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Journal of Virology, January 2008, p. 20, Vol. 82, No. 1
0022-538X/08/$08.00+0     doi:10.1128/JVI.02379-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Polerovirus transmission is regulated by unknown components of the receptor-mediated endocytotic pathways that the virus uses to transverse aphid gut and salivary tissues. Yang et al. (p. 291-299) compare the proteomes of F₂ aphid genotypes and identify proteins that are linked to vector competency. Four proteins specifically inherited in vector genotypes also bind to virus particles. Two of them have homology to luciferase or cyclophilin proteins, which both function in macromolecular transport. These findings are the first to link specific aphid proteins with vector capacity.

Human Cytomegalovirus Inactivates the Anaphase-Promoting Complex through Multiple Pathways

Cell-cycle dysregulation induced by human cytomegalovirus is associated with the inactivation of the anaphase-promoting complex (APC), an E3 ubiquitin ligase. Tran et al. (p. 529-537) have identified mechanisms involved in the inactivation of the APC, which include the dissociation of the complex itself, relocalization of its subunits, and modification of its activator, Cdh1. The involvement of multiple mechanisms in APC inactivation points to the importance of disabling the APC for a productive infection.

Structural Changes in Neurons in Experimental Rabies

In natural and experimental rabies, standard histopathology shows inflammatory changes but few morphological alterations in infected neurons. These observations have led to the concept that rabies virus induces neuronal dysfunction without significant structural change. Scott et al. (p. 513-521) evaluated rabies virus-infected transgenic mice expressing yellow fluorescent protein. Using a combination of epifluorescence microscopy and electron microscopy, marked abnormalities were observed in neuronal processes, including dendrites, axons, and presynaptic nerve endings. Injury to neuronal processes may therefore explain the severe clinical disease and fatal outcome in rabies.

Onset of Intestinal Epithelial Barrier Dysfunction during Primary Human Immunodeficiency Virus Infection

Gastrointestinal dysfunction and impaired mucosal defenses occur commonly in chronic human immunodeficiency virus (HIV) infection. Sankaran et al. (p. 538-545) report that disruption of the intestinal epithelial barrier develops during early HIV infection, prior to the long-term effects of HIV infection on the immune system. Rapid onset of HIV-associated intestinal epithelial barrier dysfunction during primary HIV infection may be driven by an imbalance between immune response and mucosal repair and regeneration. These findings emphasize the importance of early therapeutic intervention strategies for limiting mucosal damage.

MyD88 Is a Heavyweight in Antiviral Adaptive Immunity

Signaling pathways dependent on Toll-like receptor (TLR)/MyD88 and RIG-I-like helicase/IPS-1 are essential for innate immune responses to RNA viruses. However, the involvement of these signaling pathways in T-cell activation is poorly understood. Jung et al. (p. 196-206) demonstrate that MyD88, but not IPS-1, is required for the generation of virus-specific cytotoxic T lymphocytes in response to lymphocytic choriomeningitis virus (LCMV) infection by regulating type I interferon production in plasmacytoid dendritic cells. These findings highlight the importance of TLRs in mounting adaptive immunity to LCMV.

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content