viruses using the polymerase chain reaction (PCR).

Methods. Thirty temporal artery biopsies from 30 patients suspected of having GCA within a period of 1 yr were examined. Thirteen patients had classical GCA, two had biopsy-negative GCA, 10 patients had polymyalgia rheumatica and five patients had other conditions. DNA was extracted from frozen biopsies and PCR was used to amplify genes from Chlamydia pneumoniae, parvovirus B19 and each of the eight human herpes viruses: herpes simplex viruses HSV-1 and 2, Epstein–Barr virus, cytomegalovirus, varicella zoster virus and human herpes viruses HHV-6, -7 and -8.

Results. In all 30 biopsies, PCR was negative for DNAs of parvovirus B19, each of the eight human herpes viruses and C. pneumoniae.

Conclusions. We found no evidence of DNA from parvovirus B19, human herpes virus or C. pneumoniae in any of the temporal arteries. These agents do not seem to play a unique or dominant role in the pathogenesis of GCA.


KEY WORDS: Giant cell arteritis, Temporal artery biopsy, Parvovirus B19, Chlamydia pneumoniae, HSV-1, HSV-2, EBV, CMV, VZV, HHV-6, HHV-7, HHV-8.

Correspondence to: J. Helweg-Larsen, Copenhagen HIV programme, Department of Infectious Diseases 144, Hvidovre University Hospital, 2650 Hvidovre, Denmark.

Rheumatology 2002; 41: 445-449

© 2002 British Society for Rheumatology




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