Table 2 Effect of autophagy modulators on coronavirus
From: Role and clinical implication of autophagy in COVID-19
Coronavirus | Cell lines | Protein/pathway | Main results | Refs |
|---|---|---|---|---|
MHV | DBT cells | ATG5 | Autophagy is required for coronaviruses replication complexes. | [125] |
HCV | C5B cells | ATG5 | Autophagy is required for HCV replication. | [126] |
MHV | MEFs | ATG5 | ATG5 is not required for MHV‑A59 replication. | [88] |
MHV | HeLa, MEFs | LC3-I | LC3-I rather than intact autophagy process is required for MHV replication. | [91] |
PEDV | HEK293T cells | MARCHF8, ATG5 | Inhibition of selective autophagy pathway promotes PEDV replication. | [127] |
MERS-CoV | HuH7 cells | ERK/MAPK, PI3K/AKT/mTOR | Inhibition of ERK/MAPK and PI3K/AKT/mTOR pathways inhibits MERS-CoV replication. | [92] |
HCoV-NL63 | HEK 293T, HeLa and MCF-7 cells | LC3, BECN1 | PLP2-TM triggers incomplete autophagy process by interacting with BECN1 thereby modulating virus replication and antiviral innate immunity. | [128] |
PEDV | IPEC-J2 cells | PI3K/AKT/mTOR | Autophagy induced by NSP6 of PEDV promotes virus replication via PI3K/AKT/mTOR pathway. | [129] |
MERS-CoV | HEK293T cells | BECN1 | MERS-CoV invasion reduces BECN1 levels and autolysosome formulated for virus replication. | [78] |
MHV-A59 and SARS-CoV-2 | Murine 17Cl1 fibroblasts | ULK1 | PLpro of MHV-A59 and SARS-CoV-2 cleaves ULK1 and thus disrupting autophagy and inducing viral pathogenesis. | [80] |
SARS-CoV-2 | HeLa, Vero-E6 and HEK293T cells | UVRAG | SARS-CoV-2 ORF3a induces an incomplete autophagy response by interacting with UVRAG. | [130] |