No detection of parvovirus b19 or herpesvirus dna in giant cell arteritis

NO DETECTION OF PARVOVIRUS B19 OR HERPESVIRUS DNA IN GIANT CELL ARTERITIS

Journal of Clinical Virology 31 (2004) 11-15

Alicia Rodriguez-Pla, Josep A. Bosch-Gil, Juan E. Echevarria-Mayo, Jose Rossello-Urgell, Roser Solans-Laque, Pere Huguet-Redecilla, John H. Stone, Miquel Vilardell-Tarres

Abstract:

Background: Compelling arguments exist for a role of infectious agent in giant cell arteritis (GCA). Parvovirus B19 and several herpesviruses have focused the attention in recent years, but the few studies to date have yielded inconsistent results.

Objectives: To study the relationship between the presence of parvovirus B19 DNA or major known herpesviruses and histopathological features of GCA.

Study design: Between January 1997 and March 2002, 147 consecutive temporal artery biopsies were performed in our center because of a clinical suspicion of GCA. Using polymerase chain reaction (PCR) procedures validated by the World Health Organization and employed routinely by our laboratory, we examined the paraffin-embedded specimens for DNA from parvovirus B19, herpes simplex viruses (HSV) 1 and 2, Epstein-Barr virus (EBV), varicella-zoster virus (VZV), human cytomegalovirus (HCMV), and human herpesvirus 6 (HHV-6). We investigated positive results further with immunohistochemistry studies.

Results: Fifty of the 147 temporal artery biopsies (34%) showed histological features of GCA. Three biopsies (2.5% were initially PCR positive for parvovirus B19. None of the herpesvirus PCR assays were positive. Upon repeat testing by both PCR and immunohistochemistry, none of the three initially positive parvovirus B19 assays were confirmed. The results of both positive and negative control assays in these studies validated these findings. We confirmed the presence of amplifiable DNA in the temporal artery biopsy specimens using PCR primers for beta-globin and indoleamine 2,3-dioxygenase (IDO).

Conclusions: The results of our study do not support a role in the etiopathogenesis of GCA for either parvovirus or any of these six herpesviruses