Endotoxin treatment of equine infectious anaemia virus-infected horse macrophage cultures decreases production of infectious virus.
Endotoxin treatment of equine infectious anaemia virus-infected horse macrophage cultures decreases production of infectious virus.
复制标题
对马传染性贫血病毒感染的马巨噬细胞培养物进行内毒素处理可减少传染性病毒的产生。
DOI：
10.1099/0022-1317-79-4-747
复制
发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Carpenter,S
中科院分区：
文献类型：
--
作者：
Smith,TA;Davis,E;Carpenter,S
慢病毒在免疫系统的细胞中复制，并且免疫细胞的激活已显示调节病毒复制。为了确定巨噬细胞激活对马传染性贫血病毒（EIAV）复制的影响，从20匹不同的马中建立了原代马巨噬细胞培养物（HMC），感染EIAV无毒力株，并用5 μg/ml细菌内毒素刺激。测定从HMC收集的上清液中是否存在肿瘤坏死因子（TNF-α）和感染性病毒的产生。结果表明，马传染性贫血病毒的体外复制在不同马之间有显著差异（P <0.0001），与HMCs的处理无关。此外，与未处理的HMC相比，在用细菌内毒素刺激的HMC中EIAV复制显著降低（P <0.0001）。用细菌内毒素处理病毒感染的细胞后，未发现病毒复制与TNF-α产生之间存在显著相关性。然而，当HMCs在病毒感染前用内毒素处理时，EIAV复制的抑制与内毒素水平的增加成正比。用PCR和RT-PCR分别扩增感染后不同时间点的EIAV前病毒DNA和mRNA序列。结果表明，EIAV复制的早期事件，直到并包括多剪接的mRNA的转录，没有被抑制的EIAV感染的巨噬细胞与细菌内毒素的治疗。这表明内毒素处理抑制了病毒复制周期中的转录后步骤。
Lentiviruses replicate in cells of the immune system, and activation of immune cells has been shown to modulate virus replication. To determine the effects of macrophage activation on replication of equine infectious anaemia virus (EIAV), primary horse macrophage cultures (HMCs) were established from 20 different horses, infected with an avirulent strain of EIAV, and stimulated with 5 μg/ml of bacterial endotoxin. Supernatants collected from HMCs were assayed for the presence of tumour necrosis factor (TNF-α) and for production of infectious virus. Results indicated that EIAV replicationin vitrovaried significantly (P⩽ 0·0001) from horse to horse, regardless of the treatment of HMCs. Also, EIAV replication was significantly (P⩽ 0·0001) decreased in HMCs stimulated with bacterial endotoxin as compared to untreated HMCs. No significant correlation was found between virus replication and production of TNF-αfollowing treatment of virus-infected cells with bacterial endotoxin. However, when HMCs were treated with endotoxin prior to virus infection, inhibition of EIAV replication was proportional to increasing levels of endotoxin. PCR and RT-PCR were used to amplify EIAV proviral DNA and mRNA sequences, respectively, at various time-points following infection. The results indicated that the early events of EIAV replication, up to and including transcription of multiple-spliced mRNAs, were not inhibited by treatment of EIAV-infected macrophages with bacterial endotoxin. This suggests that endotoxin treatment inhibits a posttranscriptional step in the virus replication cycle.