Structural Biology of Flaviviral Replication and Opportunities for Drug Design in Visual Studio .NET

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Structural Biology of Flaviviral Replication and Opportunities for Drug Design
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KRISHNA MURTHY
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Center for Biophysical Sciences and Engineering, University of Alabama at Birmingham
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INTRODUCTION
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Flaviviral diseases are widespread in tropical regions and are caused by infections due to viruses such as dengue, yellow fever, Japanese encephalitis, and West Nile. Information that has been obtained from genetic, molecular biological, biochemical, and structural studies has elucidated the key processes involved in the life cycle of aviviruses and identi ed several therapeutic targets. These include viral structural proteins such as the envelope protein and nonstructural proteins such as the viral protease, helicase, RNA polymerase, and methyl transferase. This chapter summarizes the information that is currently available on each of these proteins and the work that is being done to target them using suitable inhibitory compounds.
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FLAVIVIRAL DISEASES
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The Flavivirus genus of Flaviviridae numbers approximately seventy identi ed members and includes many potent human pathogens.1 These include yellow fever, dengue, Japanese encephalitis, and West Nile viruses, among others. Flaviviruses are arboviruses transmitted by ticks or mosquitoes. Although successful eradication of aviviral vectors have banished infections from North America, aviviruses pervade many of the tropical regions of the world, causing death, disease, and
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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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STRUCTURAL BIOLOGY OF FLAVIVIRAL REPLICATION
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enormous economic damage. For a comprehensive series of reviews on aviviral structure, replication, evolution, pathogenesis, immunity, epidemiology, detection, diagnosis, and vaccine development, the reader is referred to recent volumes of Advances in Virus Research.2 Some reviews on potential drug design strategies against aviviral diseases are also available.3 5 Only brief background sketches of some of these topics that are relevant to a discussion of potential pharmacological targets will be presented here. Currently, dengue viruses (Den) are by far the most widespread and most virulent and pose the largest public health thereat. Quiescent mosquito reservoirs of the four serotypes of dengue (Den 1 4) in almost all tropical regions result in eruptions of frequent epidemics among the resident human population. It has been estimated that approximately 2.5 billion people, 40% of the world s population, live in areas that are endemic to dengue viruses and are at risk for infection.6 Estimated annual dengue infections number 100 million, with 500,000 cases of dengue hemorrhagic fever, resulting in an average of 25,000 deaths.7 Japanese encephalitis (JE), St. Louis encephalitis (SLE), and tickborne encephalitis (TBE) are also prevalent in many tropical regions, although they affect smaller proportions of the human population.8 11 West Nile virus (WNV), also present in many tropical regions, has been recently reintroduced into North America and has rapidly spread into many temperate regions.12 14 Other members that have recently infected human populations include Kyasanur Forest disease (KFD) virus, Omsk hemorrhagic fever (OHF) virus, and the Alkhurma virus.15 17 Besides being signi cant public health threats, Den, KFD, and OHF are thought to have bioterrorism potential.18 Vaccines are available to provide immunity against some of the aviviruses. The highly ef cacious YF17D vaccine currently provides immunity against the eponymous yellow fever virus, once the most widespread of aviviruses.19 Vaccines are also either available or in the advanced clinical trial stages for TBE, JE, and WNV.20 25 Progress on development of vaccines for KFD is also being made.26,27 The four serotypes of dengue appear to present a harder problem for vaccine design, because dengue infections are subject to antibody-dependent enhancement (ADE). Infection of any of the four serotypes results in the usually survivable dengue fever. However, a subsequent infection by a different serotype causes the more frequently fatal dengue hemorrhagic fever/dengue shock syndrome; apparently due to non-neutralizing cross-reaction of antibodies from the rst infection with the heterotypic virus followed by ef cient uptake of the antibody-bound virus via Fcg and complement receptors. Thus, although tetravalent dengue vaccines are under clinical trials, their ef cacy is yet to be demonstrated.21,28 32
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