ArticleBiochimica et biophysica acta2005
JNK and PI3k/Akt signaling pathways are required for establishing persistent SARS-CoV infection in Vero E6 cells.
Article in Biochimica et biophysica acta, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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67 citing papers in PubMed, 112 citations in OpenAlex.
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- Duvelisib for Critically Ill Patients With Coronavirus Disease 2019: An Investigator-Initiated, Randomized, Placebo-Controlled, Double-Blind Pilot Trial.Open forum infectious diseases · 2023Article
- Multiscale network analysis identifies potential receptors for SARS-CoV-2 and reveals their tissue-specific and age-dependent expression.FEBS letters · 2023Article
- Molecular mechanisms of human coronavirus NL63 infection and replication.Virus research · 2023Review
- Editorial: Immune response to respiratory viruses and respiratory viral infections in susceptible populations.Frontiers in medicine · 2023Article
- PI3K/Akt/Nrf2 mediated cellular signaling and virus-host interactions: latest updates on the potential therapeutic management of SARS-CoV-2 infection.Frontiers in molecular biosciences · 2023Review
- Live and let die: signaling AKTivation and UPRegulation dynamics in SARS-CoVs infection and cancer.Cell death & disease · 2022Review
- COVID-19 liver and gastroenterology findings: AnWorld journal of hepatology · 2022Article
- PI3K/Akt/mTOR pathway: a potential target for anti-SARS-CoV-2 therapy.Immunologic research · 2022Review
- The SARS-CoV2 and mitochondria: the impact on cell fate.Acta bio-medica : Atenei Parmensis · 2022Review
- The PI3K/Akt/mTOR pathway: A potential pharmacological target in COVID-19.Drug discovery today · 2022Review
- The probable role and therapeutic potential of the PI3K/AKT signaling pathway in SARS-CoV-2 induced coagulopathy.Cellular & molecular biology letters · 2022Review
- SARS-CoV-2 modulates inflammatory responses of alveolar epithelial type II cellsFrontiers in immunology · 2022Article
- Molecular pathways involved in COVID-19 and potential pathway-based therapeutic targets.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Recent Progress in the Development of Opaganib for the Treatment of Covid-19.Drug design, development and therapy · 2022Review
- A pathway map of signaling events triggered upon SARS-CoV infection.Journal of cell communication and signaling · 2021Article
- Multi-level inhibition of coronavirus replication by chemical ER stress.Nature communications · 2021Article
- Multifunctional inhibitors of SARS-CoV-2 by MM/PBSA, essential dynamics, and molecular dynamic investigations.Journal of molecular graphics & modelling · 2021Article
- BRD4 targeting nanotherapy prevents lipopolysaccharide induced acute respiratory distress syndrome.International journal of pharmaceutics · 2021Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistence was established after most of the SARS-CoV-infected Vero E6 cells died. RNA of the defective interfering virus was not observed in the persistently infected cells by Northern blot analysis. SARS-CoV diluted to 2 PFU failed to establish persistence, suggesting that some particular viruses in the seed virus did not induce persistent infection. Interestingly, a viral receptor, angiotensin converting enzyme (ACE)-2, was down-regulated in persistently infected cells. G418-selected clones established from parent Vero E6 cells, which were transfected with a plasmid containing the neomycin resistance gene, were infected with SARS-CoV, resulting in a potential cell population capable of persistence in Vero E6 cells. Our previous studies demonstrated that signaling pathways of extracellular signal-related kinase (ERK1/2), c-Jun N-terminal protein kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3'-kinase (PI3K)/Akt were activated in SARS-CoV-infected Vero E6 cells. Previous studies also showed that the activation of p38 MAPK by viral infection-induced apoptosis, and a weak activation of Akt was not sufficient to protect from apoptosis. In the present study, we showed that the inhibitors of JNK and PI3K/Akt inhibited the establishment of persistence, but those of MAPK/ERK kinase (MEK; as an inhibitor for ERK1/2) and p38 MAPK did not. These results indicated that two signaling pathways of JNK and PI3K/Akt were important for the establishment of persistence in Vero E6 cells.
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