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This work was supported in part from the VIRUS-HOST interaction programme (Comunidad de Madrid) and by grants from the Ministerio de Ciencia e Innovacion (SAF2006-09810; SAF2008-02036) and the Fundacion Mutua Madrilena (FMM 2008). The institutional support from Fundacion Ramon Areces is also acknowledged. E.D was a recipient of VIRUS-HOST programme postdoctoral contract. R.T. was a recipient of the SAF2006-09810 contract and I.V. was a researcher of Ramon y Cajal Programme. The elaboration of this work took about 2 years and the estimated cost was 3000 euros excluding salaries. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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Toribio, ReneAutor o CoautorDiversity in Viral Anti-PKR Mechanisms: A Remarkable Case of Evolutionary Convergence
Publicado en:Plos One. 6 (2): e16711- - 2011-01-01 6(2), DOI: 10.1371/journal.pone.0016711
Autores: Domingo-Gil, Elena; Toribio, Rene; Luis Najera, Jose; Esteban, Mariano; Ventoso, Ivan;
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Resumen
Most viruses express during infection products that prevent or neutralize the effect of the host dsRNA activated protein kinase (PKR). Translation of Sindbis virus (SINV) mRNA escapes to PKR activation and eIF2 phosphorylation in infected cells by a mechanism that requires a stem loop structure in viral 26S mRNA termed DLP to initiate translation in the absence of functional eIF2. Unlike the rest of viruses tested, we found that Alphavirus infection allowed a strong PKR activation and eIF2 alpha phosphorylation in vitro and in infected animals so that the presence of DLP structure in mRNA was critical for translation and replication of SINV. Interestingly, infection of MEFs with some viruses that express PKR inhibitors prevented eIF2 alpha phosphorylation after superinfection with SINV, suggesting that viral anti-PKR mechanisms could be exchangeable. Thus, translation of SINV mutant lacking the DLP structure (Delta DLP) in 26S mRNA was partially rescued in cells expressing vaccinia virus (VV) E3 protein, a known inhibitor of PKR. This case of heterotypic complementation among evolutionary distant viruses confirmed experimentally a remarkable case of convergent evolution in viral anti-PKR mechanisms. Our data reinforce the critical role of PKR in regulating virus-host interaction and reveal the versatility of viruses to find different solutions to solve the same conflict.
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Impacto bibliométrico. Análisis de la aportación y canal de difusión
El trabajo ha sido publicado en la revista Plos One debido a la progresión y el buen impacto que ha alcanzado en los últimos años, según la agencia WoS (JCR), se ha convertido en una referencia en su campo. En el año de publicación del trabajo, 2011, se encontraba en la posición 12/85, consiguiendo con ello situarse como revista Q1 (Primer Cuartil), en la categoría Biology.
Desde una perspectiva relativa, y atendiendo al indicador del impacto normalizado calculado a partir del Field Citation Ratio (FCR) de la fuente Dimensions, arroja un valor de: 1.79, lo que indica que, de manera comparada con trabajos en la misma disciplina y en el mismo año de publicación, lo ubica como trabajo citado por encima de la media. (fuente consultada: Dimensions Jul 2025)
De manera concreta y atendiendo a las diferentes agencias de indexación, el trabajo ha acumulado, hasta la fecha 2025-07-26, el siguiente número de citas:
- WoS: 14
- Scopus: 19
- Europe PMC: 10