作者: Margarita Maria-Panou , Emma L Prescott , Daniel L Hurdiss , Gemma Swinscoe , Michael Hollinshead
DOI: 10.3390/IJMS19030902
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摘要: BK polyomavirus (BKPyV; hereafter referred to as BK) causes a lifelong chronic infection and is associated with debilitating disease in kidney transplant recipients. Despite its importance, aspects of the virus life cycle remain poorly understood. In addition structural proteins, late region genome encodes for an auxiliary protein called agnoprotein. Studies on other agnoproteins have suggested that may contribute virion infectivity. Here, we demonstrate essential role agnoprotein release. Viruses lacking fail release from host cells do not propagate wild-type levels. this, infectivity or morphogenesis. Instead, expression correlates nuclear egress virions. We binding partner α-soluble N-ethylmaleimide sensitive fusion (NSF) attachment (α-SNAP) necessary release, siRNA knockdown α-SNAP prevents These data highlight novel begin reveal mechanism by which polyomaviruses leave infected cell.