Journal of Virology, February 2008, p. 1627, Vol. 82, No. 4
0022-538X/08/$08.00+0 doi:10.1128/JVI.02709-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Human herpesvirus 8 (HHV-8) is the etiological agent of Kaposi's sarcoma. Sander et al. (p. 1908-1922) used a systems biology approach to determine the localization of 85 HHV-8-encoded proteins in mammalian cells. Among the most surprising findings was the detection of antiapoptotic viral FLIP in the nucleus, whereas cellular FLIPs are exclusively localized in the cytoplasm. This work provides a useful reference for further studies on the interactions and functions of HHV-8-encoded proteins.
Reverse Genetics for Type I Feline Coronavirus
Feline coronaviruses (FCoV) can cause harmless persistent enteric infections and fatal feline infectious peritonitis (FIP). Although it is thought that mutations arising during persistent infections lead to generation of FIP-inducing viruses, the mechanisms of fatal FIP remain elusive. Tekes et al. (p. 1851-1859) have established a reverse genetics system for the prevalent type I FCoV and used this approach to analyze FCoV replication in feline monocytic cells. This system will lead to an enhanced understanding of FCoV replication and help elucidate the molecular determinants of FIP.
Mechanisms of Neurodevelopmental Damage in Early Central Nervous System Infection
Central nervous system infection in early life can have a profound impact on cognition and social behavior. Williams et al. (p. 1748-1758) provide evidence, using a neonatal rat model of bornavirus infection, that neurodegeneration in the hippocampus, a key region for learning and memory, is associated with accumulation of zinc and enhanced activation of poly(ADP-ribose) polymerase-1 and caspase-3. These findings provide insight into the mechanisms underlying neurodevelopmental damage and set the groundwork for pharmacological interventions that may reduce morbidity and mortality.
Target of Autologous Neutralization Antibodies in Human Immunodeficiency Virus Type 1 Subtype C Infection
Human immunodeficiency virus type 1 (HIV-1) induces potent but highly type-specific neutralizing antibodies within the first year of infection. Moore et al. (p. 1860-1869) found that individuals infected with subtype C HIV-1 strains have antibodies directed to the variable regions of the envelope glycoprotein (V1/V2, V4, and V5) that contribute to autologous neutralization. However, epitopes in the C3-V4 region are the major targets. The C3 region contains the highly variable alpha-2 helix as well as parts of the CD4-binding site. Identification of the precise epitopes in this region will provide important information about accessible regions of transmitted viruses that may inform vaccine design.
A New Tool To Study Nonenveloped Virus Entry
A common theme in nonenveloped virus entry is the participation of hydrophobic, virally encoded polypeptides, presumably in host membrane breaching for particle or genome delivery to the cytoplasm. Studying the entry-specific role of these polypeptides is challenging, since they probably have multiple functions in the viral life cycle. Walukiewicz et al. (p. 2025-2027) found that the membrane-active gamma peptide in flock house virus (FHV) can be supplied in trans during entry, via noninfectious viruslike particles, to rescue infectivity of a maturation-defective FHV. The entry-specific role of gamma protein can now be investigated by mutagenesis of viruslike particles.
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