Correction for Bailey et al., J. Virol. 80 (13) 6441-6457.
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Journal of Virology, July 2006, p. 6197, Vol. 80, No. 13
0022-538X/06/$08.00+0     doi:10.1128/JVI.00918-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

IRES Aids Simian Virus 40 Structural Protein Synthesis

Late in simian virus 40 (SV40) infection, when abundant virion structural proteins are synthesized, the virus inhibits cap-dependent translation. How then are the structural proteins translated? Yu and Alwine (p. 6553-6558) have found internal ribosome entry sites (IRESs) within the mRNA for at least one of the virion structural proteins, VP3. The release of ribosomes from cap-dependent translation, coupled with the use of IRESs, may enhance translation of late mRNAs and facilitate virion structural protein synthesis at late times in infection.

The Immune Evasion Epicenter? Coxsackievirus B3 Carries Out a Coordinated Attack on the Golgi Complex To Inhibit Host Secretion

Despite replicating to very high titers within the host, coxsackieviruses do not elicit strong CD8+ T-cell responses. Several elegant studies have attempted to ascribe immune evasion to a shutoff of host protein secretion by a single viral polypeptide. In this study, Cornell et al. (p. 6637-6647) show that three viral proteins physically and functionally target the Golgi apparatus. The viral 2B and 2BC proteins move to the Golgi, where they diminish the egress of trafficking proteins. The 3A protein goes a step further; even when expressed in transfected cells, in the absence of its normal consorts, this protein travels to and almost completely disrupts the Golgi complex. This work has implications for vaccine design.

Adenovirus RID Inhibits Signaling Triggered by Lipopolysaccharide and Interleukin-1ß

The adenovirus RID protein complex induces cell surface downregulation of several receptors, including TNFR1. Delgado-Lopez and Horwitz (p. 6378-6386) describe novel pathways targeted by RID and suggest new mechanisms of RID action. RID inhibits signaling induced by lipopolysaccharide (LPS) and interleukin-1ß (IL-1ß) in addition to tumor necrosis factor alpha. However, cell surface levels of TLR4 and the IL-1 receptor are not downregulated. Although the LPS and IL-1ß pathways share many components, the extent of their inhibition by RID differs. This work expands the molecular repertoire of adenovirus to target two important inflammatory pathways, with a wide array of potential applications.

Pseudorabies Virus Suppresses the Interferon Innate Immune Response

The interferon (IFN) system serves as the front line of host defense against viral infection. Brukman and Enquist (p. 6345-6356) have found that pseudorabies virus (PRV, an alphaerpesvirus) infection of nonnatural host fibroblasts causes a decrease in the expression of a subset of antiviral genes normally induced by IFN-ß. This reduction in transcript levels is accompanied by inhibition of phosphorylation of STAT1, a transcriptional activator that functions in IFN signal transduction. The reduced transcription of particular IFN-stimulated genes may explain the invariable lethality of PRV infection across a wide variety of nonnatural hosts.

Clonal Expansion May Allow Human Immunodeficiency Virus Type 1 Persistence in Patients on Highly Active Antiretroviral Therapy

Combination therapy for human immunodeficiency virus type 1 (HIV-1) infection can reduce viremia to less than the detection limit of ultrasensitive clinical assays. However, the virus persists in latently infected CD4+ T cells, and low levels of free virus are found in the plasma. Bailey et. al. (p. 6441-6457) have analyzed this residual viremia and found that in many patients it consists of a small number of viral clones that are released over prolonged periods without evolution, possibly by cells other than circulating CD4+ T cells. This result suggests that a major mechanism of HIV-1 persistence involves clonal expansion of infected cells rather than viral replication.

Journal of Virology, July 2006, p. 6197, Vol. 80, No. 13
0022-538X/06/$08.00+0     doi:10.1128/JVI.00918-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




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