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In the absence of substantive genomic proofreading, some RNA viruses have a high rate of genomic mutagenesis. Davis and van den Pol (p. 1625-1630) have put this mutagenesis to use by employing a negative-strand RNA virus, vesicular stomatitis virus (VSV), that contains an inserted nonviral gene, in this case one encoding a fluorescent protein. The recombinant VSV not only generates novel mutations in the inserted gene but also expresses the altered gene in infected cells, allowing rapid detection of mutations leading to novel proteins. In experiments using this virus, mutations are observed in a red fluorescent protein that lead to altered spectral characteristics.
Herpes simplex virus type 1 (HSV-1) depends on long-distance intracellular transport in axons to establish latent infections in sensory ganglia. Antinone and Smith (p. 1504-1512) performed a live-cell imaging study of HSV-1 trafficking to the neuronal cell body and defined the kinetics of the axon transport process and the structural composition of the translocating viral particles. The underlying process is remarkably conserved with a veterinary herpesvirus, pseudorabies virus, but differs in that HSV-1 selectively transports a small fraction of the VP16 transactivator protein to the neuronal cell body.
An extended product of nonstructural protein NS1, termed NS1′, is often detected during infection with members of the Japanese encephalitis serogroup of flaviviruses that cause neuroinvasive disease. However, the origin and role of this protein in viral pathogenesis are not known. Melian et al. (p. 1641-1647) now provide conclusive evidence that NS1′ is the product of a −1 ribosomal frameshift triggered by a canonical slippery heptanucleotide motif located at the beginning of the NS2A gene and a downstream RNA pseudoknot structure. Mutagenesis of West Nile virus reveals that NS1′ plays a critical role in viral neuroinvasiveness.
An optimal human immunodeficiency virus (HIV) vaccine will likely induce broad and potent neutralizing antibodies. Human monoclonal antibodies 2F5 and 4E10 target the conserved membrane-proximal external region (MPER) of HIV envelope glycoprotein gp41 and are broadly neutralizing. However, the capacity of these antibodies to protect against viral challenge has not been determined. Hessell, et al. (p. 1302-1313) show that 2F5 and 4E10 completely protect against rectal challenge by a chimeric SIV/HIV (SHIV) strain. These findings suggest that the gp41 MPER should be used as a vaccine target.
Simian immunodeficiency virus SVIcpz is the source of SIVgor and human immunodeficiency virus (HIV-1). Viruses from the SIVcpz/SIVgor lineage have been transmitted to humans on at least four occasions. Peeters et al. (p. 1464-1476) report that SIV infection in wild gorillas is limited to a handful of sites. The overall low prevalence and low genetic diversity of SIVgor strains are consistent with recent infection. However, SIV infection is not new in gorillas, as illustrated by the presence of isolated hotspots with highly infected gorilla communities that remain a potential source for infection of humans.