Open AccessDifferences in Kaposi sarcoma‐associated herpesvirus‐specific and herpesvirus‐non‐specific immune responses in classic Kaposi sarcoma cases and matched controls in Sicily
Author(s) -
Amodio Emanuele,
Goedert James J.,
Barozzi Patrizia,
Riva Giovanni,
Firenze Alberto,
Bonura Filippa,
Viviano Enza,
Romano Nino,
Luppi Mario
Publication year - 2011
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2011.02032.x
Subject(s) - elispot , kaposi's sarcoma associated herpesvirus , medicine , immunology , antigen , immune system , kaposi's sarcoma , herpesviridae , virology , virus , t cell , human herpesvirus , viral disease
Kaposi sarcoma (KS) might develop because of incompetent immune responses, both non‐specifically and specifically against the KS‐associated herpesvirus (KSHV). Peripheral blood mononuclear cells from 15 classic (non‐AIDS) KS cases, 13 KSHV seropositives (without KS) and 15 KSHV‐seronegative controls were tested for interferon‐γ T‐cell (enzyme‐linked immunospot [Elispot]) responses to KSHV‐latency‐associated nuclear antigen (LANA), KSHV‐K8.1 and CMV/Epstein–Barr virus (EBV) peptide pools. The forearm and thigh of each participant was also tested for delayed‐type hypersensitivity (DTH) against common recall antigens. Groups were compared with Fisher exact test and multinomial logistic regression to calculate odds ratios (OR) and 95% confidence intervals (CI). A KSHV Elispot response was detected in 10 (67%) classic KS cases, 11 (85%) KSHV seropositives (without KS) and two (13%) seronegative controls. All four cases with KSHV‐LANA responses had current KS lesions, whereas five of six cases with KSHV‐K8.1 responses had no lesions ( P = 0.048). No case responded to both LANA and K8.1. Compared with the seronegative controls, the risk for classic KS was inversely related to DTH in the thigh (OR 0.71, 95% CI 0.55–0.94, P = 0.01), directly associated with DTH in the forearm (OR 1.35, 95% CI 1.02–1.80, P = 0.04) and tended to be increased fivefold per KSHV Elispot response (OR 5.13, 95% CI 0.86–30.77, P = 0.07). Compared with KSHV seropositives (without KS), the risk for classic KS was reduced fivefold (OR 0.20, CI 0.03–0.77, P = 0.04) per KSHV response. The CMV/EBV Elispot responses were irrelevant. Deficiency of both KSHV‐specific and KSHV‐non‐specific immunity is associated with classic KS. This might clarify why Kaposi sarcoma responds to immune reconstitution. ( Cancer Sci 2011; 102: 1769–1773)