PMC:7640975 / 60882-62534 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7640975","sourcedb":"PMC","sourceid":"7640975","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7640975","text":"Of note, it is of great significance to compare our proteomics data with those of the newly emergent severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2),78,79 which caused the Coronavirus Disease 2019 (COVID-19) Pandemic and has posed a serious global public health emergency. Recently, Appelberg et al. conducted an integrative proteo-transcriptomics analysis of Huh7 cells responding to SARS-CoV-2 infection, and identified ErbB, HIF-1, mTOR, and TNF signaling pathways that were significantly regulated during SARS-CoV-2 infection in vitro.78 They further demonstrated that the Akt inhibitor MK-2206, targeting the mTOR signaling pathway, was able to significantly reduce the replication of SARS-CoV-2. Moreover, another recent study investigated the translatome and proteome of Caco-2 cells in response to SARS-CoV-2 infection in vitro, and discovered that several cellular pathways linked to translation, proteostasis, splicing, carbon metabolism, and nucleotide metabolism were reshaped during viral infection.79 On this basis, the authors tested two translation inhibitors, cycloheximide and emetine, for their ability to suppress SARS-CoV-2 replication, and found that both pharmaceuticals significantly decreased the replication of SARS-CoV-2 in Caco-2 cells. Undoubtedly, by comparing the similarities and differences of cellular proteomes between PDCoV- and SARS-CoV-2-infected host cells, it is possible to find some common signaling pathways and key adaptor molecules that function to inhibit viral replication, and thus provide valuable clues for screening of therapeutic drugs for PDCoV and designing novel antiviral 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