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Sent on Friday, 2010 Jul 30
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Nat Med. 2010 Jul;16(7):729. Pharmacogenetics raises new legal questions. Hutson S.
	PMID: 20613735 [PubMed - indexed for MEDLINE]

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Sent on Tuesday, 2010 Jul 27
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Science. 2010 Jul 9;329(5988):174-80. HIV persistence and the prospect of long-term drug-free remissions for HIV-infected individuals. Trono D, Van Lint C, Rouzioux C, Verdin E, Barré-Sinoussi F, Chun TW, Chomont N. School of Life Sciences and Frontiers-in-Genetics Program, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. Didier.trono@epfl.ch Abstract HIV infection can persist in spite of efficacious antiretroviral therapies. Although incomplete inhibition of viral replication may contribute to this phenomenon, this is largely due to the early establishment of a stable reservoir of latently infected cells. Thus, life-long antiviral therapy may be needed to control HIV. Such therapy is prone to drug resistance and cumulative side effects and is an unbearable financial burden for regions of the world hit hardest by the epidemic. This review discusses our current understanding of HIV persistence and the limitations of potential approaches to eradicate the virus and accordingly pleads for a joint multidisciplinary effort toward two highly related goals: the development of an HIV prophylactic vaccine and the achievement of long-term drug-free remissions in HIV-infected individuals.
	PMID: 20616270 [PubMed - indexed for MEDLINE]

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Sent on Friday, 2010 Jul 23
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Nature. 2010 Jun 10;465(7299):697-9. Blood-vessel formation: Bridges that guide and unite. Schmidt T, Carmeliet P.
	PMID: 20535192 [PubMed - indexed for MEDLINE]
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2.	Nature. 2010 Jun 10;465(7299):779-82. Epub 2010 May 16. Moonlighting bacteriophage proteins derepress staphylococcal pathogenicity islands. Tormo-Más MA, Mir I, Shrestha A, Tallent SM, Campoy S, Lasa I, Barbé J, Novick RP, Christie GE, Penadés JR. Centro de Investigación y Tecnología Animal, Instituto Valenciano de Investigaciones Agrarias (CITA-IVIA), Apdo. 187, Segorbe, Castellón 12400, Spain. Abstract Staphylococcal superantigen-carrying pathogenicity islands (SaPIs) are discrete, chromosomally integrated units of approximately 15 kilobases that are induced by helper phages to excise and replicate. SaPI DNA is then efficiently encapsidated in phage-like infectious particles, leading to extremely high frequencies of intra- as well as intergeneric transfer. In the absence of helper phage lytic growth, the island is maintained in a quiescent prophage-like state by a global repressor, Stl, which controls expression of most of the SaPI genes. Here we show that SaPI derepression is effected by a specific, non-essential phage protein that binds to Stl, disrupting the Stl-DNA complex and thereby initiating the excision-replication-packaging cycle of the island. Because SaPIs require phage proteins to be packaged, this strategy assures that SaPIs will be transferred once induced. Several different SaPIs are induced by helper phage 80alpha and, in each case, the SaPI commandeers a different non-essential phage protein for its derepression. The highly specific interactions between different SaPI repressors and helper-phage-encoded antirepressors represent a remarkable evolutionary adaptation involved in pathogenicity island mobilization.
	PMID: 20473284 [PubMed - indexed for MEDLINE]
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Sent on Thursday, 2010 Jul 22
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Nature. 2010 Jun 24;465(7301):1079-83. Subcapsular sinus macrophages prevent CNS invasion on peripheral infection with a neurotropic virus. Iannacone M, Moseman EA, Tonti E, Bosurgi L, Junt T, Henrickson SE, Whelan SP, Guidotti LG, von Andrian UH. Immune Disease Institute and Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. Matteo_Iannacone@hms.harvard.edu Abstract Lymph nodes (LNs) capture microorganisms that breach the body's external barriers and enter draining lymphatics, limiting the systemic spread of pathogens. Recent work has shown that CD11b(+)CD169(+) macrophages, which populate the subcapsular sinus (SCS) of LNs, are critical for the clearance of viruses from the lymph and for initiating antiviral humoral immune responses. Here we show, using vesicular stomatitis virus (VSV), a relative of rabies virus transmitted by insect bites, that SCS macrophages perform a third vital function: they prevent lymph-borne neurotropic viruses from infecting the central nervous system (CNS). On local depletion of LN macrophages, about 60% of mice developed ascending paralysis and died 7-10 days after subcutaneous infection with a small dose of VSV, whereas macrophage-sufficient animals remained asymptomatic and cleared the virus. VSV gained access to the nervous system through peripheral nerves in macrophage-depleted LNs. In contrast, within macrophage-sufficient LNs VSV replicated preferentially in SCS macrophages but not in adjacent nerves. Removal of SCS macrophages did not compromise adaptive immune responses against VSV, but decreased type I interferon (IFN-I) production within infected LNs. VSV-infected macrophages recruited IFN-I-producing plasmacytoid dendritic cells to the SCS and in addition were a major source of IFN-I themselves. Experiments in bone marrow chimaeric mice revealed that IFN-I must act on both haematopoietic and stromal compartments, including the intranodal nerves, to prevent lethal infection with VSV. These results identify SCS macrophages as crucial gatekeepers to the CNS that prevent fatal viral invasion of the nervous system on peripheral infection. PMCID: PMC2892812 [Available on 2010/12/1]
	PMID: 20577213 [PubMed - indexed for MEDLINE]
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2.	Nature. 2010 Jun 24;465(7301):1000-1. Human genome at ten: Science after the sequence. Butler D.
	PMID: 20577184 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2010 Jul 21
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1.	Lancet. 2010 Jun 26;375(9733):2194. The Human Genome Project: 10 years later. [No authors listed]
	PMID: 20609954 [PubMed - indexed for MEDLINE]

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Sent on Friday, 2010 Jul 16
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1.	Nature. 2010 Jun 3;465(7298):526. Mouse megascience. [No authors listed]
	PMID: 20520665 [PubMed - indexed for MEDLINE]

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Sent on Wednesday, 2010 Jul 14
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1.	Science. 2010 Jul 2;329(5987):75-8. Sequencing of 50 human exomes reveals adaptation to high altitude. Yi X, Liang Y, Huerta-Sanchez E, Jin X, Cuo ZX, Pool JE, Xu X, Jiang H, Vinckenbosch N, Korneliussen TS, Zheng H, Liu T, He W, Li K, Luo R, Nie X, Wu H, Zhao M, Cao H, Zou J, Shan Y, Li S, Yang Q, Asan, Ni P, Tian G, Xu J, Liu X, Jiang T, Wu R, Zhou G, Tang M, Qin J, Wang T, Feng S, Li G, Huasang, Luosang J, Wang W, Chen F, Wang Y, Zheng X, Li Z, Bianba Z, Yang G, Wang X, Tang S, Gao G, Chen Y, Luo Z, Gusang L, Cao Z, Zhang Q, Ouyang W, Ren X, Liang H, Zheng H, Huang Y, Li J, Bolund L, Kristiansen K, Li Y, Zhang Y, Zhang X, Li R, Li S, Yang H, Nielsen R, Wang J, Wang J. BGI-Shenzhen, Shenzhen 518083, China. Comment in: Science. 2010 Jul 2;329(5987):40-1. Abstract Residents of the Tibetan Plateau show heritable adaptations to extreme altitude. We sequenced 50 exomes of ethnic Tibetans, encompassing coding sequences of 92% of human genes, with an average coverage of 18x per individual. Genes showing population-specific allele frequency changes, which represent strong candidates for altitude adaptation, were identified. The strongest signal of natural selection came from endothelial Per-Arnt-Sim (PAS) domain protein 1 (EPAS1), a transcription factor involved in response to hypoxia. One single-nucleotide polymorphism (SNP) at EPAS1 shows a 78% frequency difference between Tibetan and Han samples, representing the fastest allele frequency change observed at any human gene to date. This SNP's association with erythrocyte abundance supports the role of EPAS1 in adaptation to hypoxia. Thus, a population genomic survey has revealed a functionally important locus in genetic adaptation to high altitude.
	PMID: 20595611 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Jul 2;329(5987):40-1. Evolution. Genes for high altitudes. Storz JF. School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, USA. jstorz2@unl.edu Comment on: Science. 2010 Jul 2;329(5987):75-8. Science. 2010 Jul 2;329(5987):72-5.
	PMID: 20595602 [PubMed - indexed for MEDLINE]
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3.	Science. 2010 Jul 2;329(5987):38-9. Genetic technologies. Synthetic "life," ethics, national security, and public discourse. Cho MK, Relman DA. Stanford University, Stanford, CA 94305, USA. micho@stanford.edu Comment on: Science. 2010 Jul 2;329(5987):52-6.
	PMID: 20595601 [PubMed - indexed for MEDLINE]
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4.	Science. 2010 Jul 2;329(5987):32-3. Variability of our somatic (epi)genomes. Sgaramella V.
	PMID: 20595596 [PubMed - indexed for MEDLINE]
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5.	Science. 2010 Jul 2;329(5987):24-7. Epigenetics. The seductive allure of behavioral epigenetics. Miller G.
	PMID: 20595592 [PubMed - indexed for MEDLINE]
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6.	Science. 2010 Jul 2;329(5987):72-5. Epub 2010 May 13. Genetic evidence for high-altitude adaptation in Tibet. Simonson TS, Yang Y, Huff CD, Yun H, Qin G, Witherspoon DJ, Bai Z, Lorenzo FR, Xing J, Jorde LB, Prchal JT, Ge R. Eccles Institute of Human Genetics, University of Utah School of Medicine, Salt Lake City, UT 84112, USA. Comment in: Science. 2010 Jul 2;329(5987):40-1. Abstract Tibetans have lived at very high altitudes for thousands of years, and they have a distinctive suite of physiological traits that enable them to tolerate environmental hypoxia. These phenotypes are clearly the result of adaptation to this environment, but their genetic basis remains unknown. We report genome-wide scans that reveal positive selection in several regions that contain genes whose products are likely involved in high-altitude adaptation. Positively selected haplotypes of EGLN1 and PPARA were significantly associated with the decreased hemoglobin phenotype that is unique to this highland population. Identification of these genes provides support for previously hypothesized mechanisms of high-altitude adaptation and illuminates the complexity of hypoxia-response pathways in humans.
	PMID: 20466884 [PubMed - indexed for MEDLINE]
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Sent on Saturday, 2010 Jul 10
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Science. 2010 Jun 25;328(5986):1640-1. Ecology. Time to tap Africa's livestock genomes. Hanotte O, Dessie T, Kemp S. School of Biology, University of Nottingham, Nottingham NG7 2RD, UK.
	PMID: 20576875 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Jun 25;328(5986):1703-5. Epub 2010 May 27. c-di-AMP secreted by intracellular Listeria monocytogene s activates a host type I interferon response. Woodward JJ, Iavarone AT, Portnoy DA. Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA. Abstract Intracellular bacterial pathogens, such as Listeria monocytogenes, are detected in the cytosol of host immune cells. Induction of this host response is often dependent on microbial secretion systems and, in L. monocytogenes, is dependent on multidrug efflux pumps (MDRs). Using L. monocytogenes mutants that overexpressed MDRs, we identified cyclic diadenosine monophosphate (c-di-AMP) as a secreted molecule able to trigger the cytosolic host response. Overexpression of the di-adenylate cyclase, dacA (lmo2120), resulted in elevated levels of the host response during infection. c-di-AMP thus represents a putative bacterial secondary signaling molecule that triggers a cytosolic pathway of innate immunity and is predicted to be present in a wide variety of bacteria and archea.
	PMID: 20508090 [PubMed - indexed for MEDLINE]
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3.	Science. 2010 Jun 25;328(5986):1689-93. Epub 2010 May 20. ATP-binding cassette transporters and HDL suppress hema topoietic stem cell proliferation. Yvan-Charvet L, Pagler T, Gautier EL, Avagyan S, Siry RL, Han S, Welch CL, Wang N, Randolph GJ, Snoeck HW, Tall AR. Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY 10032, USA. ly2159@columbia.edu Comment in: Science. 2010 Jun 25;328(5986):1641-2. Abstract Elevated leukocyte cell numbers (leukocytosis), and monocytes in particular, promote atherosclerosis; however, how they become increased is poorly understood. Mice deficient in the adenosine triphosphate-binding cassette (ABC) transporters ABCA1 and ABCG1, which promote cholesterol efflux from macrophages and suppress atherosclerosis in hypercholesterolemic mice, displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of the stem and progenitor cell population containing Lin(-)Sca-1(+)Kit+ (LSK) in the bone marrow. Transplantation of Abca1(-/-) Abcg1(-/-) bone marrow into apolipoprotein A-1 transgenic mice with elevated levels of high-density lipoprotein (HDL) suppressed the LSK population, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atherosclerosis. The findings indicate that ABCA1, ABCG1, and HDL inhibit the proliferation of hematopoietic stem and multipotential progenitor cells and connect expansion of these populations with leukocytosis and accelerated atherosclerosis.
	PMID: 20488992 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2010 Jul 07
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	N Engl J Med. 2010 Jul 1;363(1):87-9. Immunotherapy for sepsis--a new approach against an ancient foe. Hotchkiss RS, Opal S. Department of Anesthesiology, Washington University School of Medicine, St. Louis, USA.
	PMID: 20592301 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2010 Jun 5;375(9730):1940. Synthetic cell created in a laboratory. [No authors listed]
	PMID: 20569821 [PubMed - indexed for MEDLINE]
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1.	Nat Med. 2010 May;16(5):517-8. The enemy within: dormant retroviruses awaken. Engel ME, Hiebert SW. Comment on: Nat Med. 2010 May;16(5):571-9, 1p following 579.
	PMID: 20448571 [PubMed - indexed for MEDLINE]

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1.	Science. 2010 Jun 18;328(5985):1570-3. Epub 2010 May 13. MiR-33 contributes to the regulation of cholesterol homeostasis. Rayner KJ, Suárez Y, Dávalos A, Parathath S, Fitzgerald ML, Tamehiro N, Fisher EA, Moore KJ, Fernández-Hernando C. Department of Medicine, Leon H. Charney Division of Cardiology and the Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY 10016, USA. Comment in: Science. 2010 Jun 18;328(5985):1495-6. Abstract Cholesterol metabolism is tightly regulated at the cellular level. Here we show that miR-33, an intronic microRNA (miRNA) located within the gene encoding sterol-regulatory element-binding factor-2 (SREBF-2), a transcriptional regulator of cholesterol synthesis, modulates the expression of genes involved in cellular cholesterol transport. In mouse and human cells, miR-33 inhibits the expression of the adenosine triphosphate-binding cassette (ABC) transporter, ABCA1, thereby attenuating cholesterol efflux to apolipoprotein A1. In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-density lipoprotein (HDL). Lentiviral delivery of miR-33 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels. Conversely, silencing of miR-33 in vivo increases hepatic expression of ABCA1 and plasma HDL levels. Thus, miR-33 appears to regulate both HDL biogenesis in the liver and cellular cholesterol efflux.
	PMID: 20466885 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Jun 18;328(5985):1566-9. Epub 2010 May 13. MicroRNA-33 and the SREBP host genes cooperate to contro l cholesterol homeostasis. Najafi-Shoushtari SH, Kristo F, Li Y, Shioda T, Cohen DE, Gerszten RE, Näär AM. Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA. Comment in: Science. 2010 Jun 18;328(5985):1495-6. Abstract Proper coordination of cholesterol biosynthesis and trafficking is essential to human health. The sterol regulatory element-binding proteins (SREBPs) are key transcription regulators of genes involved in cholesterol biosynthesis and uptake. We show here that microRNAs (miR-33a/b) embedded within introns of the SREBP genes target the adenosine triphosphate-binding cassette transporter A1 (ABCA1), an important regulator of high-density lipoprotein (HDL) synthesis and reverse cholesterol transport, for posttranscriptional repression. Antisense inhibition of miR-33 in mouse and human cell lines causes up-regulation of ABCA1 expression and increased cholesterol efflux, and injection of mice on a western-type diet with locked nucleic acid-antisense oligonucleotides results in elevated plasma HDL. Our findings indicate that miR-33 acts in concert with the SREBP host genes to control cholesterol homeostasis and suggest that miR-33 may represent a therapeutic target for ameliorating cardiometabolic diseases.
	PMID: 20466882 [PubMed - indexed for MEDLINE]
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1.	Lancet. 2010 May 29;375(9729):1896-905. Postexposure protection of non-human primates against a lethal Ebola virus challenge with RNA interference: a proof-of-concept study. Geisbert TW, Lee AC, Robbins M, Geisbert JB, Honko AN, Sood V, Johnson JC, de Jong S, Tavakoli I, Judge A, Hensley LE, Maclachlan I. National Emerging Infectious Diseases Laboratories Institute, Boston University School of Medicine, Boston, MA 02118, USA. geisbert@bu.edu Comment in: Lancet. 2010 May 29;375(9729):1850-2. Abstract BACKGROUND: We previously showed that small interfering RNAs (siRNAs) targeting the Zaire Ebola virus (ZEBOV) RNA polymerase L protein formulated in stable nucleic acid-lipid particles (SNALPs) completely protected guineapigs when administered shortly after a lethal ZEBOV challenge. Although rodent models of ZEBOV infection are useful for screening prospective countermeasures, they are frequently not useful for prediction of efficacy in the more stringent non-human primate models. We therefore assessed the efficacy of modified non-immunostimulatory siRNAs in a uniformly lethal non-human primate model of ZEBOV haemorrhagic fever. METHODS: A combination of modified siRNAs targeting the ZEBOV L polymerase (EK-1 mod), viral protein (VP) 24 (VP24-1160 mod), and VP35 (VP35-855 mod) were formulated in SNALPs. A group of macaques (n=3) was given these pooled anti-ZEBOV siRNAs (2 mg/kg per dose, bolus intravenous infusion) after 30 min, and on days 1, 3, and 5 after challenge with ZEBOV. A second group of macaques (n=4) was given the pooled anti-ZEBOV siRNAs after 30 min, and on days 1, 2, 3, 4, 5, and 6 after challenge with ZEBOV. FINDINGS: Two (66%) of three rhesus monkeys given four postexposure treatments of the pooled anti-ZEBOV siRNAs were protected from lethal ZEBOV infection, whereas all macaques given seven postexposure treatments were protected. The treatment regimen in the second study was well tolerated with minor changes in liver enzymes that might have been related to viral infection. INTERPRETATION: This complete postexposure protection against ZEBOV in non-human primates provides a model for the treatment of ZEBOV-induced haemorrhagic fever. These data show the potential of RNA interference as an effective postexposure treatment strategy for people infected with Ebola virus, and suggest that this strategy might also be useful for treatment of other emerging viral infections. FUNDING: Defense Threat Reduction Agency. Copyright 2010 Elsevier Ltd. All rights reserved.
	PMID: 20511019 [PubMed - indexed for MEDLINE]