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A remarkably wide variety of human neurotrophic viruses—ranging from her-pes simplex 1 (HSV-1; Herpesviridae; dsDNA genome) to Hantavirus (HTV; Bunyaviridae; (−)ssRNA genome) to human immunodeficiency virus (HIV; Retroviridae; (+)ssRNA genome) are asso-ciated with the rapid up-regulation of the NF-kB-sensitive pro-inflammatory microRNA-146a (miRNA-146a) in the host shortly after infection. This signifi-cant miRNA-146a up-regulation appears to be beneficial to the infecting virus as part of an immune-evasion strategy. Interestingly, miRNA-146a is also signif-icantly up-regulated in several human central nervous system (CNS) disor-ders. These include Alzheimer’s disease (AD) and prion disease where miRNA-146a participates in pro-inflammatory and innate-immune signaling. This opinion paper will comment on some recently clarified roles for the NF-kB-regulated, pro-inflammatory miRNA-146a in viral-induced cellular dysfunction, and how anti-miRNA-146a and/or related therapeutic strategies may be benefi-cial in the clinical management of a broad spectrum of viral-mediated CNS disease. The 22 nucleotide, non-coding, sin-gle stranded RNA (ssRNA) miRNA-146a
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Hill et al. (2015) studied this question.
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