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To: Seeker of Truth who wrote (37308)	8/19/2003 7:20:08 AM
From: smolejv@gmx.net	Read Replies (1) \| Respond to of 74559

>>In the consequent struggle for survival are not the fittest those who don't kill the patients, but merely cause a (contagious) cold<< The final result (after the 10th inning or later) says nothing about how the game proceeds from 1st to 10th (dynamics of it - predator-prey for instance). One can easily envisage a virus (HIV, SARS, Ebola) to finish off with the human race to return to / stick to chimpanzees/swine or birds/gorillas (?) after the game - place where it came from. A short interlude in the game of viri. Quite easy, yes. Probable? Not very much. It's all a question of probabilities, where one-time events (crossing the inter-species barrier for instance) are, well, 10sigma events.

To: Seeker of Truth who wrote (37308)	8/19/2003 8:40:22 AM
From: Henry Niman	Respond to of 74559

The virus mutates frequently (as many as 3 times each time it divides) because it does not have a proof reading function - my posts have frequent errors even with a spell checker. Beacuse there are so many variant version, there is ample opportunity to select for virus that offers a selection advantage. This is a new virus in humans, so the selection process is hard at work. It produced many stable mutations back in the fall of 2002 and winter of 2003. In fact these mutations are so stable that they are found in virtually all human isolates (there are about 50 early mutations). Since jumping from the Metropole Hotel, it has accumulated addition mutations which are still pretty regional. The isolates with the most mutations are in Taiwan, where the case mortality rate was highest before the epidemic abruptly stopped. Some, including myself, think that the halt was largely due to seasonal factors. The Surrey outbreak happened in the summer, so it is not clear if the virus is less fatal, or seasonal co-factors are missing. The sequence of the first 200 nucleotides (out of about 30,000) show no mutations, but 200 is not very predictive of 30,000 (although it shows that the virus in Surrey is not a distant relative and is probably virtually identical to the SARS CoV. A virus that just replicates without killing its host should be pretty selectable. However, some of the selection for replication in the host may simultaneously select for lethality. Unfortuantely, I think it is much too early in the process for the virus to have found the most advantageous genetic composition. Therefore I am not confident that the virus in Surrey is anywhere near then end of the mutational line. In fact because of the season, I am not sure that the virus has any significant genetic differences than the lethal virus seen in Toronto. I suspect the virus in Surrey is related most closely to the SARS virus transmitted at Surrey Memorial Hospital last April. BC only had 4 probable SARS cases and two involved the virus at Surrey Memorial, so that virus wasn't very transmissible and no one died in BC in the earlier outbreak. However, the current virus in Surrey is certainly very transmissible (151 or 302 patients and staff have symptoms) and the three pneumonia linked deaths are under investigation (early media reports indicated at least one had tested positive for the virus which if true would confirm the first SARS fatality in BC).