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SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Picornavirus 3CD proteins are multifunctional proteins, serving as proteases, as precursors to the viral 3C protease and 3D RNA-dependent RNA polymerase, and as RNA-binding proteins that regulate many essential processes during viral infection. Marcotte et al. (p. 3583-3596) have determined the structure of poliovirus 3CD. The structure strongly suggests that 3CD autoprocessing is intermolecular, provides insights into why 3CD lacks polymerase activity, and, together with mutational data, suggests models for how interactions of 3CD with 3D^pol up-regulate cre-dependent uridylylation of genome-linked protein VPg.

The Transcriptional Coactivator ALY Functions on a Viral Enhancer

Type B leukemogenic virus (TBLV), a strain of mouse mammary tumor virus that causes lymphomas in mice, contains a T-cell-specific enhancer within its long terminal repeat. Mertz et al. (p. 3503-3513) show that enhancer activity is elevated by ALY, a transcriptional coactivator that elevates RUNX1 activity on cellular enhancers but also has a role in RNA export. ALY synergizes with both RUNX1 and c-Myb on the TBLV enhancer, demonstrating for the first time that ALY functions on a viral enhancer to increase the activity of several transcription factors. These data suggest a central role for ALY in T-cell enhancer function.

Adenovirus IVa2 Protein Nucleates Encapsidation of Viral DNA

The adenovirus IVa2 protein is present in at least two complexes that bind to the packaging sequence of the viral chromosome, implicating this protein in the encapsidation process. The mechanism by which IVa2 facilitates this process is not clear. Tyler et al. (p. 3447-3454) report the purification of IVa2 and an analysis of its interaction with the packaging sequence. The findings demonstrate that IVa2 assembles into a multisubunit complex on the DNA. This work supports a model by which IVa2 nucleates encapsidation.

The Mimivirus Genome Encodes a Novel Eukaryotic Transporter Protein

Mitochondrial carrier proteins have been found to date only in eukaryotes, where they transport compounds across the mitochondrial inner membrane to link the metabolic pathways of the cytosol and the mitochondrial matrix. Monné et al. (p. 3181-3186) report a novel mitochondrial carrier in the genome of the giant virus, Mimiviridae mimivirus, and show that the protein transports dATP and dTTP. Because the enormous 1.2-megabase mimivirus genome is rich in adenine and thymine nucleotides, the virus may be using this protein to target the host mitochondria as an additional source of deoxynucleotides necessary for its replication.

Disorganization of the Cellular Cytoskeleton by the Rotavirus Enterotoxin

Rotavirus is a major cause of childhood gastroenteritis. Expression of the rotavirus enterotoxin NSP4 alone or during rotavirus infection of cells induces an increase in intracellular calcium. Berkova et al. (p. 3545-3553) show that this increase in intracellular calcium leads to reorganization of the actin cytoskeleton by altering the activation state of the actin polymerizing protein, cofilin. Activated cofilin leads to an increase in cellular F-actin content in both NSP4-expressing cells and rotavirus-infected cells. In this manner, the rotavirus enterotoxin is similar to bacterial toxins that cause calcium-dependent cytoskeletal disorganization.

A Type I Interferon Response Characterizes T Cells in Progressive Human Immunodeficiency Virus Type 1 Infection

The molecular basis of peripheral T-cell dysfunction in human immunodeficiency virus type 1 (HIV-1) infection is currently unknown. Through transcriptional profiling of pure CD4⁺ and CD8⁺ T-cell populations from HIV-1-infected patients at various stages of disease, Hyrcza et al. (p. 3477-3486) demonstrate that both T-ell subsets show a persistent interferon response. This state appears as early as 2 months following acute infection and persists for years afterwards. However, this response is absent in long-term nonprogressors. Thus, a chronic interferon response may be a hallmark of T-cell dysfunction in progressive HIV-1 infection.

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