question: How do antiviral drugs work, and how to they differ from antibacterial drugs?
comment: First you have to understand a key difference between bacteria and viruses. Bacteria reproduce and multiple by growing and then dividing. So one bacteria gets big and then splits into two and then those two each split into two and so on and so forth. Viruses can't multiply on their own like this. Viruses instead need a host (like a person). They basically break into the cells of the host and trick the host's own cells into make more viruses. Because viruses use the host's own cells, it's difficult to make medicines that attack just the viruses. A lot of antivirals are design to attack some stage of this process whereas a lot of antibacterial drugs are design to attack the bacteria themselves.
passages: Section::::Chemical.:Antivirals.
  
  Antiviral drugs are a class of medication used specifically for treating viral infections. Like antibiotics, specific antivirals are used for specific viruses. 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.
   Antiviral drug
  
  Antiviral drugs are a class of medication used specifically for treating viral infections rather than bacterial ones. Most antivirals are used for specific viral infections, while a broad-spectrum antiviral is effective against a wide range of viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit their development.
   Specific antiviral drugs are used to treat some viral infections. These drugs prevent viruses from reproducing by inhibiting essential stages of the virus's replication cycle in infected cells. Antivirals are used to treat HIV, hepatitis B, hepatitis C, influenza, herpes viruses including varicella zoster virus, cytomegalovirus and Epstein-Barr virus. With each virus, some strains have become resistant to the administered drugs.
   Morpholino oligos have been used to experimentally suppress many viral types:
  
  BULLET::::- caliciviruses
  
  BULLET::::- flaviviruses (including WNV)
  
  BULLET::::- dengue
  
  BULLET::::- HCV
  
  BULLET::::- coronaviruses
  
  Section::::Approaches by life cycle stage.:During viral synthesis.:Translation/ribozymes.
  
  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.
   Many antiviral drugs are designed to treat infections by retroviruses, mostly HIV. Important antiretroviral drugs include the class of protease inhibitors. Herpes viruses, best known for causing cold sores and genital herpes, are usually treated with the nucleoside analogue acyclovir. Viral hepatitis is caused by five unrelated hepatotropic viruses (A-E) and can be treated with antiviral drugs depending on the type of infection. influenza A and B viruses have become resistant to neuraminidase inhibitors such as oseltamivir and the search for new substances is on.
  
  Section::::Chemical.:Antiparasitics.
   Antiviral drugs are often nucleoside analogues (fake DNA building-blocks), which viruses mistakenly incorporate into their genomes during replication. The life-cycle of the virus is then halted because the newly synthesised DNA is inactive. This is because these analogues lack the hydroxyl groups, which, along with phosphorus atoms, link together to form the strong "backbone" of the DNA molecule. This is called DNA chain termination. Examples of nucleoside analogues are aciclovir for Herpes simplex virus infections and lamivudine for HIV and Hepatitis B virus infections. Aciclovir is one of the oldest and most frequently prescribed antiviral drugs.
   Section::::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.
   An alternative way to treat viral infections would be antiviral drugs in which the drug blocks the virus's replication cycle. The specificity of an antiviral drug is the key to its success. These drugs are toxic to both the virus and the host but in order to minimize their damage they are developed in such a way as to be more toxic to the virus than to the host. The efficiency of an antiviral drug is measured by the chemotherapeutic index, given by:
  
  Section::::Additional links.
  
  BULLET::::- molecular biology
  
  BULLET::::- phage, the virus of bacteria/prokaryotes
  
  BULLET::::- viral plaque
   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 antibodies purified from infected individuals are also used as a treatment for hepatitis B.
  
  Section::::Acquired resistance.
   Interference with post translational modifications or with targeting of viral proteins in the cell is also possible.
  
  Section::::Approaches by life cycle stage.:During viral synthesis.:Protease inhibitors.
   This stage of viral replication can be inhibited in two ways:
  
  BULLET::::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.
  
  BULLET::::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.
   Section::::Approaches by life cycle stage.:During viral synthesis.:Reverse transcription.
  
  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. This approach is more commonly associated with the inhibition of reverse transcriptase (RNA to DNA) than with "normal" transcriptase (DNA to RNA).
  
  The first successful antiviral, aciclovir, 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.
   Antiviral drugs typically target key components of viral reproduction; for example, oseltamivir targets influenza neuraminidase, while guanosine analogs inhibit viral DNA polymerase. Resistance to antivirals is thus acquired through mutations in the genes that encode the protein targets of the drugs.
   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 part of the standard treatment for hepatitis B and C, and other interferons are also being investigated as treatments for various diseases.
   Another target is integrase, which integrate the synthesized DNA into the host cell genome.
  
  Section::::Approaches by life cycle stage.:During viral synthesis.:Transcription.
  
  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.
  
  Section::::Approaches by life cycle stage.:During viral synthesis.:Translation/antisense.
   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's 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.
   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 complementary molecule 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.
   Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic (also termed antibacterial), antifungal and antiparasitic drugs, or antiviral drugs based on monoclonal antibodies. Most antivirals are considered relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which are not medication but deactivate or destroy virus particles, either inside or outside the body. Natural antivirals are produced by some plants such as eucalyptus and Australian tea trees.
  
  Section::::Medical uses.
   A ribozyme antiviral to deal with hepatitis C has been suggested, 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.
  
  Section::::Approaches by life cycle stage.:During viral synthesis.:Protein processing and targeting.
   List of antiviral drugs
  
  This is a list of antiviral drugs.
  
  Section::::A.
  
  BULLET::::- Abacavir Use for HIV
  
  BULLET::::- Acyclovir (Aciclovir) Use for herpes e.g. Chicken pox
  
  BULLET::::- Adefovir Use for chronic Hepatitis B
  
  BULLET::::- Amantadine Use for influenza
  
  BULLET::::- Amprenavir(Agenerase) Use for inhibition of HIV
  
  BULLET::::- Ampligen
  
  BULLET::::- Arbidol
  
  BULLET::::- Atazanavir
  
  BULLET::::- Atripla (fixed dose drug)
  
  Section::::B.
  
  BULLET::::- Balavir
  
  Section::::C.
  
  BULLET::::- Cidofovir
  
  BULLET::::- Combivir (fixed dose drug)
  
  Section::::D.
  
  BULLET::::- Dolutegravir
  
  BULLET::::- Darunavir
  
  BULLET::::- Delavirdine
  
  BULLET::::- Didanosine
  
  BULLET::::- Docosanol
  
  Section::::E.
  
  BULLET::::- Edoxudine
  
  BULLET::::- Efavirenz
  
  BULLET::::- Emtricitabine
  
  BULLET::::- Enfuvirtide
  
  BULLET::::- Entecavir
  
  BULLET::::- Ecoliever
  
  Section::::F.
  
  BULLET::::- Famciclovir
  
  BULLET::::- Fixed dose combination (antiretroviral)
   Protease inhibitors have also been seen in nature. A protease inhibitor was isolated from the Shiitake mushroom ("Lentinus edodes"). The presence of this may explain the Shiitake mushroom's noted antiviral activity "in vitro".
  
  Section::::Approaches by life cycle stage.:Assembly.
  
  Rifampicin acts at the assembly phase.
  
  Section::::Approaches by life cycle stage.:Release phase.
   Vaccines bolster the body's immune system to better attack viruses in the "complete particle" stage, outside of the organism's cells. They traditionally consist of an attenuated (a live weakened) or inactivated (killed) version of the virus. These vaccines can, in very rare cases, harm the host by inadvertently infecting the host with a full-blown viral occupancy . 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.
   Section::::Production.
  
  Section::::Production.:Development.
   Section::::Anti-viral targeting.
   There is little evidence to support the use of antivirals such as aciclovir and valacyclovir although they may reduce initial viral shedding. Although antivirals are not recommended for people with simple infectious mononucleosis, they may be useful (in conjunction with steroids) in the management of severe EBV manifestations, such as EBV meningitis, peripheral neuritis, hepatitis, or hematologic complications.
  
  Although antibiotics exert no antiviral action they may be indicated to treat bacterial secondary infections of the throat, such as with streptococcus (strep throat). However, ampicillin and amoxicillin are not recommended during acute Epstein–Barr virus infection as a diffuse rash may develop.
  