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Review

Review Review articles synthesize the best available evidence on a topic relevant to the pathogens community.

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The Battle between Rotavirus and Its Host for Control of the Interferon Signaling Pathway

  • Michelle M. Arnold,

    Affiliation: Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

    Current address: Department of Microbiology and Immunology, Louisiana State University Health Sciences Center - Shreveport, Shreveport, Louisiana, United States of America

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  • Adrish Sen,

    Affiliation: Department of Medicine and Microbiology and Immunology, Stanford University, Stanford, California, and VA Palo Alto Health Care System, Palo Alto, California, United States of America

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  • Harry B. Greenberg,

    Affiliation: Department of Medicine and Microbiology and Immunology, Stanford University, Stanford, California, and VA Palo Alto Health Care System, Palo Alto, California, United States of America

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  • John T. Patton mail

    jpatton@niaid.nih.gov

    Affiliation: Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Published: January 24, 2013
  • DOI: 10.1371/journal.ppat.1003064

Reader Comments (1)

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Cited evidence does not support a role for NSP1 in rotavirus inhibition of STAT 1 nuclear accumulation

Posted by bcoulson on 29 Jan 2013 at 04:35 GMT

We originally reported our discovery of the ability of rotaviruses to inhibit the nuclear accumulation of STAT 1 and STAT 2 in 2009 [1]. In this 2013 review by M. Arnold and associates, it is stated at the bottom of column 1 on page 5 that this suppression of STAT 1 signalling we originally reported would seem likely to be mediated by the rotavirus non-structural protein NSP1. However, our experiments showed that NSP1 expressed alone did not affect IFN-induced gene expression in a reporter system [1], and no other reports on this subject have since been published. Thus, the published evidence does not support a role for NSP1 in the rotavirus inhibition of STAT 1 nuclear accumulation that was originally observed.

We suggest that the text be amended in a manner similar to the following:

Also worth noting is a study showing that rotavirus suppresses IFN signalling by inhibiting STAT1 nuclear accumulation [58]. The viral mediator of this effect has not been identified, although NSP1 does not appear to have a major role based on the studies reported to date [58].

1. Holloway G, Truong TT, Coulson BS (2009) Rotavirus antagonizes cellular antiviral responses by inhibiting the nuclear accumulation of STAT1, STAT2, and NF-kappaB. J Virol 83: 4942-4951.

No competing interests declared.