Enhancement of porcine circovirus 2 replication in porcine cell lines by IFN-γ before and after treatment and by IFN-α after treatment
Enhancement of porcine circovirus 2 replication in porcine cell lines by IFN-γ before and after treatment and by IFN-α after treatment
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DOI：
10.1089/jir.2005.25.684
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发表时间：
2005-11-01
影响因子：
2.3
通讯作者：
Nauwynck, HJ
中科院分区：
文献类型：
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作者：
Meerts, P;Misinzo, G;Nauwynck, HJ
猪免疫系统的刺激导致猪圆环病毒2（PCV 2）在体内的复制增加。在本研究中，我们研究了各种细胞因子（白细胞介素-1 [IL-1]，IL-6，IL-10，肿瘤坏死因子-α [TNF-α]，干扰素-α [IFN-α]和IFN-γ）是否能够影响体外PCV 2感染。在IL-1、IL-6、TNF-α或IL-10处理的细胞中未观察到变化。然而，已证实IFN-α和IFN-γ影响猪肾细胞（PK-15）和猪单核细胞（3D 4/31）中的PCV 2感染。在接种之前、期间或之后向培养基中添加IFN-γ使PK-15细胞中PCV 2抗原阳性细胞的数量分别增加418%、171%和691%，并且使3D 4/31细胞中PCV 2抗原阳性细胞的数量分别增加706%、114%和423%。IFN-α预处理减少了感染的PK-15细胞的数量。当在接种后加入IFN-α时，IFN-α在PK-15细胞中使PCV 2感染增强529%，在3D 4/31细胞中增强308%。两种IFN对PCV 2感染的作用是剂量依赖性的，并且可以用IFN-α或IFN-γ中和抗体阻断。白细胞衍生的猪IFN-γ诱导对PCV 2感染的类似作用。用IFN-γ处理PK-15培养物导致后代病毒的产量增加20倍。共聚焦显微镜研究表明，IFN-γ对PCV 2感染的增强作用是通过增加PCV 2病毒样颗粒（VLP）的内化实现的。IFN-γ处理不改变VLP与细胞的结合或感染细胞中PCV 2蛋白的表达动力学。据我们所知，这项研究报告的第一个增强病毒感染的治疗与I型或II型干扰素。
Stimulation of the porcine immune system causes increased replication of porcine circovirus 2 (PCV2) in vivo. In the present study, we investigated whether various cytokines (interleukin-1 [IL-1], IL-6, IL-10, tumor necrosis factor-alpha [TNF-alpha], interferon-alpha [IFN-alpha], and IFN-gamma) are able to influence PCV2 infection in vitro. No changes were observed in IL-1, IL-6, TNF-alpha, or IL-10-treated cells. However, it was demonstrated that IFN-alpha and IFN-gamma influenced PCV2 infection in porcine kidney cells (PK-15) and porcine monocytic cells (3D4/31). IFN-gamma added to the culture medium before, during, or after inoculation increased the number of PCV2 antigen-positive cells, respectively, by 418%, 171%, and 691% in PK-15 cells and by 706%, 114%, and 423% in 3D4/31 cells. IFN-alpha pretreatment decreased the number of infected PK-15 cells. When it was added after inoculation, IFN-alpha enhanced PCV2 infection by 529% in PK-15 cells and by 308% in 3D4/31 cells. The effect of both IFNs on PCV2 infection was dose dependent and could be blocked with IFN-alpha or IFN-gamma neutralizing antibodies. Leukocyte-derived porcine IFN-gamma induced a similar effect on PCV2 infection. Treatment of PK-15 cultures with IFN-gamma caused a 20 times higher production of progeny virus. Confocal microscopy studies showed that the enhancing effect of IFN-gamma on PCV2 infection was achieved by increased internalization of PCV2 virionlike particles (VLPs). Binding of the VLPs to the cell or expression kinetics of PCV2 proteins in infected cells were not altered by IFN-gamma treatment. To our knowledge, this study reports the first enhancement of a viral infection by treatment with type I or type II IFNs.