Subversion of the cellular autophagy pathway by viruses.
Autophagy is a cellular process that creates double-membraned vesicles, engulfs and degrades cytoplasmic material, and generates and recycles nutrients. A recognized participant in the innate immune response to microbial infection, a functional autophagic response can help to control the replication of many viruses. However, for several viruses, there is functional and mechanistic evidence that components of the autophagy pathway act as host factors in viral replicative cycles, viral dissemination, or both. Investigating the mechanisms by which viruses subvert or imitate autophagy, as well as the mechanisms by which they inhibit autophagy, will reveal cell biological tools and processes that will be useful for understanding the many functional ramifications of the double-membraned vesicle formation and cytosolic entrapment unique to the autophagy pathway.
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. karlak@stanford.edu
Karla
K
Kirkegaard
D000818:Animals; D001343:Autophagy / Q000276:immunology*; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D014777:Virus Diseases / Q000276:immunology* / Q000821:virology; D014779:Virus Replication; D014780:Viruses / Q000276:immunology*