Title Bovine Viral Diarrhea Virus Infection Induces Autophagy in MDBK Cells
Author Qiang Fu1, Huijun Shi1, Yan Ren2, Fei Guo2, Wei Ni3, Jun Qiao1, Pengyan Wang1, Hui Zhang1, and Chuangfu Chen1*
Address 1College of Animal Science and Technology, Shihezi University, Shihezi 832003, Xinjiang, P.R. China, 2College of Medicine, Shihezi University, Shihezi 832003, Xinjiang, P.R. China, 3College of Life Science, Shihezi University, Shihezi 832003, Xinjiang, P.R. China
Bibliography Journal of Microbiology, 52(7),619-625, 2014,
DOI 10.1007/s12275-014-3479-4
Key Words bovine viral diarrhea virus NADL, autophagy, Madin-Darby Bovine Kidney (MDBK) cells, autophagosome, GFP-LC3
Abstract Bovine viral diarrhea virus (BVDV) is an enveloped, positive-sense, single-stranded RNA virus that belongs to the genus Pestivirus (Flaviviridae). The signaling pathways and levels of signaling molecules are altered in Madin-Darby Bovine Kidney (MDBK) cells infected with BVDV. Autophagy is a conservative biological degradation pathway that mainly eliminates and degrades damaged or superfluous organelles and macromolecular complexes for intracellular recycling in eukaryotic cells. Autophagy can also be induced as an effective response to maintain cellular homeostasis in response to different stresses, such as nutrient or growth factor deprivation, hypoxia, reactive oxygen species exposure and pathogen infection. However, the effects of BVDV infection on autophagy inMDBK cells remain unclear. Therefore, we performed an analysis of autophagic activity after BVDV NADL infection using real-time PCR, electron microscopy, laser confocal microscopy, and Western blotting analysis. The results demonstrated that BVDV NADL infection increased autophagic activity and significantly elevated the expression levels of the autophagy-related genes Beclin1 and ATG14 inMDBK cells. However, the knockdown of Beclin1 and ATG14 by RNA interference (RNAi) did not affect BVDV NADL infection-related autophagic activity. These findings provided a novel perspective to elaborate the effects of viral infection on the host cells.