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Access through your institution Buy or subscribe Type I interferons have critical antiviral functions, but their main cellular targets are unclear. In _PLOS Pathogens_, Diamond and

colleagues use conditional deletion of the receptor for type I interferons (IFNAR) to determine the key cells that require signaling via type I interferons to mediate resistance to infection

with West Nile Virus (WNV). As expected, germline deletion of IFNAR leads to rapid death after WNV infection but, unexpectedly, conditional deletion of IFNAR specifically in dendritic

cells, granulocytes, macrophages or monocytes results in an equally severe pathology. The morbidity of WNV-infected mice with germline or conditional deletion of IFNAR is due to sepsis and

includes elevated viral loads and cytokine production by IFNAR-deficient cells. The signaling adaptor MAVS is at the vertex of several key antiviral recognition pathways, and deletion of

MAVS in conjunction with deletion of IFNAR largely normalizes cytokine production but leaves WNV loads high. The action of type I interferons in myeloid cells, therefore, is essential in

controlling the permissiveness and pathology of WNV. _PLoS Pathog._ (17 April 2014) doi:10.1371/journal.ppat.1004086 This is a preview of subscription content, access via your institution

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about institutional subscriptions * Read our FAQs * Contact customer support Authors * Zoltan Fehervari View author publications You can also search for this author inPubMed Google Scholar

RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Fehervari, Z. Interferon targets. _Nat Immunol_ 15, 537 (2014). https://doi.org/10.1038/ni.2906 Download

citation * Published: 19 May 2014 * Issue Date: June 2014 * DOI: https://doi.org/10.1038/ni.2906 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this

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