RT Journal Article
T1 Severe acute respiratory syndrome coronavirus envelope protein regulates cell stress response and apoptosis.
A1 DeDiego, Marta L.
A1 Nieto-Torres, José Luis
A1 Jiménez-Guardeño, José Manuel
A1 Regla-Nava, Jose Ángel
A1 Álvarez, Enrique
A1 Oliveros, Juan Carlos
A1 Zhao, Jincun
A1 Fett, Craig
A1 Perlman, Stanley
A1 Enjuanes, Luis
K1 Síndrome respiratorio agudo grave
K1 COVID-19 - Influencia y consecuencias
AB Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE or with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigargin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a measure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE.
PB PLOS
YR 2011
FD 2011
LK https://hdl.handle.net/10630/33286
UL https://hdl.handle.net/10630/33286
LA eng
NO his work was supported by grants from the Ministry of Science and Innovation of Spain (BIO2007-60978 and BIO2010-16705), the EuropeanCommunity’s Seventh Framework Programme (FP7/2007-2013) under the project ‘‘EMPERIE’’ EC Grant Agreement number 223498, and U.S. National Institutes ofHealth (R56 AI079424-01A1 and 2PO1 AI060699). Marta L. DeDiego received a contract from the project ‘‘EMPERIE’’ EC Grant Agreement number 223498. Thefunders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 26 feb 2026