This post is different from previous ones I've made. I'm going to try to put current problems and controversies into a broader biological perspective. This will not appeal to everyone. The problem I'm grappling with is a fundamental one with implications far beyond the moment. Abstractions mentioned are likely to be unfamiliar. This does not mean they are vague, sloppy or inapplicable, only different.
Darwin struggled with a central problem of biology which he rightly used in the title of his famous work 'the origin of the species'. Considering the state of the art at the time, he did a remarkable job of demonstrating that random variation and natural selection were observed facts. In the end, however, he had trouble with the apparent existence of fixed species on many time scales. This doesn't say he was wrong, only that theoretical biology was incomplete.
In the 1970s, a radical thesis called 'punctuated equilibrium' came into vogue. By that time there was sufficient fossil evidence to show that many species undergo remarkably little change for long periods of time, until they disappear. This was, in a sense, a general observation rather than a theory of how this came to be. If there was a comprehensive underlying framework, it passed most biologists by. You can get a remarkable range of explanations from various biologists today.
The revolution in molecular biology was just getting underway at that time. If anyone proposed a human genome project back then, it could be demonstrated to be absurd. Since that time there has been a great deal of work, but if there has been an 'origin of the quasispecies' it has escaped me. This is what would be needed to explain the evolution of retroviral sequences.
We see a situation in the discussion of viral species which can easily explain diffusion away from an ancestral species, but has to rely on near miracles or vast times for the origin of those species. This is particularly apparent in the debate over the origin of XMRV. The problem is much more general.
When researchers chase contamination, their focus is very narrow. They aren't thinking about general biological principles. Most of the time they aren't able to trace the exact path by which contamination occurred. Even in successful cases, the story is unlikely to get written up and published. It becomes part of the folklore of the field. Assumptions are unlikely to be exposed to critical reappraisal.
One principle of large scale evolution is that convergent evolution never produces identical species. You may find a marsupial small-animal predator that resembles a fox, but detailed examination will always reveal a huge catalog of differences. It might have a jaw that works like a fox's jaw, but the bones forming it will have a different embryological origin. You can't simply move the jaw from one species to an unrelated species.
At the level of molecular evolution of quasispecies, things are less clear. Recombination is not limited to the same species or genus. Convergence to a particular sequence can take place in a specific environment.
We can talk about the 'fitness landscape' in a particular environment as if it were a kind of topographic map. The different coordinates would correspond to different sequences, while the altitude would give you the likelihood that sequence will replicate well in that environment. Small-scale evolution can then lead to hill climbing, which ends at a peak. Many similar sequences may converge on the same peak.
In the language of dynamical systems the altitude is reversed. Now you replace hill climbing with a process like water running downhill. The region leading to a particular common end point is called a basin of attraction, and the end point is called an attractor.
Mathematically, this can be modeled as an iterated map which converges to a fixed point. The property of having a fixed point is very general, but it is typically true of non-linear maps. Most of the convenient mathematics taught in schools is linear.
A fixed point is not the only possible outcome. Another possibility is a limit cycle, where the same sequence of states repeats endlessly. There is even a stranger possibility appropriately called a 'strange attractor'. (Poincar type-three motion for high-brows.)
At this time, I only need to consider a fixed point. In a very simple environment, like a carefully-tended cell line, the fitness landscape can be simple, dominated by a single peak/attractor with a large basin of attraction. In this case random changes will destroy many sequences, but a sequence with a rapid rate of replication will likely come to dominate. It doesn't need to defend against predation, because there is none in this environment. It doesn't have to grub up nutrients, humans will supply them. All it need do is replicate as fast as it can.
What I'm suggesting here is that a sequence like VP62 is a fixed point in the environment where culturing takes place. If any one of a range of sequences are present in the original sample, over time these will converge on VP62. Change the environment, and you may get VP35, or the virus contaminating 22Rv1.
This is only possible if there is a sequence in the basin of attraction leading to those fixed points to begin with. It will also require some number of cycles of replication to perform the small-scale evolution required to converge. A highly-specific test for a particular sequence will initially fail. After some number of cycles of replication, it may succeed. This does not require a miracle. It should be expected to happen.
This fits a number of observations in the present controversy.
Blog entry posted by anciendaze, Jun 28, 2011.