Tuesday, July 14, 2009

How do mutations arise in RNA viruses?

As we understand more about the human genome, it becomes equally important to understand its relationship with the genomic environment. In the case of RNA viruses such as SARS, Hepatitis C or Influenza, an inappropriate interaction with a viral genome can result in death. The human genome defends itself by to engineering specific immunological factors (T cells, antibodies) that selectively target viral antigens. However, RNA viruses can rapidly mutate, escape immunological defenses and even become resistant to therapeutic drugs. A contemporary example is the ability of the Flu virus to mutate a single amino acid, rendering it resistant to Tamiflu. Most of our fundamental knowledge in genomics and molecular biology has accrued from the study of model virus systems. However, there is a remarkable lacuna in our understanding of the molecular mechanisms of RNA viral mutation. The current dogma is that such errors arise because of the lack of a proof reading function during replication. In short, a default concept. However, given that it is advantageous to mutate, one suspects that there are viral factors that actively catalyze mutagenesis. Perhaps the somatic hypermutation of the immunoglobulin genes is an attractive metaphor. In any event, much more attention should be devoted to investigating these mechanisms. It would be tragic if the current H1N1 pandemic further illuminates our lack of knowledge
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