Dysregulation in Akt/mTOR/HIF-1 signaling identified by proteo-transcriptomics of SARS-CoV-2 infected cells

Emerg Microbes Infect. 2020 Dec;9(1):1748-1760. doi: 10.1080/22221751.2020.1799723.

Abstract

How severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infections engage cellular host pathways and innate immunity in infected cells remains largely elusive. We performed an integrative proteo-transcriptomics analysis in SARS-CoV-2 infected Huh7 cells to map the cellular response to the invading virus over time. We identified four pathways, ErbB, HIF-1, mTOR and TNF signaling, among others that were markedly modulated during the course of the SARS-CoV-2 infection in vitro. Western blot validation of the downstream effector molecules of these pathways revealed a dose-dependent activation of Akt, mTOR, S6K1 and 4E-BP1 at 24 hours post infection (hpi). However, we found a significant inhibition of HIF-1α through 24hpi and 48hpi of the infection, suggesting a crosstalk between the SARS-CoV-2 and the Akt/mTOR/HIF-1 signaling pathways. Inhibition of the mTOR signaling pathway using Akt inhibitor MK-2206 showed a significant reduction in virus production. Further investigations are required to better understand the molecular sequelae in order to guide potential therapy in the management of severe coronavirus disease 2019 (COVID-19) patients.

Keywords: Akt/mTOR/HIF-1; MK-2206; SARS-CoV-2; proteomics; transcriptomics.

MeSH terms

  • Betacoronavirus / pathogenicity*
  • COVID-19
  • Cell Line
  • Chromatography, Liquid
  • Coronavirus Infections / genetics
  • Coronavirus Infections / metabolism
  • Coronavirus Infections / virology*
  • Gene Expression Profiling / methods*
  • Gene Expression Regulation
  • High-Throughput Nucleotide Sequencing
  • Humans
  • Hypoxia-Inducible Factor 1 / genetics
  • Hypoxia-Inducible Factor 1 / metabolism
  • Pandemics
  • Pneumonia, Viral / genetics
  • Pneumonia, Viral / metabolism
  • Pneumonia, Viral / virology*
  • Proteomics / methods*
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • SARS-CoV-2
  • Signal Transduction*
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism
  • Tandem Mass Spectrometry

Substances

  • Hypoxia-Inducible Factor 1
  • MTOR protein, human
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases

Grants and funding

The study is funded by the Swedish Research Council [grant number 2017-01330, UN]. A. M. is supported by the Swedish research Council [2018-05766 and 2017-03126]. J.M.P. is supported by the Canada 150 Research Chair program and CIHR rapid Response COVID-19 grant. K.S. acknowledges the funding from the Office of Research (Early Concept Grant, Bond Life Sciences Center), University of Missouri, Columbia, MO.