RIG-I like receptor sensing of host RNAs facilitates the cell-intrinsic immune response to KSHV infection

Yang Zhao, Xiang Ye, William Dunker, Yu Song and John Karijolich ()
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Yang Zhao: Vanderbilt University School of Medicine
Xiang Ye: Vanderbilt University School of Medicine
William Dunker: Vanderbilt University School of Medicine
Yu Song: Vanderbilt University School of Medicine
John Karijolich: Vanderbilt University School of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract The RIG-I like receptors (RLRs) RIG-I and MDA5 are cytosolic RNA helicases best characterized as restriction factors for RNA viruses. However, evidence suggests RLRs participate in innate immune recognition of other pathogens, including DNA viruses. Kaposi’s sarcoma-associated herpesvirus (KSHV) is a human gammaherpesvirus and the etiological agent of Kaposi’s sarcoma and primary effusion lymphoma (PEL). Here, we demonstrate that RLRs restrict KSHV lytic reactivation and we demonstrate that restriction is facilitated by the recognition of host-derived RNAs. Misprocessed noncoding RNAs represent an abundant class of RIG-I substrates, and biochemical characterizations reveal that an infection-dependent reduction in the cellular triphosphatase DUSP11 results in an accumulation of select triphosphorylated noncoding RNAs, enabling their recognition by RIG-I. These findings reveal an intricate relationship between RNA processing and innate immunity, and demonstrate that an antiviral innate immune response can be elicited by the sensing of misprocessed cellular RNAs.

Date: 2018
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DOI: 10.1038/s41467-018-07314-7

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