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SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

The recurring dangers of cross-species viral infections have focused attention on the significance of nonspecific membrane interactions in viral replication. Orynbayeva et al. (p. 1140-1147) used new chromatic vesicle and cell assays to investigate the binding and penetration of vaccinia virus into lipid bilayers. The results emphasize the role of specific lipid molecules and lipid domains in promoting binding and insertion of virions. This work highlights the potential of new chromatic platforms for studies of virus interactions with the cell surface.

A Severe Acute Respiratory Syndrome Coronavirus Membrane Protein Accelerates Viral Replication

The severe acute respiratory syndrome coronavirus (SARS-CoV) encodes a novel 63-residue membrane protein, protein 6, that functions as a virulence factor, increasing the neuropathogenicity of a related murine coronavirus. Tangudu et al. (p. 1220-1229) report that protein 6 colocalizes on intracellular membranes with replicating murine coronavirus RNAs and replicase-associated proteins and also coimmunoprecipitates with viral RNAs. The presence of protein 6 correlates strikingly with increased viral RNA synthesis. These findings suggest that SARS-CoV protein 6 creates intracellular environments fostering robust coronavirus RNA-dependent RNA synthesis, a feature that may explain its capacity to increase virulence in mice.

The ERK Signal Transduction Pathway Mediates Cellular Toxicity by the Ebola Virus Glycoprotein

Ebola virus causes damage to cells by high-level expression of the viral glycoprotein (GP), but the mechanism responsible for this effect was previously unknown. Zampieri et al. (p. 1230-1240) now show that the activity of ERK-2 kinase is reduced by the GP. Expression of a dominant-negative ERK-2 mutant or small interfering RNA-mediated knockdown of ERK-2 potentiated GP-induced toxicity, while constitutively active ERK-2 protected against this effect, implicating the ERK pathway as a mediator of Ebola virus cytopathicity. This study provides insight into the molecular events in Ebola virus pathogenesis and suggests potential cellular targets to ameliorate disease.

Nef Promotes Evasion of Proteasome-Dependent Restriction by Human Immunodeficiency Virus Type 1

The multifunctional accessory protein Nef enhances human immunodeficiency virus type 1 (HIV-1) infectivity by a mechanism that is poorly defined despite intensive study. Qi and Aiken (p. 1534-1536) report that treatment of cells with proteasome inhibitors selectively enhances their permissiveness to infection by Nef-defective HIV-1. These findings suggest that Nef promotes infection by reducing the susceptibility of the HIV-1 core to proteasomal degradation in target cells.

Immune Responses Induced by Adenovirus via TLR9 Recognition

Adenovirus induces a potent innate immune response following systemic administration in vivo, hampering its efficacy as a gene delivery vector. Mechanisms involved in innate immune activation by adenovirus have remained elusive. Iacobelli-Martinez and Nemerow (p. 1305-1312) now demonstrate a role for adenovirus DNA-TLR9 interactions in the induction of type I interferons (IFNs) by human plasmacytoid dendritic cells. Interestingly, adenovirus serotypes that use CD46 for cell attachment induce more-potent IFN responses than CAR-utilizing adenovirus serotypes, revealing a role for specific receptor-mediated entry pathways in TLR9 activation.

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