S-Adenosylhomocysteine Hydrolase Inhibitors as a Source of Anti-Filovirus Agents in .NET

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S-Adenosylhomocysteine Hydrolase Inhibitors as a Source of Anti-Filovirus Agents
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STEWART W. SCHNELLER and MINMIN YANG
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Department of Chemistry and Biochemistry, Auburn University
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INTRODUCTION
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There is evidence that, upon infection, the loviruses inhibit the natural production of interferon in the host cells. This effect can be reversed by the carbocyclic nucleoside 3-deazaneplanocin A and, possibly, 3-deazaaristeromycin, which are inhibitors of S-adenosylhomocysteine hydrolase. This effect is further manifested in blocking viral mRNA processing. This chapter outlines the infectious properties of the loviruses Ebola and Marburg; the current status of therapeutic (vaccine and drug) development; the role that interferon immunotherapy can play in therapy design; the biochemical stages associated with inhibiting viral mRNA and its relationship to anti- loviral agents; and the status of current efforts to avail signi cant amounts of 3-deazaneplanocin A and 3-deazaaristerocmycin for further therapeutic investigations.
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FILOVIRUSES
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The small lipid enveloped zoonotic RNA viruses that are responsible for viral hemorrhagic fevers (VHFs) exist in four taxonomic families: the Filoviridae (Ebola and Marburg), Arenaviridae (Junin, Lassa, Tacaribe, Machupo, Guanarito), Bunyaviridae (Hantavirus, Rift Valley fever, Crimean-Congo HF), and Flaviviridae (yellow fever, dengue).1,2 The VHF designation is the result of the damage that occurs to the vascular system following infection.2 This often is accompanied by
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Antiviral Drug Discovery for Emerging Diseases and Bioterrorism Threats. Edited by Paul F. Torrence Copyright # 2005 John Wiley & Sons, Inc.
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S-ADENOSYLHOMOCYSTEINE HYDROLASE INHIBITORS
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hemorrhaging, which in some instances is severe and life-threatening.2 Many of the VHFs have been identi ed as possible bioweapons against civilians because of (1) high morbidity and mortality, (2) person-to-person transmission, (3) low dose/high infectivity with delivery by aerosol, (4) unavailability of treatment methods, (5) pathogen availability, (6) stressful circumstances the infection would cause for health care workers, (7) capability of large-scale production, (8) environmental stability, and (9) previous research on the pathogens.1 In the latter regard, there are reports that the hemorrhagic fevers have been weaponized,1,3,4 and that until 1992, the Soviet Union/Russia produced large quantities of Marburg ( lo), Ebola ( lo), Lassa (arena), Junin (arena), and Machupo ( avi) viruses.1 Successful infection of nonhuman primates with aerosolized Ebola,5 Marburg,6 Lassa,7 and New World arenaviruses8 has also been documented.1 There is also reason to believe that the loviruses were subjected to biotechnology modi cations either to enhance their pathogenicity and/or to produce agents with characteristics not typical of the virus,3 which mousepox experiments appeared to have validated.9 The possibility that some of the scientists who worked on these projects (as well as with smallpox) may now be in countries capable of bioterrorism activities adds to the concerns. Interestingly, prior to 1969, yellow fever and Rift Valley fever were being developed in the U.S. offensive biological weapons program.1,10 Of the hemorrhagic fevers, the loviruses Ebola (EBO) and Marburg (MBG) cause the most severe effects in humans with fever and death appearing within a few days.11 There is a single species of Marburg. Marburg was the rst lovirus discovered (1967); this occurred at a vaccinia production facility in Marburg, Germany, where workers came in contact with monkey carriers imported from Uganda. Marburg virus, however, remains con ned to Africa. Ebola virus was encountered (1976) at a missionary hospital in Zaire (now the Democratic Republic of the Congo), where it reached epidemic proportions. The lovirus genus contains four subtypes of Ebola: (1) Zaire, (2) Sudan, and (3) Ivory Coast, which infect human, and (4) Reston, which causes disease only in nonhuman primates. Ebola-Zaire (EBO-Z) causes the most virulent VHF in humans.1 While the natural reservoir for the loviruses remains unknown,12 their potency requires that they be handled in a BSL-4 containment facility. There are, presently, no vaccines or therapeutic candidates available for combating Ebola and Marburg viruses but they are urgently needed.13 18
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THERAPEUTIC AGENTS FOR FILOVIRUSES
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Despite recent animal model advances in vaccine development to protect against the effects of lovirus infection, a number of issues must be resolved before vaccines qualify for human use. This places the need for therapeutics as a priority. Efforts in this regard have been limited,14 until recently, because of insuf cient biochemical information on loviral replication at the molecular level. By analyzing the similarities in loviral replication with the more thoroughly studied
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