Viral Evolution? Not a problem

The infamous swine flu virus is teetering on the edge of a world wide pandemic, with signs of resistance to the Governments stockpile of Tamiflu. It’s a relief to note the work being done in genetics to develop a new generation of antiviral drugs. Michael Goldblatt from the biotech company, Functional Genetics, is one of a group of researchers that believe they have found the key to viral evolution or at least preventing infection from slight mutations, which render conventional antiviral useless in treating the new strains. At present the antiviral blocks replication by binding to the viral protein, which relies on drug specificity for each individual strain of viral infection? The discoveries by Goldblatt rely on the basis that viruses are dependant on their hosts. They hijack normal host cells processes to facilitate viral propagation and deceive the host into making copies of the virus. Some of these host proteins that are in fact essential for the replication of the virus are not required by the cell for its normal functioning and survival. The proposal is to disable these proteins in order to block viral replication. Many viral strains are found to use the TSG101 protein, as it is involved in mediating intracellular transport and when hijacked plays a role in viral budding and release of the virus. By using this form of transport however is leaves a ‘fingerprint’ of human protein, one by which multiple viruses use as their mechanism for attack, and therefore is not specific mechanism to each virus. It has been found that there are many viral families that rely on this one mechanism for viral propagation, and as a result you have a therapeutic that can identify and block every virus that uses this mechanism.

Philip Thorpe, a pharmacologist at the University of Texas Medical Centre, has developed an antibody that is able to bind to these ‘fingerprinted’ infected cells, and destroys it to prevent further replication. The antiviral drugs on the market today do not take into consideration the ease in which the virus can mutate when the drug is interacting with the viral protein. It is not clear however, how a virus can mutate to such a great degree to change the mechanism by which they infect cells, which appears to be a far sure and more effective angle to approach to take when trying to prevent the spread of viral infection. There is the probability that a virus will eventually overcome this, but how far away that time is, is uncertain, and definitely not obvious.

By Dion Zunker (42063519)

Original Article: New scientist; Bob Holmes (10 August 2009); Magazine issue 2720; http://www.newscientist.com/article/mg20327200.100-how-to-cure-diseases-before-they-have-even-evolved.html