Journal of Virology, September 2006, p. 8847, Vol. 80, No. 18
0022-538X/06/$08.00+0 doi:10.1128/JVI.01582-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Finding the Right Partner during Capsid AssemblyThe production of icosahedral virus particles demands accuracy in the macromolecular interactions that are required for assembly. Alphavirus capsid assembly involves the formation of a nucleic acid-dependent dimer that initiates assembly of icosahedral capsids. Although this dimer can be formed through contacts within the C-terminal region of the capsid protein, Hong et al. (p. 8848-8855) now show that helix I found in the N-terminal region is essential for stabilizing the dimer. Moreover, helix I is the primary determinant that controls the accuracy of dimer formation. This checkpoint arises from discrimination between binding partners through specific amino acid interactions and is imperative for functional capsid assembly.
Murine Leukemia Virus Engineered To Infect Nondividing Cells
The mechanisms by which different retroviruses are transported passively, as in murine leukemia virus (MLV), or actively, as in human immunodeficiency virus, into the nucleus are poorly understood. Yu and Schaffer (p. 8981-8988) used a novel, library-based protein engineering technique to select for an MLV variant that is capable of infecting terminally differentiated neurons in vitro and in vivo. This new variant could aid in the understanding of retroviral intracellular transport and in the development of retroviral vectors for gene therapy.
Type I Interferon-Counteracting Activity Associated with the Arenavirus Nucleoprotein
Arenaviruses merit significant attention as tractable model systems to study acute and persistent viral infections and as clinically important human pathogens, including several causative agents of severe hemorrhagic fever (HF), chiefly Lassa fever virus. Arenavirus-induced HF disease is associated with the host's inability to mount an effective antiviral immune response. Martínez-Sobrido et al. (p. 9192-9199) show that the arenavirus nucleoprotein (NP) blocks the nuclear translocation and transcription activity of IRF-3, which results in a robust inhibition of type I interferon (IFN) production. This IFN-counteracting activity of NP may contribute to the failure of the host innate antiviral response to control the replication of pathogenic arenaviruses.
Role for Mouse Mammary Tumor Virus Envelope in Mammary Tumor Induction
Mouse mammary tumor virus (MMTV) causes mammary tumors by insertional activation of cellular oncogenes, but it has been proposed that the virus also contributes directly to transformation. Here, Ross et al. (p. 9000-9008) show that mammary tumor induction by milk-transmitted virus was greatly attenuated and the pattern of oncogene insertional activation was altered when an immunoreceptor tyrosine-based activation motif (ITAM) in the envelope protein was altered. These findings suggest that ITAM signaling participates in MMTV-mediated tumorigenesis and that inappropriate expression of such signaling molecules in epithelial cells represents a novel transformation mechanism.
Journal of Virology, September 2006, p. 8847, Vol. 80, No. 18
0022-538X/06/$08.00+0 doi:10.1128/JVI.01582-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
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