In my previous two articles (here and here), I explored some of the background information concerning the integration of retroviral elements into primate genomes and the various arguments for common descent which are based on them. I explored, in some detail, the evidence for common descent based on the shared placement of retroviral sequences. In this final article, I will discuss the two remaining points which are raised in the popular-level article which I have been examining.
Regarding shared “mistakes” between primate genomes, this argument again assumes that mutations are random and are unlikely to occur convergently. Cuevas et al. (2002), however, have documented, in retroviruses, the occurrence of molecular convergenes in 12 variable sites in independent lineages. Some of these convergent mutations even took place in intergenic regions (changes in which are normally thought to be selectively neutral) and also in synonymous sites. The authors also note that this observation is fairly widespread among HIV-1 virus clones in humans and in SHIV strains isolated from macaques, monkeys and humans.
As the authors note,
One of the most amazing features illustrated in Figure 1 is the large amount of evolutionary convergences observed among independent lineages. Twelve of the variable sites were shared by different lineages. More surprisingly, convergences also occurred within synonymous sites and intergenic regions. Evolutionary convergences during the adaptation of viral lineages under identical artificial environmental conditions have been described previously (Bull et al. 1997; Wichman et al. 1999; Fares et al. 2001). However, this phenomenon is observed not only in the laboratory. It is also a relatively widespread observation among human immunodeficiency virus (HIV)-1 clones isolated from patients treated with different antiviral drugs; parallel changes are frequent, often following a common order of appearance (Larder et al. 1991; Boucher et al. 1992; Kellam et al. 1994; Condra et al. 1996; Martinez-Picado et al. 2000). Subsequent substitutions may confer increasing levels of drug resistance or, alternatively, may compensate for deleterious pleiotropic effects of earlier mutations (Molla et al. 1996; Martinez-Picado et al. 1999; Nijhuis et al. 1999). Also, molecular convergences have been observed between chimeric simian-human immunodeficiency viruses (strain SHIV-vpu+) isolated from pig-tailed macaques, rhesus monkeys, and humans after either chronic infections or rapid virus passage (Hofmann-Lehmann et al. 2002).
I could cite several other similar studies. For another case example, see Bull et al. (1997).
LTRs And Phylogeny
The other argument offered by the article pertains to primate phylogenies in relation to long terminal repeat (LTR) sequences. Because LTRs are identical at the time of integration, it is argued, if the 5′ and 3′ LTR sequences are very different with respect to one another, this should correspond with an older insertion. The problem is that the pattern is nothing like as neat and tidy as many Darwinists would like us to think.
One of the main difficulties associated with trying to construct phylogenies based on the divergence between the 5′ and 3′ LTRs is that it is predicated on the critical supposition that the 5′ and 3′ LTR sequences are acquiring mutations independently of one another. However, the phenomenon of cross-LTR gene conversion can result in a much smaller degree of divergence, thereby rendering this method for inferring time since integration suspect.
The authors note,
We found that gene conversion plays a significant role in the molecular evolution of LTRs in primates and rodents, but the extent is quite different. In rodents, most LTRs are subject to extensive gene conversion that reduces the divergence, so that the divergence-based method results in a serious underestimation of the insertion time. In primates, this effect is limited to a small proportion of LTRs. The most likely explanation of the difference involves the minimum length of the interacting sequence (minimal efficient processing segment [MEPS]) for interlocus gene conversion. An empirical estimate of MEPS in human is 300-500 bp, which exceeds the length of most of the analyzed LTRs. In contrast, MEPS for mice should be much smaller. Thus, MEPS can be an important factor to determine the susceptibility of LTRs to gene conversion, although there are many other factors involved. It is concluded that the divergence method to estimate the insertion time should be applied with special caution because at least some LTRs undergo gene conversion. [emphasis added]
To summarise, we have observed over the last three blog posts that the case for primate common ancestry is not nearly as cut and dried as many evolutionary biologists would like to make out. While one can find a handful of ERVs which occupy the same loci, further inspection reveals that they are often independent events.
In the absence of a feasible naturalistic mechanism to account for how evolution from a common ancestor could have occurred, how can we be so sure that it did occur? In such a case, one ought to reasonably expect there to be some quite spectacular evidence for common ancestry. Unfortunately for Darwinists, however, the evidence for common ancestry is paper thin on the ground.