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Explore Apps. About About Drugs. They should be distinguished from viricides , which are not medication but deactivate or destroy virus particles, either inside or outside the body.
Natural viricides are produced by some plants such as eucalyptus and Australian tea trees. Researchers are working to extend the range of antivirals to other families of pathogens.
Designing safe and effective antiviral drugs is difficult because viruses use the host's cells to replicate. This makes it difficult to find targets for the drug that would interfere with the virus without also harming the host organism's cells.
Moreover, the major difficulty in developing vaccines and anti-viral drugs is due to viral variation. 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 pressure placed on the medical profession to deal with the human immunodeficiency virus HIV , the cause of acquired immunodeficiency syndrome AIDS.
The first experimental antivirals were developed in the s, 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 into the cultures chemicals which they thought might 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 effective antivirals which had few side effects.
Only in the s, when the full genetic sequences of viruses began to be unraveled, did researchers begin to learn how viruses worked in detail, and exactly what chemicals were needed to thwart their reproductive cycle.
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 by 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.
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 and instead 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.
Some species of mushrooms have been found to contain multiple antiviral chemicals with similar synergistic effects.
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 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's white blood cells known as "helper T cells", and identifies these target cells through T-cell surface receptors designated " CD4 " and " CCR5 ".
HIV infects a cell through fusion with the cell membrane, which requires two different cellular molecular participants, CD4 and a chemokine receptor differing depending on the cell type.
At least one of these entry inhibitors—a biomimetic peptide called Enfuvirtide , or the brand name Fuzeon—has received FDA approval and has been in use for some time.
Potentially, one of the benefits from the use of an effective entry-blocking or entry-inhibiting agent is that it potentially may not only prevent the spread of the virus within an infected individual but also the spread from an infected to an uninfected individual.
One possible advantage of the therapeutic approach of blocking viral entry as opposed to the currently dominant approach of viral enzyme inhibition is that it may prove more difficult for the virus to develop resistance to this therapy than for the virus to mutate or evolve its enzymatic protocols.
Inhibitors of uncoating have also been investigated. Amantadine and rimantadine have been introduced to combat influenza.
These agents act on penetration and uncoating. 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.
Some scientists are making the case that a vaccine against rhinoviruses, the predominant cause of the common cold, is achievable.
Vaccines that combine dozens of varieties of rhinovirus at once are effective in stimulating antiviral antibodies in mice and monkeys, researchers have reported in Nature Communications in Rhinoviruses are the most common cause of the common cold; other viruses such as respiratory syncytial virus , parainfluenza virus and adenoviruses can cause them too.
Rhinoviruses also exacerbate asthma attacks. Although rhinoviruses come in many varieties, they do not drift to the same degree that influenza viruses do.
A mixture of 50 inactivated rhinovirus types should be able to stimulate neutralizing antibodies against all of them to some degree. A second approach is to target the processes that synthesize virus components after a virus invades a cell.
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.
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