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Journal of Virology, November 2006, p. 10907-10908, Vol. 80, No. 22
0022-538X/06/$08.00+0     doi:10.1128/JVI.02071-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

The class II fusion proteins of alphaviruses and flaviviruses contain a membrane-proximal stem region predicted to be important in fusion protein rearrangement and membrane fusion. Using the alphavirus Semliki Forest virus, Liao and Kielian (p. 11362-11369) show that the stem plays a role in virus assembly. Surprisingly, however, the conserved length and specific sequence of the stem are not required for membrane fusion. This work reveals a new function for the alphavirus stem and provides important information about potential strategies to inhibit class II membrane fusion reactions.

Recoating Genetics for Rotavirus

Rotavirus lacks an efficient reverse genetics system. Trask and Dormitzer (p. 11293-11304) show that adding recombinant outer-capsid proteins to authentic rotavirus subviral particles increases their infectivity by a factor of 10⁷, yielding recoated particles as infectious as purified virions. The spike protein, VP4, must be added before the shell protein, VP7, to produce highly infectious particles. Strict dependence on VP4 concentration indicates that in vitro assembly requires low affinity VP4-VP4 interactions. This system will allow efficient production of infectious particles with recombinant outer-capsid proteins to study membrane penetration by this nonenveloped virus.

Casein Kinase I- Is Important for Hepatitis C Virus NS5A Hyperphosphorylation

Hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is heavily phosphorylated. A switch between a basally phosphorylated form and a hyperphosphorylated form of NS5A appears to regulate HCV replication. Quintavalle et al. (p. 11305-11312) show that the isoform of the casein kinase I (CKI) family of kinases is required for NS5A hyperphosphorylation. Moreover, attenuation of CKI- expression inhibits production of HCV RNA. These findings suggest that CKI- might serve as a new target for therapeutic intervention against HCV infection.

African Swine Fever Virus Slows Membrane Transport

African swine fever virus (ASFV) causes loss of the trans-Golgi network (TGN), an organelle essential for protein transport and secretion. Netherton et al. (p. 11385-11392) show that ASFV infection markedly reduces the rate of protein delivery to the plasma membrane, including newly synthesized major histocompatibility complex class 1 proteins. These findings suggest that disruption of vesicular transport at the TGN provides ASFV with a mechanism to diminish surface expression of important immune surveillance molecules, which may serve as a mechanism to evade host immune responses.

Heat Shock Protein Influences Measles Virus Virulence

The major inducible 70-kDa heat shock protein (hsp72) exhibits a dynamic range of expression under physiological conditions and is increased after fever. Although 70-kDa heat shock proteins are required for replication of several DNA and RNA viruses, nothing is known about how variability in this virus-host interaction influences the outcome of in vivo infection. Carsillo et al. (p. 11031-11039) show that elevated levels of hsp72 in neurons increase measles virus (MV) neurovirulence in a mouse model, an effect mediated by the stimulation of viral transcription by hsp72. Thus, viral transcriptional responsiveness to hsp72 is an important determinant of MV virulence.

Immune Response to Adenovirus Starts from the Very Beginning

Adenovirus-derived vectors for gene transfer, even those devoid of all residual viral genes, are known to activate a complex immune response that limits transgene expression. A role for viral capsid proteins has been suspected, but the mechanism is not known. Tamanini et al. (p. 11241-11254) provide evidence that the innate immune response starts from the initial binding of the adenovirus fiber to the coxsackievirus and adenovirus receptor. In addition to suggesting a new role for this receptor, these findings should foster design of improved adenovirus-based, gene-transfer vectors that will induce diminished inflammatory responses.

Vaccination against Influenza by Using an NS1-Truncated Modified Live-Virus Vaccine

A vaccine inducing cross-protective immunity between different subtypes and genetic variants of influenza virus is highly desirable. Richt et al. (p. 11009-11018) demonstrate the efficacy of an NS1-truncated, live-attenuated influenza vaccine in pigs. The modified live-virus (MLV) vaccine completely protected against homologous and partially protected against heterosubtypic virus challenge. Importantly, MLV-vaccinated pigs can be differentiated from naturally infected animals. These results suggest that NS1-truncated MLV vaccines represent a new generation of swine influenza vaccines with great potential for use in other hosts, such as horses, dogs, birds, and humans.

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content