HSC70，HSPA1A, and HSP90AB1 Facilitate Ebola Virus trVLPs to Induce Chaperone-Mediated Autophagy

Abstract

Abstract Background Ebola virus (EBOV) can induce autophagy to benefit the virus life cycle, but detailed mechanisms remain to be elucidated. We previously found that EBOV GP and VP40 proteins interact with host chaperones, including HSC70 (HSPA8), HSPA1A, and HSP90AB1, which are probably associated with chaperone-mediated autophagy (CMA). Methods We developed EBOV-trVLPs to model the EBOV life cycle, infected 293T cells with trVLPs, evaluated CMA by GFP-LC3 and RFP-LAMP1 co-localization, transmission electron microscopy (TEM) observation, and immunoblot analysis. Results The data suggest that EBOV-trVLPs may induce autophagy via CMA, but are not constrained by the CMA pathway. HSC70, HSPA1A and HSP90AB1 participate in and regulate the CMA induced by EBOV-trVLPs. Conclusions This is the first study of CMA induced by EBOV-trVLPs and provides insight into viral-host interactions that are presumably related to CMA.