5 Feb 2009


My colleagues were surprised when I celebrated the 200th anniversary of the birth of Charles Darwin in a public talk on hepatitis B recently.

Explaining the evolutionary theory to non-specialists is a bit tricky, but people working on antiviral therapy use the theory all the time. The essence of the evolutionary theory is ‘survival of the fittest’. During reproduction, gene mutations sometimes result in phenotypic changes in an organism. Most of the mutations are hazardous, but a minority confers competitiveness. Organisms bearing more competitive mutations have a better chance of giving birth to offsprings, and eventually the new gene will dominate the population. People working with viruses are seeing a fast-forward version of evolution. Viruses replicate quickly and produce a lot of mutations because of their lack of proof-reading during gene transcription. When an antiviral drug is given to a patient, viral mutants that do not fear the drug will replicate more effectively and soon become the dominant strain.

Actually, before Darwin published his book On the Origin of Species, a few other scientists had already noticed the gradual phenotypic changes of animals and plants. However, most considered the changes a well-planned evolution by God. It was Darwin who spotted that the changes were random, and the evolution was driven by natural selection – ‘survival of the fittest’. For those with basic knowledge on genetics, the theory may seem pretty easy to understand. However, one must remember that genetics did not exist at Darwin’s time (although Gregor Mendel was actually humbly doing his cross-breeding experiments at roughly the same time). Imagine how difficult it would be for me to explain the last paragraph again without describing anything about genes and mutations.

Like all great theories, the implications extend well beyond the original territories. I will elaborate this further next week.

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