Restriction factor compendium for influenza A virus reveals a mechanism for evasion of autophagy

细胞生物学 生物 甲型流感病毒 自噬 病毒复制 寄主因子 病毒 病毒学 遗传学 细胞凋亡
作者
Laura Martin‐Sancho,Shashank Tripathi,Ariel Rodríguez-Frandsen,Lars Pache,María Teresa Sánchez-Aparicio,Michael McGregor,Kelsey M. Haas,Danielle L. Swaney,Thông Nguyen,João I. Mamede,Christopher Churas,Dexter Pratt,Sara Brin Rosenthal,Laura Riva,Courtney Nguyen,Nish Beltran-Raygoza,Stephen Soonthornvacharin,Guojun Wang,David Jimenez‐Morales,Paul D. De Jesus,Hong M. Moulton,David A. Stein,Max W. Chang,Christopher Benner,Trey Ideker,Randy A. Albrecht,Judd F. Hultquist,Nevan J. Krogan,Adolfo García‐Sastre,Sumit K. Chanda
出处
期刊:Nature microbiology 卷期号:6 (10): 1319-1333 被引量:28
标识
DOI:10.1038/s41564-021-00964-2
摘要

The fate of influenza A virus (IAV) infection in the host cell depends on the balance between cellular defence mechanisms and viral evasion strategies. To illuminate the landscape of IAV cellular restriction, we generated and integrated global genetic loss-of-function screens with transcriptomics and proteomics data. Our multi-omics analysis revealed a subset of both IFN-dependent and independent cellular defence mechanisms that inhibit IAV replication. Amongst these, the autophagy regulator TBC1 domain family member 5 (TBC1D5), which binds Rab7 to enable fusion of autophagosomes and lysosomes, was found to control IAV replication in vitro and in vivo and to promote lysosomal targeting of IAV M2 protein. Notably, IAV M2 was observed to abrogate TBC1D5-Rab7 binding through a physical interaction with TBC1D5 via its cytoplasmic tail. Our results provide evidence for the molecular mechanism utilised by IAV M2 protein to escape lysosomal degradation and traffic to the cell membrane, where it supports IAV budding and growth.
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