BK Polyomavirus Hijacks Extracellular Vesicles for En Bloc Transmission.

摘要: Most people are asymptomatic carriers of the BK polyomavirus (BKPyV), but mechanisms persistence and immune evasion remain poorly understood. Furthermore, BKPyV is responsible for nephropathies in kidney transplant recipients. Unfortunately, sole therapeutic option to modulate immunosuppression, which increases risk rejection. Using iodixanol density gradients, we observed that Vero renal proximal tubular epithelial infected cells release two populations infectious particles, one cosediments with extracellular vesicles (EVs). Electron microscopy confirmed a single vesicle could traffic tens viral particles. In contrast naked virions, EV-associated particles (eBKPyVs) were not able agglutinate red blood did use cell surface sialylated glycans as an attachment factor, demonstrating different entry pathways involved each type particle. However, also eBKPyV equally sensitive neutralization by serum seropositive patient or commercially available polyvalent immunoglobulin preparations, occurred at postattachment step, after endocytosis. conclusion, our work shows new mechanism likely plays critical role during primary infection persistence, reactivation, BKPyV.IMPORTANCE Reactivation recipients, frequently lead graft loss. The used this virus understood, patients still lacking. Here, show can be released into EVs, enabling infect using alternative pathway. This provides view pathogenesis. Even though find any decreased sensitivity neutralizing antibodies when comparing study raises important questions about developing prevention strategies based on induction administration antibodies. Deciphering pathway enable identification targets prevent nephropathies. It better understanding pathophysiology other polyomaviruses associated human diseases.