Uberbug ping.
From a purely Darwiian standpoint, a really well-adapted virus causes little or no ill effect on its host.
I hate sloppy scietific writing.
The experience with Tamiflu during the Air Force Academy H1N1 outbreak in July seems to indicate that it doesn’t shorten duration of illness or decrease infectivity. I discussed that with another Critical Care doc and his response was, “Then what the F*** are we doing?”
Evolution of living organisms occurs through natural selection of genetic variation.
Thus the selective pressure of the mutagen and the increased genetic variation caused by the mutagen may well give rise to a genetic variation with beneficial (for the virus) attributes.
But as Jewbacca points out, the most beneficial variation for a virus is where they are highly infectious but cause little or no detrimental outcomes to the host species.
Simply put, medicine has long held the idea that the way to defeat a pathogenic disease is by killing it. But this invokes natural selection, as these pathogens don’t want to be killed. So it adapts to protect itself.
A better way is to interfere with the mechanisms the pathogens use to invade and replicate. This makes it much more difficult for natural selection to create an organism that can get by such defenses.
I see that nobody seemed to have learned much from anti-biotics.
That should have been the first thing that they considered that anti-viral resistant forms of viruses would crop up just as the anti-biotic resistant strains of bacteria did and so not prescribed stuff like Tamiflu prophylactically.
My daughter came down with the swine flu (they could trace the transmission from someone who was tested and confirmed to have it) and my PCP wrote out a prescription for everyone in the family. She took it because she caught it within the first day or so. She knew she had been exposed so when she started showing symptoms, it was no surprise. The rest of us were exposed as well and we THINK that my youngest daughter had it as well, but aren’t sure. She wasn’t sick enough.
The article isn’t exactly correct that it would make the viruses stronger. What it would do is that if stronger strains became anti-viral resistant, they would be harder to treat and more prevalent because they couldn’t be treated, and so be more likely to kill.
BTW, did you notice that the swine flu just kind of died out on its own? It was just about the time my oldest caught it, about Oct, IIRC, and then that was about the last you heard about it. I haven’t even heard of the regular flu being much of an issue.
By giving something that accelerates mutation to a very large number of infectious agents, in this case a strain of a virus, you increase the probability that you will kill many of not most of the viruses. But that is not good enough, it will most likely as well produce a virus that will cause problems.
It only takes one surviving virus that takes over the cell to multiply into several. The viral burst size, i.e., the number of viruses produced in a cell, can be very substantial from 50 to tens of thousands.
This was a result that could be anticipated before it was done.