On the cover: The malaria causing Plasmodium parasites must coordinate the salvage of host factors with de novo biosynthesis pathways in order to meet the unique demands of each intracellular stage of their life cycle. In this issue, Yu, Fidock, and colleagues (pp. 567–578) report that the parasite's fatty acid biosynthesis enzyme FabI is required for the liver stages of Plasmodium development but is dispensable for its growth in the blood stage. Cover shows the three phases of Plasmodium liver-stage development: schizont (magenta), cytomere (light green), and merozoite (yellow). Hepatoma cells infected with P. berghei sporozoites were stained with antisera against parasite SERA proteases and the exported protein 1, localizing in the parasitophorous vacuole membrane. Colors were computer generated to label the different parasite stages. Nuclei (blue) were stained with Hoechst.
Chlamydia-containing vacuole expanding as the bacteria replicate, filling the host cell cytoplasm. Time-lapse microscopy for 20 hr. Movie by Kumar and Valdivia. Also see the paper by Huang et al. in the current issue.
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Next issue: January 22, 2008
Gorben P. Pijlman, Anneke Funk, Natasha Kondratieva, Jason Leung, Shessy Torres, Lieke van der Aa, Wen Jun Liu, Ann C. Palmenberg, Pei-Yong Shi, Roy A. Hall, and Alexander A. Khromykh
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Pijlman et al. discover that flavivirus, a group of medically important encephalitic RNA viruses, exploit the action of host nucleases to produce a unique, highly structured noncoding RNA, which is essential for virus-induced cytopathicity and pathogenicity. Preview by Pierson. |
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Charrel-Dennis et al. report that the extracellular bacterial pathogen, group B streptococcus (GBS) induces type I interferon production in infected macrophages via the intracellular recognition of GBS DNA. | |
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Yu et al. show that Plasmodium fatty acid synthesis enzyme FabI is required for liver infection, yet is not the principle target in parasites of the FabI inhibitor triclosan. Preview by Spalding and Prigge. | |
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Peterson et al. show that blood-borne apolipoprotein B sequesters the Staphylococcus aureus quorum sensing signal, thereby inhibiting invasive infection. Preview by Horswill and Nauseef. |
Current Biology, December 2008
Vera Göhre, Thomas Spallek, Heidrun Häweker, Sophia Mersmann, Tobias Mentzel, Thomas Boller, Marta de Torres, John W. Mansfield, and Silke RobatzekImmunity, December 2008
Stephen A. Migueles, Christine M. Osborne, Cassandra Royce, Alex A. Compton, Rohan P. Joshi, Kristin A. Weeks, Julia E. Rood, Amy M. Berkley, Jonah B. Sacha, Nancy A. Cogliano-Shutta et al.Trends in Parasitology, December 2008 FREE
James G. Beeson, Faith H.A. Osier, and Christian R. EngwerdaChemistry & Biology, November 2008
Margaret Cooley, Siri Ram Chhabra, and Paul Williams