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| April 2014 Volume 12 Number 4 | |||||||||||||||||||||||||||||||||||||||||||||||
| In this issue
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| Comment: ND4BB: addressing the antimicrobial resistance crisis John H. Rex p231 | doi:10.1038/nrmicro3245 The Innovative Medicines Initiative (IMI) recently launched its third public-private partnership, ENABLE (European Gram-negative Antibacterial Engine), to tackle the shortage of effective antimicrobial drugs for Gram-negative pathogens. Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
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| NEWS AND ANALYSIS | Top | ||||||||||||||||||||||||||||||||||||||||||||||
| GENOME WATCH Found in translation Lia Chappell p238 | doi:10.1038/nrmicro3243 This month's Genome Watch highlights a recent study that used high-throughput sequencing to identify the mRNAs that are actively translated during the life cycle of a protozoan parasite. | |||||||||||||||||||||||||||||||||||||||||||||||
| REVIEWS | Top | ||||||||||||||||||||||||||||||||||||||||||||||
| The cryptic sexual strategies of human fungal pathogens Iuliana V. Ene & Richard J. Bennett p239 | doi:10.1038/nrmicro3236 Although once thought to be clonal, and thus undergo asexual reproduction, accumulating evidence now suggests that many human fungal pathogens retain sexual reproductive machinery and undergo sexual or parasexual reproduction. Iuliana V. Ene and Richard J. Bennett discuss the sexual cycles of three of the most prominent human pathogens — Candida albicans, Cryptococcus neoformans and Aspergillus fumigatus. Abstract | Full Text | PDF | Supplementary information | |||||||||||||||||||||||||||||||||||||||||||||||
| The co-pathogenesis of influenza viruses with bacteria in the lung Jonathan A. McCullers p252 | doi:10.1038/nrmicro3231 Mortality from influenza viruses is strongly linked to secondary bacterial invaders. Here, Jonathan A. McCullers reviews viral and bacterial virulence factors that contribute to the pathogenesis of co-infections by disrupting physical barriers, dysregulating immune responses and delaying a return to homeostasis. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| Explaining microbial genomic diversity in light of evolutionary ecology Otto X. Cordero & Martin F. Polz p263 | doi:10.1038/nrmicro3218 Wild populations of bacteria and archaea show high levels of genotypic diversity. In this Review, Cordero and Polz discuss recent studies that show that this diversity arises owing to social and ecological interactions, which have important consequences for microbial ecology and population dynamics. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| Bordetella pertussis pathogenesis: current and future challenges Jeffrey A. Melvin, Erich V. Scheller, Jeff F. Miller & Peggy A. Cotter p274 | doi:10.1038/nrmicro3235 The causative agent of whooping cough, Bordetella pertussis, has recently re-emerged as a serious public health concern. Here, Cotter, Miller and colleagues discuss the pathogenesis of pertussis, the shortcomings of current vaccines and the future challenges that need to be addressed for the development of more effective therapeutic strategies. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| PERSPECTIVES | Top | ||||||||||||||||||||||||||||||||||||||||||||||
| OPINION In search of a new paradigm for protective immunity to TB Cláudio Nunes-Alves, Matthew G. Booty, Stephen M. Carpenter, Pushpa Jayaraman, Alissa C. Rothchild & Samuel M. Behar p289 | doi:10.1038/nrmicro3230 Protective immunity against tuberculosis is multifactorial, and correlates of protection — either during natural infection or after vaccination — are lacking. Here, Behar and colleagues discuss why it is time to look beyond interferon-γ for protective mechanisms against Mycobacterium tuberculosis. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| OPINION Targeting virulence: can we make evolution-proof drugs? Richard C. Allen, Roman Popat, Stephen P. Diggle & Sam P. Brown p300 | doi:10.1038/nrmicro3232 Antivirulence drugs are a promising avenue to revitalize the antimicrobial drug-development pipeline, and it has been claimed that such compounds will generate much weaker selection for resistance than traditional antibiotics. Sam P. Brown and colleagues examine this claim and argue that, although resistance to antivirulence drugs may emerge, the crucial factor is whether or not this resistance will spread. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
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| *2012 Journal Citation Report (Thomson Reuters, 2013) |
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