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paradoxical interplay of viral and cellular functions矛盾的相互作用的病毒和细胞功能
Viruses 2011, 3, 272-277; doi:10.3390/v3030272
OPEN ACCESS
viruses
ISSN 1999-4915
/journal/viruses
Commentary
Paradoxical Interplay of Viral and Cellular Functions
Esteban Domingo 1,2
1 Centro de Biología Molecular Severo Ochoa (CSIC-UAM), C/ Nicolás Cabrera, 1, Cantoblanco,
Madrid 28049, Spain
2 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd),
Barcelona 08036, Spain; E-Mail: edomingo@cbm.uam.es; Tel.: +34-91-1964540;
Fax: +34-91-1964420
Received: 9 February 2011; in revised form: 3 March 2011 / Accepted: 7 March 2011 /
Published: 15 March 2011
Abstract : Some cellular editing functions can restrict the replication of some viruses but
contribute to completion of the life cycle of others. A recent study has identified an
isoform of the adenosine deaminase acting on RNA type 1 (ADAR 1) as required for
embryogenesis, and as a restriction factor for a number of important RNA virus
pathogens [1]. The dual implication of key cellular functions in the innate immunity
against viruses, or, paradoxically, as mediators of virus replication is interpreted in the
light of the concept of virus-host coevolution and tinkering proposed for general evolution
by François Jacob decades ago.
Keywords: RNA virus; host-virus interaction; coevolution
1. Introduction
A recent publication by M.B. Oldstone and colleagues at the Scripps Research Institute of La Jolla
ha
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