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SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Herpesviruses utilize several cellular pathways and machineries to accomplish entry. Delboy et al. (p. 3381-3390) provide intriguing new evidence that delivery of penetrated herpes simplex virus (HSV) capsids to the nuclear periphery is facilitated by proteasomal degradation. Surprisingly, entry does not require the host ubiquitination system. Proteasome activity is essential regardless of whether endocytosis or direct penetration routes are used. This work identifies an important relationship between the proteasome and incoming HSV capsids, potentially providing a new target for therapeutic intervention.

IRF-3 Regulates the Switch from Apoptosis to Persistent Infection by Paramyxoviruses

Infection of human cells with Sendai virus (SeV) or human parainfluenza virus type 3 causes apoptosis by activation of the caspase 8 pathway. Peters et al. (p. 3500-3508) report that cell death is markedly accelerated by inhibiting the action of phosphatidylinositol 3-kinase. Conversely, apoptosis is blocked by inhibiting IRF-3. When IRF-3 is absent or its activation by the RIG-I pathway is avoided, SeV establishes persistent infection. Persistently infected cells continuously produce infectious virions, and reintroduction of IRF-3 causes apoptosis. Thus, IRF-3 is a critical cellular factor that determines the fate of an infected cell.

Scavenger Receptor Class B Is Required for Hepatitis C Virus Uptake and Cross-Presentation by Human Dendritic Cells

Class B scavenger receptors (SR-B) are important host entry factors for hepatitis C virus (HCV) infection of hepatocytes. Barth et al. (p. 3466-3479) now show that SR-B are directly involved in uptake and cross-presentation of HCV by human dendritic cells, suggesting a functional role for SR-B in the initiation of HCV-specific immune responses. This work identifies a novel function for SR-B in viral antigen uptake and recognition, which may be important for the design of HCV vaccines and immunotherapeutics.

Simian Immunodeficiency Virus Is Directly Cytopathic in Natural Simian Immunodeficiency Virus Hosts

Sooty mangabeys naturally infected with simian immunodeficiency virus do not develop AIDS despite high levels of viremia. Gordon et al. (p. 3725-3735) provide evidence that the bulk of virus replication in these animals occurs in short-lived infected cells, most likely activated CD4⁺ T cells. This finding indicates that the absence of disease in sooty mangabeys is not due to reduced virus cytopathicity in vivo. Rather, species-specific host factors appear to be key determinants of pathogenesis during primate lentivirus infections.

Rice Yellow Mottle Virus, an RNA Plant Virus, Evolves as Rapidly as Most RNA Animal Viruses

The rate of evolution of an RNA plant virus has not been estimated using temporally spaced sequence data. Fargette et al. (p. 3584-3589) calculated the rate of evolution of rice yellow mottle virus (RYMV) from sequences of the coat protein gene of 253 isolates collected over 40 years in Africa. Using pairwise distance linear regression and Bayesian coalescent methods, RYMV was found to evolve as rapidly as most RNA animal viruses. Knowledge of the molecular clock of plant viruses now provides methods for testing a wide range of biological hypotheses.

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