Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 19, Issue 12, Pages -Publisher
MDPI
DOI: 10.3390/ijms19123940
Keywords
Flaviviridae; Autophagy; selective autophagy; Hepatitis C virus; Dengue virus; Japanese encephalitis virus; West Nile virus; Zika virus
Funding
- Ministry of Science and Technology, Taipei [MOST 102-2320-B-182-037-MY3, MOST 105-2628-B-182-001-MY3]
- Chang Gung Memorial Hospital, Taoyuan, Taiwan [CMRPD1C0211, CMRPD1D0021, CMRPD1D0022, CMRPD1D0023, CMRPD1G0281, CRRPD1F0031, CMRPG3F0571]
- National Health Research Institute, Miaoli [NHRI-EX103-10322SC, NHRI-EX104-10322SC, NHRI-EX105-10322SC, NHRI-EX106-10322SC]
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Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis. Flavivirus infections underlie multiple human diseases and thus exert an immense burden on public health worldwide. Mounting evidence indicates that host autophagy is subverted to modulate the life cycles of flaviviruses, such as hepatitis C virus, dengue virus, Japanese encephalitis virus, West Nile virus and Zika virus. The diverse interplay between autophagy and flavivirus infection not only regulates viral growth in host cells but also counteracts host stress responses induced by viral infection. In this review, we summarize the current knowledge on the role of autophagy in the flavivirus life cycle. We also discuss the impacts of virus-induced autophagy on the pathogeneses of flavivirus-associated diseases and the potential use of autophagy as a therapeutic target for curing flavivirus infections and related human diseases.
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