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Journal of Virology, November 2006, p. 10291-10292, Vol. 80, No. 21
0022-538X/06/$08.00+0     doi:10.1128/JVI.01951-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Human respiratory syncytial virus (HRSV), the main viral cause of pediatric pneumonia, is distinct from other paramyxoviruses in a number of ways. Oomens et al. (p. 10465-10477) demonstrate yet another distinctive feature of HRSV by showing that, in contrast to measles virus and simian virus 5, the cytoplasmic tail (CT) of the fusion protein F is critically important for infectious progeny production and that deletion of the CT alters F protein cellular distribution and abolishes lipid raft interaction. These results point to the F protein CT-lipid raft interaction as an early and critical step in the HRSV assembly process and therefore a potential target for therapeutic intervention.

Rotavirus NSP5 and RNA Bind at the Same Site on the NSP2 Doughnut

Viroplasms formed during viral infection provide exclusive sites for genome replication and particle assembly. Little is known about how these processes are coordinated within viroplasms. Rotavirus viroplasms form by expression of the nonstructural proteins NSP2 and NSP5. Subnanometer resolution cryoelectron microscopic analyses of these components by Jiang et al. (p. 10829-10835) localize the binding sites of NSP5 and RNA on the outside of the doughnut-shaped NSP2 octamer and suggest that the phosphoprotein NSP5 regulates NSP2-RNA interactions. This regulatory function, coupled to its phosphorylation, may provide a temporal switch to control processing of the viral transcripts during genome replication.

Functional Asymmetry in a Parvovirus Left-End Telomere Is Essential for Infectivity

While rolling hairpin DNA replication usually generates palindromic hairpin telomeres in two inverted sequence orientations, members of the genus Parvovirus have evolved an elaborate means of maintaining a single form of their left end. Burnett et al. (p. 10879-10883) use a reverse genetics strategy to disrupt this arrangement and show that the underlying asymmetry is essential for infectivity. Viable, second-site mutants regain asymmetric function in ways that suggest that the mechanism exists to prevent establishment of an active origin on the promoter-proximal arm of the hairpin.

Latent Cytomegalovirus under Tight Immune Surveillance

Recurrence of cytomegalovirus infection by reactivation from latency is a health risk in immunocompromised allograft recipients. Simon et al. (p. 10436-10456) elucidate the earliest molecular event in viral transcriptional reactivation and its sensing by CD8⁺ T lymphocytes preventing the completion of the productive infectious cycle in the immunocompetent host. Latency is identified as a dynamic state during which perpetual events of local gene desilencing in the latent viral genome result in the presentation of antigenic viral peptides to tissue-patrolling, epitope-specific, effector-memory T cells that terminate the reactivation attempt. The authors propose the existence of backup control by multiple, sequentially-ordered immunological checkpoints.

Human Immunodeficiency Virus Type 1 Vpr Causes Replication Stress in Infected CD4⁺ T Lymphocytes In Vitro and In Vivo

Vpr, a small protein encoded by human immunodeficiency virus type 1 (HIV-1), causes blockade of the cell cycle in the G₂ phase by activating ATR kinase. Zimmerman et al. (p. 10407-10418) have isolated peripheral blood lymphocytes from infected individuals and now demonstrate that infected cells in vivo are, indeed, arrested in G₂. The authors also provide evidence that primary CD4⁺ T lymphocytes, but not monocyte-derived macrophages, express ATR. This differential expression of ATR may help explain why infected CD4⁺ T lymphocytes are highly sensitive to the cytopathic effect of HIV-1, whereas macrophages can sustain viral infection for longer periods of time while remaining viable.

Molecular Signature of Influenza Virus-Infected Macaques

A multilevel macaque model of the pathogenesis of human influenza virus infection has been developed through integration of functional genomics with clinical observations, ancillary analyses, and pathology. Baas et al. (p. 10813-10828) present data suggesting the strong effect of even limited viral replication on infected and surrounding pulmonary tissues at the transcriptional and translational level, with an effect detectable in peripheral blood as early as 2 days postinfection. This important multifaceted approach will serve as a template for studies of host responses to more pathogenic influenza viruses in isolated tissues and in the intact host.

Elucidating the Molecular Evolution of Hepatitis B Virus by Investigation of Longitudinal Paired Sera over a 25-Year Period

The longitudinal molecular evolution of hepatitis B virus (HBV) is difficult to determine due to HBV genomic complexity and the need to study paired samples collected over long periods of time. Osiowy et al. (p. 10307-10314) investigated paired sera collected in 1979 and 2004 from eight HBeAg-negative, asymptomatic carriers, thus providing a unique opportunity to document the long-term molecular evolution of HBV. The results suggest that HBV sequence divergence occurs more rapidly than previously estimated and is dependent on the host immune phase.

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