What do the common cold, the flu, herpes and AIDS have in common? Viruses cause them. There's more. Hepatitis, polio, RSV, Ebola, foot-and-mouth disease, coxsackievirus, Kaposi's sarcoma, some encephalitis and HPV don't even complete the list of viral infections known to humans. Following the dawn of antibiotics, antivirals were developed and launched onto the pharmaceutical scene. As researchers discover more about the physical makeup of the virus, new approaches to disable the virus arise.
Virus Features
Bacterium proved their vital existence when scientists found they lived and grew outside of a host. Not so with viruses. Outside of a host, viruses show no sign of life. They have no metabolism, which orchestrates body function. They do not grow. Viruses depend entirely on a host in order to replicate. According to Scientific-American.com, viruses do not fit the definition of life yet they have become a real presence in humans. Replication, also called infection, becomes possible by their physical design. A fragmented bit of RNA or DNA makes up their core structure. Then, a protein sheath envelopes them from the outside. They exist for one reason only -- to replicate and grow in number.
Virus Behavior
It does not matter that viruses border between life and chemistry, they still have a way of latching on to other living things. CBC News in Canada explains how this happens. They enter the body either by going through the cell membrane or else they sit on the membrane and inject their genetic material through it and into the cell. Once infected, the cell's chemical machinery responds to the genetic information of the virus and begins making parts for creating new viruses. As the new virus bodies fill the cell, they break open the membrane, killing the cell and move on to invading other cells.
Antiviral Strategies
Once scientists understood what the virus was, they scrambled to study ways to stop its spread. According to Science Media Center.org, 2009, antivirals work on the flu virus by disabling the "N" protein molecule on the surface of the virus. At the top of the molecule the antiviral deposits a pocket of itself. Specifically, Relenza and Tamiflu work this way. "H" and "N" proteins on the top of the virus help it make its way into human cells. The "H" protein enables passageway and the "N" enables the new viruses to exit the cell's membrane and enter other cells. By tampering with the "N" protein, the medicine prevents the virus from spreading. Other influenza antivirals work by blocking molecular sites meant for viral use or by uncoating the viral sheath.
Genetic Manipulation
Acyclovir and gancyclovir treat the cytomegalovirus, CMV, an eye infection seen in AIDs patients. They accomplish by replicating the virus's genome or genetic data. Microbiology Bytes.com, 2010, explains that viruses have evolved to where their genome has specificity. This gives scientists a target for which to develop antiviral medicines. Genome replication works better in viruses than gene expression does, because viruses badly need the cell's machinery for its replication process.
Research
So far, other mechanisms remain in the testing stage. The journal "Pharmaceuticals" reported a 2010 study conducted by the School of Public Health, University of California at Berkeley. The details, though complicated and thorough, all link to their work with CPPs, cell-penetrating peptides. CPPs, the key to access into the virus, couple with other agents to gain access to the virus's genetic material. In a sense, CPP gains access for the agent and then the agent plays the role of the assassin. Some viruses have evolved to where current medications can't extinguish them. Science continues to seek new ways to "outsmart" them but have to proceed with caution. Microbiology Bytes.com put it succinctly when it wrote, "Any stage of virus replication can be a target for a drug, but the drug must be more toxic to the virus than to the host."
