An interleukin-6-related systemic inflammatory syndrome in patients co-infected with Kaposi sarcoma-associated herpesvirus and HIV but without Multicentric Castleman disease.
An interleukin-6-related systemic inflammatory syndrome in patients co-infected with Kaposi sarcoma-associated herpesvirus and HIV but without Multicentric Castleman disease.
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DOI：
10.1086/654798
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发表时间：
2010-08-01
期刊：
影响因子：
--
通讯作者：
Yarchoan R
中科院分区：
文献类型：
--
作者：
Uldrick TS;Wang V;O'Mahony D;Aleman K;Wyvill KM;Marshall V;Steinberg SM;Pittaluga S;Maric I;Whitby D;Tosato G;Little RF;Yarchoan R
卡波西肉瘤相关疱疹病毒 (KSHV) 是 HIV 感染者卡波西肉瘤 (KS) 和多中心卡斯尔曼病 (MCD) 的病原体。 KSHV-MCD 患者会出现发烧、消瘦、低蛋白血症、血细胞减少和低钠血症，这些症状与 KSHV 编码的小瓶白细胞介素 (IL)-6 (vIL-6) 和人 IL-6 的过量产生有关。我们确定了 6 名患有 KS 或 KSHV 感染血清学证据的 HIV 感染患者，他们有严重的炎症性 MCD 样症状，但我们无法诊断 MCD，并假设这些症状是由于 vIL-6 过量产生所致。对这 6 名患者的血清 vIL-6 水平进行了评估，并与 8 名有症状 KSHV-MCD 的对照患者和 32 名 KS 对照患者进行了比较。还评估了 KSHV 病毒载量、血清人 IL-6 (hIL-6) 和人 IL-10。有炎症性 MCD 样症状但无 MCD 的患者的 vIL-6 水平升高，与有症状的 KSHV-MCD 患者相当，并且显着高于对照 KS 患者（P = 0.0026）。 hIL-6、IL-10 和 KSHV 病毒载量升高也与有症状的 KSHV-MCD 患者相当，并且显着高于 KS 患者。一部分 HIV 和 KSHV 混合感染但没有 MCD 的患者可能会出现与 KSHV vIL-6、IL-6 和 KSHV 病毒载量水平升高相关的严重全身炎症症状。 KSHV 的过度裂解激活、裂解基因产物 vIL6 的产生以及相关的免疫失调可能是这些症状的病理生理学基础。对于 HIV 和 KSHV 合并感染的危重患者，必须考虑这种 IL-6 相关炎症综合征。
Kaposi sarcoma-associated herpesvirus (KSHV) is the causal agent for Kaposi sarcoma (KS) and multicentric Castleman disease (MCD) in HIV-infected patients. Patients with KSHV-MCD develop fevers, wasting, hypoalbuminemia, cytopenias, and hyponatremia that are related to overproduction of KSHV-encoded vial interleukin (IL)-6 (vIL-6) and human IL-6. We identified 6 HIV-infected patients with KS or serological evidence of KSHV infection who had severe inflammatory MCD-like symptoms but in whom we could not diagnose MCD, and hypothesized that these symptoms resulted from vIL-6 overproduction. Serum vIL-6 levels were assessed in these 6 patients and compared to 8 control patients with symptomatic KSHV-MCD and 32 control patients with KS. KSHV viral load, serum human IL-6 (hIL-6), and human IL-10 were also evaluated. Patients with inflammatory MCD-like symptoms but without MCD had elevated vIL-6 levels comparable to patients with symptomatic KSHV-MCD and significantly greater than control patients with KS (P = 0.0026). Elevated hIL-6, IL-10, and KSHV viral loads were also comparable to patients with symptomatic KSHV-MCD and significantly greater than those with KS. A subset of patients with HIV and KSHV co-infection, but without MCD, can develop severe systemic inflammatory symptoms associated with elevated levels of KSHV vIL-6, IL-6, and KSHV viral loads. Excess lytic activation of KSHV, production of the lytic gene product vIL6, and associated immunologic dysregulation may underlie the pathophysiology of these symptoms. This IL-6-related inflammatory syndrome is important to consider in critically ill patients with HIV and KSHV co-infection.
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