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 Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in infants and young children. The function of the RSV small hydrophobic (SH) protein remains elusive. Fuentes et al. (p. 8361-8366) have found that the SH protein plays a critical role in blocking cell death, thus prolonging virus replication in infected cells. This work is important for understanding the pathogenesis of RSV disease and provides a new target for therapeutic intervention.

PKR Plays Apoptosis- and Virus-Selective Roles in Human Cells

PKR, a protein kinase regulated by RNA, is a key component of the host innate immune response. Zhang and Samuel (p. 8192-8200) demonstrate by stable knockdown that PKR is important for apoptosis and protein synthesis inhibition induced by double-stranded RNA, but not tumor necrosis factor alpha, in HeLa cells. They also show, using vesicular stomatitis virus, reovirus, and adenovirus, that PKR is important for the antiviral effect of interferon against some viruses but not against others. This work extends findings from mouse cells genetically deficient in Pkr and clarifies the functions of PKR in apoptosis, signaling, and virus replication in a human cell system.

Host Cell Proteomic Analysis Reveals that Human Cytomegalovirus Targets Destruction of Focal Adhesions

Human cytomegalovirus (HCMV) infection does not inhibit host cell gene expression. Instead, transcriptional responses are controlled to promote efficient virus replication. Stanton et al. (p. 7860-7872) performed a high-throughput antibody screen comparing expression of over 1,000 cellular proteins after infection with HCMV strains AD169 and Toledo. A subset of host proteins changed dramatically in abundance after infection. In particular, suppression of connexin-43 was demonstrated along with the dispersal and degradation of focal adhesions. The disruption of focal adhesions likely influences both intercellular communication and cell motility during HCMV infection.

Adaptation of Borna Disease Virus to New Host Species

Most strains of Borna disease virus (BDV) do not replicate in mice but can be adapted by an initial passage in rats and multiple passages in mice. Ackermann et al. (p. 7933-7940) used this approach to analyze the adaptation of molecularly cloned BDV. The authors demonstrate that changes in the viral polymerase complex are responsible for this process and further show that single amino acid substitutions are sufficient to allow interspecies transmission. Finally, their data indicate that BDV adaptation and pathogenicity are partially mediated by reduced negative regulation of the viral polymerase complex through the accessory viral X protein.

Identification of Novel Rodent Herpesviruses, Including the First Gammaherpesvirus of Mus musculus

Few rodent herpesviruses are available for study as experimental models of human herpesvirus diseases. In a comprehensive search for prevously unknown rodent herpesviruses, Ehlers et al. (p. 8091-8100) discovered a plethora of novel rodent beta- and gammaherpesviruses (GHVs), whereas alphaherpesviruses were not identified. This work has led to the identification of the first GHV of Mus musculus (MmusRHV1), a member of a novel group of rodent GHVs that is clearly distinct from murine herpesvirus 68-like rodent GHV.

Compensatory Mutation Restores Fitness Cost of Human Immunodeficiency Virus Escape Mutation

The HLA-B*5703 allele is associated with low viral loads during human immunodeficiency virus (HIV) infection. However, the underlying mechanism is unknown. Crawford et al. (p. 8346-8351) provide data suggesting that one contributory factor is the selection of escape mutations that reduce viral replicative capacity in epitopes presented by this allele. A mutation in the Gag p24 epitope KF11 reduces viral fitness, which is partially restored by the subsequent appearance of a second mutation in the same epitope. The capacity of HIV to adapt via the selection of compensatory mutations to immune-mediated selection has implications for vaccine development.

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 Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content