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Journal of Virology, March 2006, p. 2075, Vol. 80, No. 5
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.5.2075.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Diverse mechanisms are used by single-stranded RNA viruses to initiate RNA synthesis. Deng et al. (p. 2337-2348 ) show that the mechanism of RNA replication initiation differs for influenza virus vRNA and cRNA promoters. Initiation occurs internally on the cRNA promoter, resulting in the synthesis of a dinucleotide that realigns with the terminal residue, whereas initiation is terminal on the vRNA promoter. Such a mechanism might have evolved to maintain genome integrity and may operate in other RNA viruses.

Activity of Autographa californica Multiple Nucleopolyhedrovirus (AcMNPV) in Mammalian Cells

Baculovirus has been used as a biopesticide and a gene-transfer vector in insect and mammalian cells. Fujita et al. (p. 2390-2395) provide evidence that AcMNPV is capable of expressing some viral genes at the transcription level in mammalian cells through the usual pathway of infection. These results emphasize the significance of studying the molecular details of baculovirus-mammalian cell interactions to facilitate the use of baculoviruses in the agrobiological, pharmaceutical, and medical fields.

Vesicular Stomatitis Virus Mutant Stimulates Myeloid Dendritic Cells

Wild-type (wt) vesicular stomatitis virus (VSV) induces innate immune responses by activating plasmacytoid dendritic cells (DC) through Toll-like receptor 7 (TLR7). Ahmed et al. (p. 2194-2205) show that a matrix (M) protein mutant of VSV stimulates maturation of myeloid DC, which do not express TLR7, and thus has the potential to activate a broader population of DC than wt VSV. These data support the utility of M protein mutants as therapeutic agents for antitumor therapies and vaccines due to their capacity to induce maturation of several DC subsets, leading to the efficient activation of T cells.

A New West Nile Virus Vaccine Candidate Based on Inhibition of Interferon Antagonism

Targeted disruption of viral antagonism of the host interferon (IFN) response is emerging as a promising approach for the development of attenuated viral vaccines. Liu et al. (p. 2396-2404) show that a single amino acid substitution in the nonstructural protein, NS2A, of the Australian subtype of West Nile virus (Kunjin), abolishes viral inhibition of IFN induction and attenuates viral virulence in mice. Despite its attenuation, immunization of mice with the mutant Kunjin virus provided complete protection against lethal challenge with the pathogenic New York 99 strain of West Nile virus. This work illustrates the importance of the host IFN response in determining the outcome of flavivirus infection and establishes a novel approach for the development of live-attenuated flavivirus vaccines.

Efficient Neuronal Infection by Microsome-Associated Prions

The mechanisms by which transmissible spongiform encephalopathy (TSEs) agents, or prions, infect cells are unknown. Baron et al. (p. 2106-2117) use a new neuronal cell model of TSE infection to show that infection with microsome-associated PrP-res, the disease-specific isoform of prion protein, is much more efficient than that with purified, membrane-free PrP-res. This work provides evidence that association of PrP-res with membranes, perhaps acting with other microsomal components, facilitates intercellular transfer of PrP-res and TSE infectivity.

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