Dengue Virus by Timothy P. Endy, In-Kyu Yoon, Mammen P Mammen (auth.), Alan

By Timothy P. Endy, In-Kyu Yoon, Mammen P Mammen (auth.), Alan L. Rothman (eds.)

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42 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Abstract Dengue virus is sensed in mammalian cells by Toll-like receptors and DExD/H box RNA helicases, triggering a Type 1 interferon response. Interferon acts upon infected and noninfected cells by stimulating the JAK/STAT signaling pathway resulting in the activation of interferon stimulated genes that lead cells toward the establishment of an antiviral response.

Harris et al. 2005a), supporting the idea that reduction of RNA synthesis contributes to attenuation of DENV1 and DENV4 vaccine strains that harbor the same deletion (Durbin et al. 2006; Durbin et al. 2005; Whitehead et al. 2003). At the very 30 terminus of the DENV genome, the highly stable and conserved DENV 30 SL plays a pivotal role in viral RNA synthesis. Mutations that altered the secondary structure of the top half of the DENV2 30 SL drastically reduced negative-strand RNA synthesis (Zeng et al.

Interestingly, mutations in the cHP have recently been shown to abolish RNA synthesis (Clyde et al. 2008), indicating a requirement for this element in translation and RNA synthesis. Sequences and structures within the DENV 30 UTR play a pivotal role in regulating negative strand RNA synthesis, which initiates at the 30 terminus of the genome. At the 50 end of the 30 UTR, deletion of the variable region (VR) in a DENV2 replicon reduced RNA synthesis in BHK cells but had no impact on RNA synthesis in C6/36 mosquito cells (Alvarez et al.

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