Estimation of human herpesvirus 8 prevalence in high-risk patients by analysis of humoral and cellular immunity
- PMID: 17627235
- DOI: 10.1097/01.tp.0000267158.23795.11
Estimation of human herpesvirus 8 prevalence in high-risk patients by analysis of humoral and cellular immunity
Abstract
Background: Immunocompromized individuals, such as patients with end-stage renal disease, transplant recipients, and HIV-infected patients, are at increased risk of acquiring human herpesvirus (HHV)-8 associated infectious complications. The prevalence of HHV-8 infection generally is determined by detection of immunoglobulin G. However, because serological assays differ greatly, estimations on the actual HHV-8 prevalence vary considerably.
Methods: HHV-8-specific cellular and humoral immunity were analyzed in 128 controls, 73 patients on dialysis, 67 transplant recipients, and 69 HIV-infected patients with the use of flow cytometry and indirect immunofluorescence microscopy.
Results: A higher seroprevalence (from 13.7% to 44.9%) was confirmed for all groups of immunocompromised individuals as compared with healthy controls (3.9%). Among immunocompetent individuals, as little as 12.5% had HHV-8 reactive T-cell frequencies greater than the detection limit. In line with a higher seroprevalence in immunosuppressed patients, HHV-8-specific T cells were detectable in 30.1% of dialysis patients, 20.9% of transplant recipients, and 24.6% of HIV-infected individuals. When combining the individual presence of either HHV-8-specific antibodies or T cells or both, the prevalence of HHV-8 infection approached 15.6% in healthy individuals and 41.1%, 40.3%, and 55.1% in dialysis patients, transplant recipients, and HIV-infected individuals, respectively.
Conclusions: The exclusive serological analysis considerably underestimates the prevalence of HHV-8 infection in all study groups. Thus, the combined quantitation of both humoral and cellular immunity may instead be a superior method to assign the individual HHV-8 status. Moreover, this study suggests that the relative contributions of humoral and cellular immunity in control of HHV-8 may be different depending on the type of immunodeficiency.
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