Respiratory virus infection of peripheral blood monocytes: correlation with ageing of cells and interferon production in vitro.
Respiratory virus infection of peripheral blood monocytes: correlation with ageing of cells and interferon production in vitro.
复制标题
外周血单核细胞呼吸道病毒感染：与细胞衰老和体外干扰素产生的相关性。
DOI：
10.1099/0022-1317-68-6-1749
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
McIntosh,K
中科院分区：
文献类型：
--
作者：
Krilov,LR;Hendry,RM;Godfrey,E;McIntosh,K
研究了呼吸道合胞病毒（RSV）和副流感病毒3型（PIV 3）感染前1、2、4和7天在体外培养的外周血单核细胞中复制的能力。接种1天大的单核细胞产生的新病毒至少比感染更老，更巨噬细胞样细胞的两种病毒少十倍。PIV 3诱导广泛的合胞体形成，而RSV引起细胞病变效应，表现为细胞变圆增加，合胞体形成最少。检测感染单核细胞的上清液中的人干扰素-α（HuIFN-α），试图解释最年轻单核细胞中病毒复制受限的原因。在PIV 3感染的细胞中，HuIFN-α的产生与新病毒的形成呈负相关。培养1天后感染的单核细胞产生800 IU/ml的HuIFN-α;较老的细胞产生100至200 IU/ml。相比之下，在第1天用RSV感染的单核细胞产生最少量的HuIFN-α（1.5IU/ml）。培养2、4或7天后，在感染RSV的细胞中检测到HuIFN-α的量增加，在第7天达到最大值400 IU/ml。进一步研究年轻单核细胞培养物中复制的明显限制可能有助于理解这些呼吸道感染的发病机制。
The ability of respiratory syncytial virus (RSV) and parainfluenza virus type 3 (PIV3) to replicate in peripheral blood monocytes culturedin vitrofor 1, 2, 4 or 7 days prior to infection was investigated. Inoculation of 1-day old monocytes produced at least tenfold less new virus than infection of the older, more macrophage-like cells for both viruses. PIV3 induced extensive syncytium formation, whereas RSV caused a cytopathic effect manifest by increased rounding of the cells with minimal syncytium formation. Supernatants of infected monocytes were assayed for human interferon-a (HuIFN-α) in an attempt to explain the restricted viral replication in the youngest monocytes. In PIV3-infected cells, HuIFN-αproduction was inversely correlated with new virus formation. Monocytes infected after 1 day in culture produced 800 IU/ml of HuIFN-α; the older cells produced 100 to 200 IU/ml. In contrast, monocytes infected on day 1 with RSV produced minimal amounts (1·5 IU/ml) of HuIFN-α. Increasing amounts of HuIFN-αwere detected in cells infected with RSV after 2, 4 or 7 days in culture, reaching a maximum of 400 IU/ml on day 7. Further investigation of the apparent restriction of replication in young monocyte cultures may be helpful in understanding the pathogenesis of these respiratory infections.