Differential regulation of the attachment of Kaposi's sarcoma-associated herpesvirus (KSHV)-infected human B cells to extracellular matrix by KSHV-encoded gB and cellular αV integrins
Differential regulation of the attachment of Kaposi's sarcoma-associated herpesvirus (KSHV)-infected human B cells to extracellular matrix by KSHV-encoded gB and cellular αV integrins
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DOI：
10.1111/j.1462-5822.2008.01149.x
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发表时间：
2008-07-01
影响因子：
3.4
通讯作者：
Akula, Shaw M.
中科院分区：
文献类型：
--
作者：
Dyson, Ossie F.;Oxendine, Telisha L.;Akula, Shaw M.
卡波西肉瘤相关疱疹病毒（KSHV）有两种复制模式：潜伏和裂解复制。从潜伏期的重新激活部分地由细胞周期决定。在此，我们试图通过探索细胞周期不同阶段细胞表面受体的表达模式来阐明细胞周期在KSHV发病机制中的重要性。在成纤维细胞、上皮细胞和KSHV感染的细胞中，α V整联蛋白表达在S期增加。使用Matrigel系统，我们开创了KSHV感染的原发性渗出性淋巴瘤细胞可以附着于细胞外基质蛋白的概念。这种附着主要通过α V整联蛋白或病毒编码的gB介导，并且分别优先发生在来自S期的细胞或来自S期的积极支持裂解感染的细胞中。受感染的B细胞附着于内皮细胞的这种能力也可能有助于感染的传播。这项工作的重点是，我们首次描述了KSHV感染的B细胞优先使用细胞（α V）或病毒（g B）受体特异性结合细胞的能力，这取决于细胞周期和感染的阶段。
Kaposi's sarcoma-associated herpesvirus (KSHV) has two modes of replications: latent and lytic replications. Reactivation from latency is dictated, in part, by the cell cycle. Herein, we have attempted to delineate the importance of cell cycle in KSHV pathogenesis by exploring the expression pattern of cell-surface receptors during different phases of the cell cycle. alpha V integrin expression is augmented during S phase in fibroblasts, epithelial and KSHV-infected cells. Using a Matrigel system, we pioneer the concept that KSHV-infected primary effusion lymphoma cells can attach to extracellular matrix proteins. This attachment is mediated primarily via alpha V integrins or virally encoded gB, and occurs preferentially in cells from S phase or cells from S phase actively supporting a lytic infection respectively. Such an ability of infected B cells to attach to endothelial cells may also aid in the dissemination of infection. The keystone of this work is that for the first time, we describe the ability of KSHV-infected B cells to preferentially use cellular (alpha V) or viral (gB) receptors to specifically bind cells, depending upon the stage of the cell cycle and infection.