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The first successful antiviral, aciclovir , is a nucleoside analogue, and is effective against herpesvirus infections.
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.
Another target is integrase , which integrate 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 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. 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 has been suggested,  and ribozyme antivirals are being developed to deal with HIV.
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.
Interference with post translational modifications or with targeting of viral proteins in the cell is also possible.
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 have also been seen in nature. A protease inhibitor was isolated from the Shiitake mushroom Lentinus edodes. Most viruses produce long dsRNA helices during transcription and replication.
In contrast, uninfected mammalian cells generally produce dsRNA helices of fewer than 24 base pairs during transcription.
In cell culture, DRACO was reported to have broad-spectrum efficacy against many infectious viruses, including dengue flavivirus , Amapari and Tacaribe arenavirus , Guama bunyavirus , H1N1 influenza and rhinovirus , and was additionally found effective against influenza in vivo in weanling mice.
It was reported to induce rapid apoptosis selectively in virus-infected mammalian cells, while leaving uninfected cells unharmed. The procaspases transactivate via cleavage, activate additional caspases in the cascade, and cleave a variety of cellular proteins, thereby killing the cell.
Rifampicin acts at the assembly 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.
Rather than attacking viruses directly, a second category of tactics for fighting viruses involves encouraging the body's immune system to attack them.
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.
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.
Antiviral resistance can be defined by a decreased susceptibility to a drug caused by changes in viral genotypes.
In cases of antiviral resistance, drugs have either diminished or no effectiveness against their target virus. The Centers for Disease Control and Prevention CDC inclusively recommends anyone six months and older to get a yearly vaccination to protect them from influenza A viruses H1N1 and H3N2 and up to two influenza B viruses depending on the vaccination.
However, vaccines are preventative and are not generally used once a patient has been infected with a virus. Additionally, the availability of these vaccines can be limited based on financial or locational reasons which can prevent the effectiveness of herd immunity, making effective antivirals a necessity.
Currently, neuraminidase inhibitors NAIs are the most frequently prescribed antivirals because they are effective against both influenza A and B.
However, antiviral resistance is known to develop if mutations to the neuraminidase proteins prevent NAI binding. Furthermore, a study published in in Nature Biotechnology emphasized the urgent need for augmentation of oseltamivir Tamiflu stockpiles with additional antiviral drugs including zanamivir Relenza.
This finding was based on a performance evaluation of these drugs supposing the H1N1 'Swine Flu' neuraminidase NA were to acquire the Tamiflu-resistance HisTyr mutation which is currently widespread in seasonal H1N1 strains.
The genetic makeup of viruses is constantly changing, which can cause a virus to become resistant to currently available treatments. The mechanisms for antiviral resistance development depend on the type of virus in question.
RNA viruses such as hepatitis C and influenza A have high error rates during genome replication because RNA polymerases lack proofreading activity.
DNA viruses are therefore less error prone, are generally less diverse, and are more slowly evolving than RNA viruses.
Billions of viruses are produced every day during the course of an infection, with each replication giving another chance for mutations that encode for resistance to occur.
Multiple strains of one virus can be present in the body at one time, and some of these strains may contain mutations that cause antiviral resistance.
Antiviral resistance has been reported in antivirals for herpes, HIV, hepatitis B and C, and influenza, but antiviral resistance is a possibility for all viruses.
National and international surveillance is performed by the CDC to determine effectiveness of the current FDA-approved antiviral flu drugs.
WHO further recommends in-depth epidemiological investigations to control potential transmission of the resistant virus and prevent future progression.
If a virus is not fully wiped out during a regimen of antivirals, treatment creates a bottleneck in the viral population that selects for resistance, and there is a chance that a resistant strain may repopulate the host.
The most commonly used method for treating resistant viruses is combination therapy, which uses multiple antivirals in one treatment regimen. This is thought to decrease the likelihood that one mutation could cause antiviral resistance, as the antivirals in the cocktail target different stages of the viral life cycle.
This minimizes exposure to unnecessary antivirals and ensures that an effective medication is being used. This may improve patient outcomes and could help detect new resistance mutations during routine scanning for known mutants.
Some notably more than others. But perhaps those who have been destabilized the most are the ones who struggle with addiction disorders.
Experts are predicting a record year for opioid-related overdosages, surpassing lasts […]. With the weather heating up across the U.
Escaping into the sun is something we are all looking forward to, especially after a winter of confinement at home. But did you know that heat-related deaths are one of the deadliest weather-related outcomes in […].
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