|Home | About | Journals | Submit | Contact Us | Français|
The respiratory syncytial virus (RSV) G protein is a 90-kDa glycoprotein that functions in viral attachment. A minor 55-kDa form of RSV G is thought to lack O-glycosylation. Kwilas et al. (p. 10710-10718) investigated the 55-kDa form and found that it is missing its C terminus. The larger form predominated in virions isolated from HEp-2 cells, but the smaller form predominated in virions isolated from Vero cells. Vero-derived virions were much less infectious for primary differentiated human airway cultures, indicating that the G protein C terminus is required for efficient infection of these cells. These findings suggest that RSV stocks prepared for animal or clinical vaccine studies should not be grown in Vero cells.
All herpesviruses encode an active ubiquitin-specific protease domain as part of their large tegument protein. Gredmark-Russ et al. (p. 10644-10652) showed that for the murine gammaherpesvirus MHV68, the activity of ORF64, which encodes this protease, contributes to replication efficiency. This work sets the stage for identification of natural substrates of ORF64 and its homologs in other herpesviruses.
Until now, strategies to directly manipulate the genomes of multicomponent single-stranded DNA nanoviruses were unavailable. Grigoras et al. (p. 10778-10787) provide conclusive evidence for the stoichiometry of genomic nanovirus DNAs and describe a way to reliably obtain functional representatives of the eight identified swarms of heterogeneous molecules. Fully infectious and sustainably insect transmissible virus can be reconstituted from such DNAs, which now allows in-depth studies of this emerging group of plant viruses.
Influenza virus can produce a spectrum of disease in humans and other animal populations. The host genetic elements underpinning this disease spectrum are largely unknown. Using a systems biology approach, Boon et al. (p. 10417-10426) found that H5N1 influenza disease in mice is associated with viral load and proinflammatory mediators and that three genomic locations segregate with severe illness. This work defines the complex nature of murine susceptibility to influenza virus infection and identifies several candidate genes that are likely involved in determining the relative severity of disease within a population.
A clinical trial of a recombinant adenovirus serotype 5 (Ad5) expressing human immunodeficiency virus (HIV) genes was halted due to an increase in HIV acquisition in vaccine recipients with pre-existing anti-Ad5 antibodies. This finding raised the possibility that T lymphocytes activated in response to vaccination might represent an increased pool of potential targets for HIV infection. Exploring this possibility, Sun et al. (p. 10596-10604) demonstrated a striking but transient T-lymphocyte activation in rhesus monkeys following Ad5 immunization. However, this global T-lymphocyte activation is unlikely to be of sufficient duration to account for the increased acquisition of HIV in the vaccine recipients.