Lostalé-Seijo Irene, Martínez-Costas José, Benavente Javier
Centro de Investigación en Química Biológica y Materiales Moleculares (CIQUS), Universidad de Santiago de Compostela, Campus Vida, 15782 Santiago de Compostela, Spain.
Centro de Investigación en Química Biológica y Materiales Moleculares (CIQUS), Universidad de Santiago de Compostela, Campus Vida, 15782 Santiago de Compostela, Spain.
Virology. 2016 Jan;487:104-11. doi: 10.1016/j.virol.2015.10.009. Epub 2015 Oct 23.
We have previously shown that the replication of avian reovirus (ARV) in chicken embryo fibroblasts (CEF) is more resistant to the antiviral action of interferon (IFN) than the replication of vesicular stomatitis virus (VSV) or vaccinia virus (VV). In this study we examined the capacity of these three viruses to induce the expression of IFN when infecting avian cells. Efficient expression of both type-α and type-β IFNs, as well as of the double-stranded RNA (dsRNA)-activated protein kinase (PKR), takes place in ARV-infected CEF, but not in cells infected with VSV or VV. PKR expression is not directly induced by ARV infection, but by the IFN secreted by ARV-infected cells. IFN induction in ARV-infected cells requires viral uncoating, but not viral gene expression, a situation similar to that reported for apoptosis induction by ARV-infected cells. However, our results demonstrate that IFN induction by ARV-infected CEF occurs by a caspase-independent mechanism.
我们之前已经表明，禽呼肠孤病毒（ARV）在鸡胚成纤维细胞（CEF）中的复制比水疱性口炎病毒（VSV）或痘苗病毒（VV）的复制对干扰素（IFN）的抗病毒作用更具抗性。在本研究中，我们检测了这三种病毒感染禽类细胞时诱导IFN表达的能力。α型和β型IFN以及双链RNA（dsRNA）激活的蛋白激酶（PKR）在ARV感染的CEF中均有效表达，但在VSV或VV感染的细胞中则不然。PKR的表达不是由ARV感染直接诱导的，而是由ARV感染细胞分泌的IFN诱导的。ARV感染细胞中的IFN诱导需要病毒脱壳，但不需要病毒基因表达，这与ARV感染细胞诱导凋亡的情况类似。然而，我们的结果表明，ARV感染的CEF诱导IFN是通过一种不依赖半胱天冬酶的机制发生的。
