Rare diseases

Varicella-zoster ‘reactivation’ link to GCA debunked in Australian study

Rheumatologists from Sydney have poured cold water on a long running hypothesis that varicella-zoster virus (VZV) reactivation is a trigger for giant cell arteritis (GCA).

A study led by Dr Anthony M. Sammel from the Royal North Shore Hospital in Sydney and published in Rheumatology included 58 consecutive patients who underwent temporal artery biopsy for suspected GCA.

All patients underwent serum testing for VZV IgM and IgG and temporal artery biopsy (TAB) sections were stained for VZV antigen using a Cell Marque Varicella Zoster Virus Mouse Cocktail Antibody.

After six months of follow up, 12 of the patients were diagnosed with biopsy-positive GCA, eight with biopsy-negative GCA and 38 were given an alternative diagnosis.

Among the biopsy-positive GCA cohort, no patients had active herpes zoster (HZ) at the time of enrolment; 67% recalled a remote history of chickenpox, 17% had a prior episode of HZ and none had received the live zoster vaccine. No significant differences in VZV exposures were seen among GCA patients and those with alternative diagnoses.

Results showed that among the patients with a diagnosis of GCA, none had a VZV-compatible clinical syndrome, VZV antigen convincingly detected on TABs or positive VZV IgM serology.

The authors noted that this was despite all patients receiving corticosteroids and none receiving antiviral therapy.

“While IgM seropositivity is a relatively insensitive marker of viral reactivation (positive in 9–69% of patients with acute HZ infections) we would have expected at least a proportion of patients to test positive if GCA was indeed a VZV reactivation syndrome,” the study authors wrote.

“[Therefore] our study refutes the hypothesis that GCA represents a VZV reactivation syndrome,” they concluded.

The authors suggested that non-specific immunohistochemistry staining might explain the high rates of VZV antigen reported in other studies.

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