• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Journal of Virology >Intracellular Tat of Human Immunodeficiency Virus Type 1 Activates Lytic Cycle Replication of Kaposis Sarcoma-Associated Herpesvirus: Role of JAK/STAT Signaling
【2h】

Intracellular Tat of Human Immunodeficiency Virus Type 1 Activates Lytic Cycle Replication of Kaposis Sarcoma-Associated Herpesvirus: Role of JAK/STAT Signaling

机译：1型人类免疫缺陷病毒的细胞内Tat激活卡波西氏肉瘤相关疱疹病毒的Lytic循环复制：JAK / STAT信号传导的作用

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Human immunodeficiency virus type 1 (HIV-1) infection significantly increases the risk of Kaposi's sarcoma (KS) occurrence in individuals infected with Kaposi's sarcoma-associated herpesvirus (KSHV). KSHV infection appears to be necessary but not sufficient for KS development without other cofactors. However, factors that facilitate KSHV to cause KS have not been well defined. Previously, we determined that human herpesvirus 6 was one of the cofactors that activated lytic cycle replication of KSHV. Here, we demonstrate that the Tat protein of HIV-1 is a potentially important factor in the pathogenesis of KS, as determined by production of lytic phase mRNA transcripts and viral proteins in BCBL-1 cells. Mechanistic studies showed ectopic expression of Tat induced the production of human interleukin-6 (huIL-6) and its receptor (huIL-6Ra) and activated STAT3 signaling. Neutralization of huIL-6 or huIL-6R or inhibition of STAT3 signaling enhanced the replication. In addition, IL-4/STAT6 signaling also partially contributed to Tat-induced KSHV replication. These findings suggest that Tat may participate in KS pathogenesis by inducing KSHV replication and increasing KSHV viral load. These data also suggest that JAK/STAT signaling may be of therapeutic value in AIDS-related KS patients.
机译：在感染了卡波西氏肉瘤相关疱疹病毒（KSHV）的个体中，人类免疫缺陷病毒1型（HIV-1）感染显着增加了卡波西氏肉瘤（KS）发生的风险。在没有其他辅助因子的情况下，KSHV感染似乎是必要的，但不足以促进KS的发展。但是，促成KSHV引起KS的因素尚未明确。以前，我们确定人疱疹病毒6是激活KSHV裂解周期复制的辅助因子之一。在这里，我们证明HIV-1的Tat蛋白是KS发病机理中的潜在重要因素，这是由BCBL-1细胞中的裂解相mRNA转录产物和病毒蛋白的产生确定的。机理研究表明，Tat的异位表达可诱导人白介素6（huIL-6）及其受体（huIL-6Ra）的产生并激活STAT3信号。 huIL-6或huIL-6R的中和或STAT3信号的抑制增强了复制。此外，IL-4 / STAT6信号也部分促成Tat诱导的KSHV复制。这些发现表明，Tat可能通过诱导KSHV复制和增加KSHV病毒载量而参与KS发病。这些数据还表明，JAK / STAT信号传导在与艾滋病相关的KS患者中可能具有治疗价值。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号