Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
J Virol. 2011 Sep;85(18):9651-4. doi: 10.1128/JVI.00316-11. Epub 2011 Jul 13.
Picornaviruses rearrange cellular membranes to form cytosolic replication sites. In the case of poliovirus and several other picornaviruses, these membranes are derived from subversion of the cellular autophagy pathway. We also reported observation of autophagosome-like structures during infection by two human rhinoviruses (HRVs), HRV-2 and HRV-14 (W. T. Jackson et al., PLoS Biol. 3:e156, 2005). Another group reported that HRV-2 does not induce autophagosomes or respond to changes in cellular autophagy (M. Brabec-Zaruba, U. Berka, D. Blaas, and R. Fuchs, J. Virol. 81:10815-10817, 2007). In this study, we tested HRV-2-infected cells for activation of autophagic signaling and changes in virus growth in response to changes in autophagy levels. Our data indicate that HRV-2 induces and subverts the autophagic machinery to promote its own replication.
小核糖核酸病毒会重新排列细胞的膜结构,以形成细胞质复制位点。在脊髓灰质炎病毒和其他几种小核糖核酸病毒的情况下,这些膜结构来源于细胞自噬途径的破坏。我们还观察到在感染两种人类鼻病毒(HRV)——HRV-2 和 HRV-14 时,存在类似自噬体的结构(W.T.杰克逊等人,《公共科学图书馆·生物学》3:e156,2005 年)。另一组研究人员报告称,HRV-2 不会诱导自噬体,也不会对细胞自噬的变化做出反应(M.布拉贝克-扎鲁巴、U.伯卡、D.布拉阿斯和 R.福克斯,《病毒学杂志》81:10815-10817,2007 年)。在这项研究中,我们检测了 HRV-2 感染细胞中的自噬信号激活情况,以及病毒生长变化对自噬水平变化的反应。我们的数据表明,HRV-2 诱导并破坏了自噬机制,以促进自身的复制。