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Journal of Virology, April 2008, p. 3813, Vol. 82, No. 8
0022-538X/08/$08.00+0     doi:10.1128/JVI.00383-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Varicella-zoster virus (VZV) is a neurotropic human herpesvirus. Reichelt et al. (p. 3971-3983) used correlative confocal and EM analysis of VZV-infected human dorsal root ganglia xenografts in the SCIDhu mouse model to investigate infection of both neurons and satellite cells and cell-cell fusion in neuron-satellite cell complexes in vivo. Satellite cell infection and polykaryon formation were shown to provide mechanisms to amplify VZV entry into neuronal cell bodies, which is necessary for VZV transfer to skin in the affected dermatome during herpes zoster infection. These mechanisms of VZV neuropathogenesis help to account for the often severe neurologic consequences of herpes zoster.

A Transcriptional Enhancer Identified for the First Time in Coronaviruses

In transmissible gastroenteritis coronavirus, transcription is mainly regulated by base pairing between leader and gene transcription-regulating sequences, with the notable exception of subgenomic (sg) mRNA N. Moreno et al. (p. 3882-3893) show that complementarity between two distant 9-nucleotide elements upstream of the N gene increases the accumulation of sg mRNA N. This work describes for the first time in coronaviruses a long-distance RNA-RNA interaction regulating transcriptional activity, specifically enhancing the transcription of a single gene.

Insight into Mechanisms of Human Epithelial Cell Immortalization by Human Papillomavirus Type 16 E6

Human papillomavirus type 16 (HPV-16) E6 is proposed to contribute to immortalization of human epithelial cells by degradation of p53 and induction of telomerase. The requirement for p53 inactivation has been debated. Another E6 target is the hAda3 protein, a p53 coactivator and component of histone acetyltransferase complexes. Shamanin et al. (p. 3912-3920) characterized immortalization-competent HPV-16 E6 mutants for the capacity to degrade p53 and hAda3. The findings suggest that inactivation of the p14ARF-p53 pathway by E6-mediated degradation of p53 or hAda3 or by cellular adaptation is essential for human epithelial cell immortalization.

Human Immunodeficiency Virus Release Is Enhanced by Modulation of Cell Adhesion Complexes

Several human immunodeficiency virus type 1 (HIV-1) regulatory proteins interact with ubiquitin ligase complexes. Salim and Ratner (p. 3932-3938) demonstrate that the HIV-1 Vpu protein diverts the SCF β-TrCP-associated ubiquitin ligase complex from the transcriptional repressor Snail, resulting in depressed levels of both total and β-catenin-associated E-cadherin cell-adhesion complexes, leading to enhanced virus release. Since E-cadherin is expressed in dendritic cells and macrophages, but not T cells, these findings suggest that the HIV-1 vpu gene may have evolved to counteract different restrictions to assembly in different cell types.

ICAM-1 Helps West Nile Virus Enter the Brain

Understanding how West Nile virus crosses the blood-brain barrier is essential to understanding the pathogenesis of West Nile encephalitis. Dai et al. (p. 4164-4168) show that ICAM-1, a molecule critical for leukocyte trafficking into the central nervous system, plays a role in this disease. In comparison to wild-type mice, ICAM-1-deficient mice are resistant to lethal West Nile encephalitis. Targeting ICAM-1 signaling may help control West Nile encephalitis.

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