Risk of classical Kaposi sarcoma by plasma levels of Epstein-Barr virusantibodies, sCD26, sCD23 and sCD30

BACKGROUND: To clarify the immunological alterations leading to classical Kaposi sarcoma (cKS) among people infected with KS-associated herpesvirus (KSHV).METHODS: In a population-based study of 119 cKS cases, 105 KSHV-seropositivecontrols, and 155 KSHV-seronegative controls, we quantified plasma solublecluster of differentiation (sCD) levels and antibodies against Epstein-Barr virusnuclear antigen-1 (anti-EBNA-1) and viral capsid antigen (anti-VCA). Differences between groups in prevalence of low-tertile anti-EBNA-1 and high-tertile anti-VCAwere compared by logistic regression. Continuous levels between groups and bypresence of cKS co-factors among controls were compared by linear regression and Mann-Whitney-Wilcoxon methods.RESULTS: Comparisons of cKS cases to seropositive controls and of seropositive toseronegative controls revealed no significant differences. However, controls withknown cKS cofactors (male sex, nonsmoking, diabetes and cortisone use) hadsignificantly lower levels of anti-EBNA (P = 0.0001 - 0.07) and anti-VCA (P =0.0001 - 0.03). Levels of sCD26 were significantly lower for male and non-smokingcontrols (Padj ≤ 0.03), and they were marginally lower with older age andcortisone use (Padj ≤ 0.09).CONCLUSIONS: Anti-EBV and sCD26 levels were associated with cofactors for cKS,but they did not differ between cKS cases and matched controls. Novel approaches and broader panels of assays are needed to investigate immunologicalcontributions to cKS.