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07-SEPTEMBER-2008 03:17:44 - Antiviral drug Antiviral drugs are a class of medication used specifically for treating viral infections. Like antibiotics for bacteria, specific antivirals are used for specific viruses. Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic, antifungal and antiparasitic drugs. They are relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which actively deactivate virus particles outside the body. Most of the antivirals now available are designed to help deal with HIV, herpes viruses best known for causing cold sores and genital herpes, but actually causing a wide range of diseases, the hepatitis B and C viruses, which can cause liver cancer, and influenza A and B viruses. Researchers are now working to extend the range of antivirals to other families of pathogens. The emergence of antivirals is the product of a greatly expanded knowledge of the genetic and molecular function of organisms, allowing biomedical researchers to understand the structure and function of viruses, major advances in the techniques for finding new drugs, and the intense pressure placed on the medical profession to deal with the human immunodeficiency virus HIV, the cause of the deadly acquired immunodeficiency syndrome AIDS pandemic. Almost all anti-microbials, including anti-virals, are subject to drug resistance as the pathogens evolve to survive exposure to the treatment. Contents 1 History 2 Virus life cycle 3 Inadequacy of vaccines 4 Anti-viral targeting technique 5 Approaches by life cycle stage 5.1 Before cell entry 5.2 During viral synthesis 5.3 Release phase 6 Immune system stimulation 7 See also 8 References History Modern medical science and practice has an array of effective tools, ranging from antiseptics to vaccines and antibiotics. One field in which medicine has historically been weak, however, is in finding drugs to deal with viral infections. Highly effective vaccines have been recently developed to prevent such diseases, but formerly, when someone contracted a virus, there was little that could be done but to recommend rest and plenty of fluids until the disease ran its course. The first experimental antivirals were developed in the 1960s, mostly to deal with herpes viruses, and were found using traditional trial-and-error drug discovery methods. Researchers grew cultures of cells and infected them with the target virus. They then introduced chemicals into the cultures they thought were likely to inhibit viral activity, and observed whether the level of virus in the cultures rose or fell. Chemicals that seemed to have an effect were selected for closer study. This was a very time-consuming, hit-or-miss procedure, and in the absence of a good knowledge of how the target virus worked, it was not efficient in discovering antivirals that were effective and had few side effects. It was not until the 1980s, when the full genetic sequences of viruses began to be unraveled, that researchers began to learn how viruses worked in detail, and exactly what chemicals were needed to thwart their reproductive cycle. Dozens of antiviral treatments are now available, and medical research is rapidly exploiting new knowledge and technology to develop more. Virus life cycle Viruses consist of a genome and sometimes a few enzymes stored in a capsule made of protein called a capsid, and sometimes covered with a lipid layer sometimes called an 'envelope'. Viruses cannot reproduce on their own, so they propagate by subjugating a host cell to produce copies of themselves, thus producing the next generation. Researchers working on such rational drug design strategies for developing antivirals have tried to attack viruses at every stage of their life cycles. Viral life cycles vary in their precise details depending on the species of virus, but they all share a general pattern: Attachment to a host cell. Release of viral genes and possibly enzymes into the host cell. Replication of viral components using host-cell machinery. Assembly of viral components into complete viral particles. Release of viral particles to infect new host cells. Inadequacy of vaccines Vaccines attack viruses when they are in the complete particle stage, outside of the organism's cells. They traditionally consist of a weakened or killed version of a pathogen. The vaccine can still cause harm to the host. Recently subunit vaccines have been devised that consist strictly of protein targets from the pathogen. They stimulate the immune system without doing serious harm to the host. In either case, when the real pathogen attacks the subject, the immune system responds to it quickly and blocks it. Vaccines are very effective on stable viruses, but are of limited use in treating a patient who has already been infected. They are also difficult to successfully deploy against rapidly mutating viruses, such as influenza the vaccine for which is updated every year and HIV. These two gaps are where antiviral drugs become useful. Anti-viral targeting technique The general idea behind modern antiviral drug design is to identify viral proteins, or parts of proteins, that can be disabled. These targets should generally be as unlike any proteins or parts of proteins in humans as possible, to reduce the likelihood of side effects. The targets should also be common across many strains of a virus, or even among different species of virus in the same family, so a single drug will have broad effectiveness. For example, a researcher might target a critical enzyme synthesized by the virus, but not the patient, that is common across strains, and see what can be done to interfere with its operation. Once targets are identified, candidate drugs can be selected, either from drugs already known to have appropriate effects, or by actually designing the candidate at the molecular level with a computer-aided design program. The target proteins can be manufactured in the lab for testing with candidate treatments by inserting the gene that synthesizes the target protein into bacteria or other kinds of cells. The cells are then cultured for mass production of the protein, which can then be exposed to various treatment candidates and evaluated with rapid screening technologies. Approaches by life cycle stage Before cell entry One anti-viral strategy is to interfere with the ability of a virus to infiltrate a target cell. The virus must go through a sequence of steps to do this, beginning with binding to a specific receptor molecule on the surface of the host cell and ending with the virus uncoating inside the cell and releasing its contents. Viruses that have a lipid envelope must also fuse their envelope with the target cell, or with a vesicle that transports them into the cell, before they can uncoat. This stage of viral replication can be inhibited in two ways: 1. Using agents which mimic the virus-associated protein VAP and bind to the cellular receptors. This may include VAP anti-idiotypic antibodies, natural ligands of the receptor and anti-receptor antibodies.clarify 2. Using agents which mimic the cellular receptor and bind to the VAP. This includes anti-VAP antibodies, receptor anti-idiotypic antibodies, extraneous receptor and synthetic receptor mimics. This strategy of designing drugs can be very expensive, and since the process of generating anti-idiotypic antibodies is partly trial and error, it can be a relatively slow process until an adequate molecule is produced. A very early stage of viral infection is viral entry, when the virus attaches to and enters the host cell. A number of entry-inhibiting or entry-blocking drugs are being developed to fight HIV. HIV most heavily targets the immune system white blood cells known as helper T cells, and identifies these target cells through T-cell surface receptors designated CD4 and CCR5. Attempts to interfere with the binding of HIV with the CD4 receptor have failed to stop HIV from infecting helper T cells, but research continues on trying to interfere with the binding of HIV to the CCR5 receptor in hopes that it will be more effective. However, two entry-blockers, amantadine and rimantadine, have been introduced to combat influenza, and researchers are working on entry-inhibiting drugs to combat hepatitis B and C virus. One entry-blocker is pleconaril. Pleconaril works against rhinoviruses, which cause the common cold, by blocking a pocket on the surface of the virus that controls the uncoating process. This pocket is similar in most strains of rhinoviruses and enteroviruses, which can cause diarrhea, meningitis, conjunctivitis, and encephalitis. During viral synthesis A second approach is to target the processes that synthesize virus components after a virus invades a cell. One way of doing this is to develop nucleotide or nucleoside analogues that look like the building blocks of RNA or DNA, but deactivate the enzymes that synthesize the RNA or DNA once the analogue is incorporated. The first successful antiviral, acyclovir, is a nucleoside analogue, and is effective against herpesvirus infections. The first antiviral drug to be approved for treating HIV, zidovudine AZT, is also a nucleoside analogue. An improved knowledge of the action of reverse transcriptase has led to better nucleoside analogues to treat HIV infections. One of these drugs, lamivudine, has been approved to treat hepatitis B, which uses reverse transcriptase as part of its replication process. Researchers have gone further and developed inhibitors that do not look like nucleosides, but can still block reverse transcriptase. Other targets being considered for HIV antivirals include RNase H - which is a component of reverse transcriptase that splits the synthesized DNA from the original viral RNA - and integrase, which splices the synthesized DNA into the host cell genome. Once a virus genome becomes operational in a host cell, it then generates messenger RNA mRNA molecules that direct the synthesis of viral proteins. Production of mRNA is initiated by proteins known as transcription factors. Several antivirals are now being designed to block attachment of transcription factors to viral DNA. Genomics has not only helped find targets for many antivirals, it has provided the basis for an entirely new type of drug, based on antisense molecules. These are segments of DNA or RNA that are designed as mirror images to critical sections of viral genomes, and the binding of these antisense segments to these target sections blocks the operation of those genomes. A phosphorothioate antisense drug named fomivirsen has been introduced, used to treat opportunistic eye infections in AIDS patients caused by cytomegalovirus, and other antisense antivirals are in development. An antisense structural type that has proven especially valuable in research is morpholino antisense. Morpholino oligos have been used to experimentally suppress many viral types including caliciviruses 1, flaviviruses including WNV 2 , Dengue 3 and HCV 4 , and coronaviruses 5 and are currently in clinical development. Yet another antiviral technique inspired by genomics is a set of drugs based on ribozymes, which are enzymes that will cut apart viral RNA or DNA at selected sites. In their natural course, ribozymes are used as part of the viral manufacturing sequence, but these synthetic ribozymes are designed to cut RNA and DNA at sites that will disable them. A ribozyme antiviral to deal with hepatitis C is in field testing, and ribozyme antivirals are being developed to deal with HIV. An interesting variation of this idea is the use of genetically modified cells that can produce custom-tailored ribozymes. This is part of a broader effort to create genetically modified cells that can be injected into a host to attack pathogens by generating specialized proteins that block viral replication at various phases of the viral life cycle. Some viruses include an enzyme known as a protease that cuts viral protein chains apart so they can be assembled into their final configuration. HIV includes a protease, and so considerable research has been performed to find protease inhibitors to attack HIV at that phase of its life cycle. Protease inhibitors became available in the 1990s and have proven effective, though they can have unusual side effects, for example causing fat to build up in unusual places. Improved protease inhibitors are now in development. Release phase The final stage in the life cycle of a virus is the release of completed viruses from the host cell, and this step has also been targeted by antiviral drug developers. Two drugs named zanamivir Relenza and oseltamivir Tamiflu that have been recently introduced to treat influenza prevent the release of viral particles by blocking a molecule named neuraminidase that is found on the surface of flu viruses, and also seems to be constant across a wide range of flu strains. Immune system stimulation A second category of tactics for fighting viruses involves encouraging the body's immune system to attack them, rather than attacking them directly. Some antivirals of this sort do not focus on a specific pathogen, instead stimulating the immune system to attack a range of pathogens. One of the best-known of this class of drugs are interferons, which inhibit viral synthesis in infected cells. One form of human interferon named interferon alpha is well-established as a treatment for hepatitis B and C, and other interferons are also being investigated as treatments for various diseases. A more specific approach is to synthesize antibodies, protein molecules that can bind to a pathogen and mark it for attack by other elements of the immune system. Once researchers identify a particular target on the pathogen, they can synthesize quantities of identical monoclonal antibodies to link up that target. A monoclonal drug is now being sold to help fight respiratory syncytial virus in babies, and another is being tested as a treatment for hepatitis B. Examination of the genomes of viruses and comparison with the human genome show that some generate proteins that mimic those used by the human immune system, confusing the immune system response. Researchers are now searching for antivirals that can recognize these intruder proteins and disable them. See also Antiretroviral drug List of antiviral drugs References June 2007 v d e Antivirals, other than for HIV primarily J05, also S01AD and D06BB Anti-herpesvirus DNA, I purine analogue guanine Aciclovir, Famciclovir, Ganciclovir, Penciclovir, Valaciclovir, Valganciclovir Vidarabine pyrimidine analogue uridine Idoxuridine, Trifluridine Brivudine Cidofovir Docosanol Fomivirsen Foscarnet Tromantadine HPV/MC DNA, I Imiquimod Podophyllotoxin Hepatitis B DNA, VII Adefovir Clevudine Interferon alfa-2b Pegylated interferon alfa-2a Entecavir Lamivudine Telbivudine Tenofovir Hepatitis C RNA, IV Pegylated interferon alpha Ribavirin Taribavirin† Boceprevir† Telaprevir† Picornavirus RNA, IV Pleconaril† Anti-influenza agents RNA, V Arbidol adamantane derivatives/M2 inhibitors Amantadine, Rimantadine neuraminidase inhibitors Oseltamivir, Zanamivir, Peramivir† HIV Reverse, VI See HIV pharm Other antiviral agents general Inosine, Interferon †Undergoing clinical trials, not FDA approved. v d e Antivirals used against HIV HAART primarily J05 Nucleoside Nucleotide Reverse Transcriptase Inhibitors NRTI Abacavir ABC° Dexelvucitabine§ Emtricitabine° Lamivudine 3TC° Tenofovir° Didanosine Zidovudine AZT Apricitabine† Stampidine† Elvucitabine† Racivir† Amdoxovir† Stavudine‡ Zalcitabine‡ Non-Nucleoside Reverse Transcriptase Inhibitors NNRTI Ateviridine§ Capravirine§ Efavirenz° Emivirine§ Lodenosine§ Nevirapine Etravirine Rilpivirine† Loviride‡ Delavirdine‡ Quinotaline§ Protease Inhibitors PI Atazanavir° Brecanavir§ Fosamprenavir° Lopinavir° Darunavir Nelfinavir Ritonavir Saquinavir Tipranavir Amprenavir‡ Indinavir‡ Entry/fusion inhibitors Aplaviroc§ Enfuvirtide Maraviroc Vicriviroc† PRO 140† Ibalizumab† Integrase inhibitors Raltegravir Elvitegravir† Maturation inhibitors Bevirimat† Vivecon† Combined formulations Combivir Atripla Trizivir Truvada Kaletra Epzicom Other experimental agents Foscarnet Hydroxyurea Synergistic enhancers Epigallocatechin gallate Portmanteau inhibitors Globoidnan A Griffithsin Diarylpyrimidines Calanolide A Cyanovirin-N Miltefosine R-roscovitine† °DHHS preferred first-line agent. †Undergoing clinical trials, not FDA approved. ‡Formerly or rarely used agent. §Development terminated. v d e Major drug groups Gastrointestinal tract/metabolism A stomach acid Antacids, H2 antagonists, Proton pump inhibitors Antiemetics Laxatives Antidiarrhoeals/Antipropulsives Anti-obesity drugs Anti-diabetics Vitamins Dietary minerals Blood and blood forming organs B Antithrombotics Anticoagulants, Antiplatelets, Thrombolytics Antihemorrhagics Cardiovascular system C cardiac therapy/antianginals Cardiac glycosides, Antiarrhythmics, Cardiac stimulant Antihypertensives Diuretics Vasodilators Beta blockers renin-angiotensin system ACE inhibitors, Angiotensin II receptor antagonists, Renin inhibitors Antihyperlipidemics Skin D Emollients Cicatrizant Antipruritics Reproductive system G Hormonal contraception Fertility agents SERMs Sex hormones Endocrine system H Corticosteroids Sex hormones Thyroid hormones Antithyroid agent Infections and infestations J, P Antibiotics Antivirals Vaccines Antifungals Antiparasitic Antiprotozoals, Anthelmintics Malignant and immune disease L Anticancer agents Immunostimulators Immunosuppressants Muscles, bones, and joints M Anabolic steroids Anti-inflammatories NSAID Antirheumatics Corticosteroids Muscle relaxants Brain and nervous system N Anesthetics General, Local Analgesics Anticonvulsants Mood stabilizers Psycholeptic Anxiolytics, Antipsychotics, Hypnotics/Sedatives Psychoanaleptic Antidepressants, Stimulants/Psychostimulants Respiratory system R Bronchodilators Decongestants H1 antagonists Other ATC V Antidotes Contrast media Radiopharmaceuticals Dressing Retrieved from http://en..org/wiki/Antiviral_drug Categories: AntiviralsHidden categories: articles needing clarification | Articles lacking sources from June 2007 | All articles lacking sources Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Türkçe Català Dansk Deutsch Español Français Italiano 日本語 Polski Svenska ไทย This page was last modified on 25 August 2008, at 19:01
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