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Published on: September 13, 2018
Limited G-Dependent Residual Infectivity of G Gene-Deleted Vesicular Stomatitis Virus
Kangyixin Sun1, Li Li1, Jia Yang1
1Guangdong Provincial Key Laboratory of Brain Connectome and Behavior, CAS Key Laboratory of Brain Connectome and Manipulation, the Brain Cognition and Brain Disease Institute, Translational Research Center for the Nervous System, Shenzhen Institutes of Advance Technology, Chinese Academy of Sciences; Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen, China; NMPA Key Laboratory for Research and Evaluation of Viral Vector Technology in Cell and Gene Therapy Medicinal Products, Key Laboratory of Quality Control Technology for Virus-Based Therapeutics, Guangdong Provincial Medical Products Administration, Shenzhen Key Laboratory of Viral Vectors for Biomedicine, Shenzhen Institutes of Advance Technology, Chinese Academy of Sciences, Shenzhen, China.
None:
Vesicular stomatitis virus (VSV) -ΔG vector particles are widely applied in vaccine development, gene delivery, and immunotherapy studies due to their high transduction efficiency and replication-defective design. However, G-pseudotyped VSV-ΔG preparations may exhibit residual multicycle infectivity associated with VSV-G-dependent entry. Therefore, in this study, we generated VSV-ΔG particles and corresponding M51R and ΔM51 derivatives to examine the relationship between G-dependent residual infectivity and post-entry innate immune regulation. Serial passage experiments were performed with removal of the inoculum and repeated PBS washing, followed by RT-PCR and Sanger sequencing of viral genomic regions. Detectable infectivity persisted transiently during early passages but progressively declined, while no evidence of restoration of the deleted VSV-G gene was identified. Neutralization with anti-VSV-G antibody markedly reduced infection, supporting the dependence of the observed residual infectivity on functional VSV-G-mediated entry. M51 mutations were associated with enhanced interferon-related signaling after infection. Together, these findings distinguish limited G-dependent residual infectivity from restoration of replication competence and highlight the need to consider such activity during the characterization and interpretation of G-pseudotyped VSV-ΔG systems.
