Journal of Virology, October 2006, p. 9927, Vol. 80, No. 20
0022-538X/06/$08.00+0 doi:10.1128/JVI.01821-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Positive-strand RNA viruses infecting eukaryotic cells exhibit specificity in packaging progeny RNA into matured virions. Annamalai and Rao (p. 10096-10108) show that packaging specificity in brome mosaic virus (BMV), a plant-infecting RNA virus, is dictated by a transient interaction between viral replicase proteins and coat protein subunits. This work also provides intriguing new evidence that packaging of BMV coat protein mRNA is functionally coupled to replication-dependent transcription and translation of coat protein subunits, a mechanism that appears to be conserved among viruses infecting plants, insects, and humans.
Cell Entry Factors for Ebola and Marburg Viruses Identified
The broad cell tropism of Ebola and Marburg viruses cannot be fully explained by host cell surface molecules reported to be involved in their infection, including C-type lectins. Shimojima et al. (p. 10109-10116) demonstrate that members of the Tyro3 family of receptor tyrosine kinases function as cell entry factors for these viruses. The results expand our understanding of the tropism and possibly extreme pathogenicity of these viruses.
Kaposi's Sarcoma-Associated Herpesvirus Infection Is Characterized by Heterogeneity of Viral Load and Life Cycle
Kaposi's sarcoma-associated herpesvirus (KSHV) intracellular viral copy number varies markedly among tumor types. Moreover, within tumors or immortalized cell lines the expression profile of viral and cellular proteins varies in each infected cell, depending on the stage of viral reactivation. Adang et al. (p. 10073-10082) examined this inherent heterogeneity by using the novel technique of multispectral imaging flow cytometry. This work has allowed an accurate estimate of intracellular viral load while defining the stage of the viral life cycle within each infected cell, potentially providing new insights into KSHV infection and biology.
A Mouse Model for Increased Vascular Permeability in Severe Dengue Disease
Lack of an appropriate animal model for dengue virus (DEN)-induced vascular permeability, the cardinal feature of dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), has impeded characterization of pathogenic mechanisms. Shresta et al. (p. 10208-10217) have developed a murine model of DHF/DSS. Mice lacking interferon receptors infected with a novel DEN2 strain died early without paralysis, carried infectious virus in both nonneuronal and neuronal tissues, exhibited increased vascular permeability, and produced significant levels of tumor necrosis factor alpha. This report represents a significant advance in development of animal models for severe DEN disease and provides mechanistic insights into DEN-induced pathology.
Human JC Virus Subtypes Exhibit Population Dynamics That Differ from Those of Human Populations
The existence of more than 14 subtypes of human JC virus (JCV), each associated with different human populations, has led to the assumption that the virus has codiverged with human populations over thousands of years. Shackelton et al. (p. 9928-9933) examined the population dynamics of JCV, which asymptomatically infects
70 to 90% of humans, and then tested the hypothesis of JCV-human codivergence with both a phylogenetic reconciliation analysis and an independent estimate of the viral nucleotide substitution rate. Neither analysis provided evidence for codivergence, indicating that JCV subtypes may not be suitable markers for inferring the history and migration patterns of human populations.
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