Virologic, hematologic, and immunologic risk factors for classic Kaposi sarcoma
Virologic, hematologic, and immunologic risk factors for classic Kaposi sarcoma
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DOI：
10.1002/cncr.22236
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发表时间：
2006-11-01
期刊：
影响因子：
6.2
通讯作者：
Goedert, James J.
中科院分区：
文献类型：
--
作者：
Brown, Elizabeth E.;Whitby, Denise;Goedert, James J.
背景经典卡波西肉瘤（CKS）是一种炎症介导的肿瘤，在存在KS相关疱疹病毒（KSHV）和免疫干扰的情况下发生。在本研究中，作者比较了CKS病例与年龄和性别匹配的KSHV血清阳性对照组（无人类免疫缺陷病毒1型感染）、病毒控制标志物、血细胞计数、CD 4阳性和CD 8阳性淋巴细胞、血清β 2-微球蛋白和新喋呤水平。实时荧光定量扩增KSHV-K6和EBV-pol基因检测病毒载量，酶联免疫吸附试验检测抗K8.1（裂解）滴度，免疫荧光法检测抗潜伏核抗原（拉娜）滴度。使用logistic回归计算比值比（OR）和95%置信区间（95% CI），并根据性别、年龄和研究地点进行调整。外周血单个核细胞（PBMC）KSHV DNA检测（P 1：1745; P 1：102，400; P = 0.03）抗体滴度与CKS风险呈正相关。与无病变的病例相比，病变病例的抗体滴度更高（P = 638个细胞/μ L; P = 0.009）。无论疾病负担如何，在病例中均观察到β 2-微球蛋白和新蝶呤无显著性升高（P >= .08）。在多变量模型中，发现CKS风险与PBMC KSHV DNA（OR为2.7; 95%CI，1.4-5.3）、高KSHV裂解抗体滴度（OR为3.7; 95%CI，1.9-7.4）和低淋巴细胞相关，特别是在年龄< 70岁的患者中（OR为8.0; 95%CI，2.7-23.7）。目前的研究结果似乎证实了KSHV的特异性，并强调了CKS发病机制中涉及的血液学和免疫学相关性。
BACKGROUND. Classic Kaposi sarcoma (CKS) is an inflammatory-mediated neoplasm that develops in the presence of KS-associated herpesvirus (KSHV) and immune perturbation. In the current study, the authors compared CKS cases with age-matched and sex-matched KSHV-seropositive controls without human immunodeficiency virus-1 infection and markers of viral control, blood Counts, CD4-positive and CD8-positive lymphocytes, and serum beta-2-microglobulin and neopterin levels.METHODS. Viral loads were detected using real-time amplification of the KSHV-K6 and EBV-pol genes, anti-K8.1 (lytic) titers were detected by enzyme-linked immunoadsorbent assay, and antilatent nuclear antigen (LANA) titers were detected using immunofluorescence. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using logistic regression adjusted for sex, age, and study site.RESULTS. Peripheral blood mononuclear cells (PBMC) KSHV DNA detection (P 1:1745; P 1:102,400; P = .03) antibody titers were found to be positively associated with CKS risk. Antibody titers were higher in cases with lesions compared with cases without lesions (P = 638 cells/mu L; P = .009). Nonsignificant elevations of beta-2-microglobulin and neopterin were observed among cases regardless of disease burden (P >= .08). In a multivariate model, the CKS risk was found to be associated with PBMC KSHV DNA (OR of 2.7; 95% CI, 1.4-5.3), a high KSHV lytic antibody titer (OR of 3.7; 95% CI, 1.9-7.4), and low lymphocytes, particularly among those patients age < 70 years (OR of 8.0; 95% CI, 2.7-23.7).CONCLUSIONS. The findings of the current study appear to corroborate the specificity of KSHV and highlight the hematologic and immunologic correlates involved in the pathogenesis of CKS.