Double-Stranded RNA Is Produced by Positive-Strand RNA Viruses and DNA Viruses but Not in Detectable Amounts by Negative-Strand RNA Viruses

By F. Weber, V. Wagner, Simon B. Rasmussen, R. Hartmann, S. Paludan. Journal of Virology, 2006

934 citations recorded by the source corpus.

Subfields: Cancer Research, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7ec61a333a6c0afe2e51ff2d05f7e2430af3d5f6

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Citations in the corpus

An evolving arsenal: viral RNA detection by RIG-I-like receptors (2014, background): “Compounding this effect, negative strand viruses such as HTNV and CCHV do not produce substantial amounts of dsRNA [40,41], thereby eluding MDA-5 detection.”
Recognition of 5′-triphosphate by RIG-I helicase requires short blunt double-stranded RNA as contained in panhandle of negative strand virus (2009, positive): “However, in the life cycle of negative strand RNA viruses, such double-stranded RNA is absent (Pichlmair et al., 2006; Weber et al., 2006), and 5′triphosphate single-stranded RNA seems the prime RIG-I ligand.”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, result): “This is in agreement with the recent finding that dsRNA accumulates in the cytoplasm during infection of permissive cells with DNA viruses, including HSV, and thus represents a potential ligand for cytosolic dsRNA receptors (380).”
RNA recognition and signal transduction by RIG‐I‐like receptors (2009, background): “Indeed, the production of abundant double-stranded replication intermediates was observed in EMCV-infected cells (64).”
SARS-Coronavirus Replication Is Supported by a Reticulovesicular Network of Modified Endoplasmic Reticulum (2008, background): “Thus, the isolated RTC appears to be protected by at least one membrane, a conclusion also drawn from similar biochemical studies on flavivirus RTCs, leading to an alternative model [42] in which flavivirus VPs would be “topologically similar” to coronavirus VPs and consist of a closed inner vesicle”
Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “Furthermore, even though dsRNA is present in very low amounts in cells infected with negative-strand RNA viruses, including influenza virus (Weber et al., 2006), the NS1 protein of influenza virus has a dsRNA-binding motif (Lu et al., 1995).”
5′-triphosphate RNA requires base-paired structures to activate antiviral signaling via RIG-I (2009, background): “The observation that viral infections recognized by RIG-I are specifically characterized by the lack of high amounts of long ( 20 bp) dsRNA in infected cells hints that our short model ligands might indeed be in the size range of natural viral ligands of RIG-I (10, 23).”
Viral evasion and subversion of pattern-recognition receptor signalling (2008, background): “Even DNA viruses can produce considerable amounts of dsRNA owing to convergent transcription (that is, when two adjacent open reading frames are transcribed at opposite directions, resulting in a partial 3′ overlap between their transcripts 62 .”
Innate Immunity to Virus Infection (2009, background): “EMCV produces high levels of dsRNA in infected cells, whereas dsRNA was barely detected in influenza virusinfected cells (28, 31).”
Inhibition of Retinoic Acid-Inducible Gene I-Mediated Induction of Beta Interferon by the NS1 Protein of Influenza A Virus (2006, background): “Third, dsRNA is likely not to be the only molecule produced during viral infection to trigger the IFN system; in fact, little dsRNA is detected in cells infected with influenza viruses (53).”
Cytosolic Sensing of Viruses (2013, background): “Picornaviruses are sensed by MDA5 and produce abundant dsRNA during infection (Pichlmair et al., 2009; Weber et al., 2006) (Table S1).”
The multifunctional NS1 protein of influenza A viruses. (2008, background): “However, dsRNA has yet to be detected in influenza A virusinfected cells (Weber et al., 2006), and it is now evident that unique components of the influenza virus ssRNA genome can be directly recognized by the cytoplasmic pathogen sensor, RIG-I (Pichlmair et al.”