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Journal of Virology, May 2008, p. 4193, Vol. 82, No. 9
0022-538X/08/$08.00+0     doi:10.1128/JVI.00534-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Many viruses interfere with host-cell translation through enzyme-catalyzed destruction of key regulatory molecules. One common mechanism is the targeted cleavage of poly(A)-binding protein (PABP), a central regulator of translation. Ilkow et al. (p. 4284-4294) now report a novel, nonenzymatic mechanism by which rubella virus capsid blocks translation by sequestering PABP into nonfunctional complexes. Moreover, because PABP sequestration can occur only when capsid levels are relatively high (late in infection), this process also may enhance assembly of nucleocapsids by blocking further translation of the viral genome.

Herpes Simplex Virus Replication Requires Cellular Phosphatase cdc25C

Herpes simplex virus 1 (HSV-1) activates the mitotic kinase, cdc2, in an ICP22-dependent manner to facilitate the expression of a subset of 2 (late-late) viral genes. The cellular phosphatase, cdc25C, is the cdc2 activator. Smith-Donald et al. (p. 4527-4532) show that cdc25C is required for HSV-1 replication and performs an essential function in addition to activating the ICP22-dependent pathway. Smith-Donald and Roizman (p. 4533-4543) show that cdc25C interacts with ICP22 and that each is phosphorylated by the viral kinases U_S3 and U_L13. Thus, HSV-1 targets and redirects the cell-cycle machinery to achieve its replication.

Novel Strategy of Type I Interferon Inhibition in Severe Acute Respiratory Syndrome Coronavirus Infection

Severe acute respiratory syndrome (SARS) coronavirus nonstructural protein 1 (nsp1) suppresses host gene expression by inhibiting translation and promoting mRNA degradation. Using a SARS coronavirus mutant carrying an altered nsp1 gene, Narayanan et al. (p. 4471-4479) have demonstrated a novel mechanism utilized by nsp1 to suppress host gene expression, including type I interferon production, in infected cells. This work highlights a critical role for nsp1 in the evasion of host interferon responses and SARS coronavirus virulence.

Papillomavirus Conformational Changes Revealed by Neutralizing Antibodies

Day et al. (p. 4638-4646) examine the dynamics of papillomavirus interactions with the cell surface. They report that exposure of broadly cross-neutralizing epitopes of the papillomavirus minor capsid protein requires a furin-cleavage-dependent conformational change. Engagement of these epitopes by anti-L2 antibodies caused virus to be released from the cell surface. The dominant class of L1-specific neutralizing antibodies, generated after virus-like particle vaccination, inhibits the conformational change required for exposure of the L2 neutralizing epitope. These findings have implications for both the evolution of human papillomavirus (HPV) serotypes and the efficacy of current and future HPV vaccines.

Multiple Molecular Clocks for Poliovirus

The rapid poliovirus evolution rate of more than 10^–2 total nucleotide substitutions per site per year facilitates high-resolution evolutionary and epidemiologic studies. However, the saturation of total nucleotide substitutions obscures relationships beyond 20 years of total evolutionary separation. Jorba et al. (p. 4429-4440) resolved different categories of nucleotide substitution into the poliovirus capsid region to calibrate five different molecular clocks whose particular rates of substitution extend over a 30-fold range. The slower molecular clocks can be used to explore deeper evolutionary relationships within and across poliovirus genotypes.

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