Evans Gareth L, Caller Laura G, Foster Victoria, Crump Colin M
Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK.
Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK
Open Biol. 2015 Aug;5(8). doi: 10.1098/rsob.150041.
BK polyomavirus (BKPyV) is a member of a family of potentially oncogenic viruses, whose reactivation can cause severe pathological conditions in transplant patients, leading to graft rejection. As with many non-enveloped viruses, it is assumed that virus release occurs through lysis of the host cell. We now show the first evidence for a non-lytic release pathway for BKPyV and that this pathway can be blocked by the anion channel inhibitor DIDS. Our data show a dose-dependent effect of DIDS on the release of BKPyV virions. We also observed an accumulation of viral capsids in large LAMP-1-positive acidic organelles within the cytoplasm of cells upon DIDS treatment, suggesting potential late endosome or lysosome-related compartments are involved in non-lytic BKPyV release. These data highlight a novel mechanism by which polyomaviruses can be released from infected cells in an active and non-lytic manner, and that anion homeostasis regulation is important in this pathway.
BK多瘤病毒(BKPyV)是一类潜在致癌病毒家族的成员,其重新激活可在移植患者中导致严重的病理状况,进而引发移植物排斥反应。与许多无包膜病毒一样,人们认为病毒通过宿主细胞裂解而释放。我们现在展示了BKPyV非裂解释放途径的首个证据,并且该途径可被阴离子通道抑制剂DIDS阻断。我们的数据显示DIDS对BKPyV病毒粒子释放具有剂量依赖性效应。我们还观察到在DIDS处理后,病毒衣壳在细胞胞质内大型LAMP-1阳性酸性细胞器中积累,这表明潜在的晚期内体或溶酶体相关区室参与了BKPyV的非裂解释放。这些数据突出了一种新机制,即多瘤病毒可通过主动且非裂解的方式从受感染细胞中释放,并且阴离子稳态调节在该途径中很重要。