Liu then goes on to discuss what he regards as facts against the endogenization theory.

  • [quote]However, there are also interesting facts against the endogenization theory.[/quote]

  • [quote]
  • (1) Endogenization of modern exogenous retroviruses is rarely observed in nature.[/quote]

The endogenization of modern exogenous retroviruses has been observed in nature. Liu has already mentioned it above - the koala endogenous retrovirus, and he has also described other evidence in support of recent endogenization events. Even if endogenization was judged to be rare, it's rarity would not be evidence against it happening! But we have to be careful about words like 'rare' in evolutionary scenarios. The evidence is that eukaryotic life is some 2 billion years old. As we have some 200,000 ERVs in our genomes, that means one endogenization event that goes on to become fixed in the population, on average, once every 10,000 years. IOW, endogenization can be rare, and still be frequent enough to account for all our ERVs.

  • [quote]
  • (2) Most modern ERVs are not actively transposing (moving around or duplicating) in the host cell genome. At least all human ERVs appear fixed in numbers and positions; although some mouse ERVs are capable of expanding in the host genome. Are the human ERVs older, therefore more degenerated and less active? If the human race is younger than the murine race, as evolutionist biologists believe, there is no reason to suppose that the human ERVs are older than those of the mouse.[/quote]

Liu seems to have a bit of a misunderstanding here about what 'evolutionist biologists believe'. Human beings are not a species that poofed into existence from nowhere, and neither are mice. For both men and mice, they and their ancestors have been around for exactly the same length of time (although there will have been more mouse ancestors, mice happening to breed like - well, like mice). If mice have acquired more ERVs more recently than humans, it is not because they are a more recent species.

  • [quote]
  • (3) Xenotropic ERVs reside in cells that have no receptor for them. Instead, envelope (env) proteins of these ERVs bind receptors on cells of other animals. How did these ERVs get into the cell, if they were not built inside? It is no surprise to read speculations like this in Retroviruses, the “Bible” of retrovirology: “It is likely that xenotropic viruses originally inserted into the germ line in a host background that encoded their cognate receptor but that the functional xenotropic viral receptor allele was subsequently lost, probably under selective pressure from exogenous xenotropic viruses.”9 The term “exogenous xenotropic virus” is difficult to conceive, if not self-contradictory.[/quote]

ERVs, as has been already explained, get into cells by inheritance, ultimately from the infection of a germline cell by an exogenous retrovirus. Cells that inherit an ERV do not, therefore, need to have the retroviral receptor. Language nitpicking aside, it is not difficult to understand that a species or its ancestors can acquire an ERV and subsequently lose the receptor that made the original acquisition possible. Easier, in fact, than the idea that a designer snuck them into a cell, for no good reason other than to pose us a puzzle.

From Coffin, 1997 [noparse][/noparse]

  • Genetics of MLV Receptors

  • The ecotropic viruses were the first class of MLVs to be identified. They comprise some of the most intensely studied retroviruses, including exogenous viruses such as Moloney MLV (Mo-MLV) and Friend MLV (Fr-MLV), as well as the endogenous virus of the AKR mouse strain, AKR MLV (AKV). A functional receptor for the ecotropic MLVs is encoded by all strains of laboratory and wild mice of the genus Mus musculus that have been examined to date. The assignment of a single genetic locus for susceptibility to ecotropic MLV infection was consistent with a single gene encoding the receptor protein. The evidence for this came from studies of somatic cell hybrids that were created by fusion of susceptible mouse cells to nonpermissive hamster cells. When cells that retained susceptibility to ecotropic MLV infection were characterized for their mouse chromosomal content, it was possible to assign the receptor gene(s) to the Rec1 locus on chromosome 5 (Gazdar et al. 1977; Oie et al. 1978; Ruddle et al. 1978).

  • Xenotropic and polytropic MLVs are present as endogenous proviruses in all inbred mice (see Chapter 8). Like ASLV receptors in chickens, the receptor for xenotropic MLV is polymorphic in mice but not in other species. Although xenotropic viruses will not infect cells from inbred strains of mice, they will infect cells derived from some wild mice and species of mice other than M. musculus (Hartley and Rowe 1975; Lander and Chattopadhyay 1984). The genetic locus for susceptibility maps to chromosome 1, and it is inseparable from the gene for the polytropic viral receptor, suggesting that alleles of this gene can serve as the receptor for both polytropic and xenotropic viruses (Kozak 1985; Hunter et al. 1991)

  • Xenotropism—the inability of an endogenous retrovirus to infect cells of the species whose germ line it inhabits—is not limited to the endogenous viruses of mice but is also seen with the subgroup E viruses of chickens and with endogenous viruses of cats and primates. It is likely that xenotropic viruses originally inserted into the germ line in a host background that encoded their cognate receptor but that the functional xenotropic viral receptor allele was subsequently lost, probably under selective pressure from exogenous xenotropic viruses.

  • Amphotropic viruses are exogenous MLVs originally isolated from some wild mouse strains. Because of their efficient infection of human cells, the amphotropic env gene is widely used in retroviral vectors (Chapter 9). The distribution of receptor activity for amphotropic viruses among species differs from that of xenotropic and polytropic viruses, as does the map location of the receptor (Garcia et al. 1991). To date, genes encoding receptors for ecotropic and amphotropic MLVs have been cloned and characterized; those for xenotropic and polytropic viruses remain to be discovered.

In other words, certain inbred strains of mice have ERVs derived from viruses that cannot infect them, but which can infect certain wild strains of mice. Liu thinks that a designer with nothing better to do than to mislead us is a better explanation than the explanation that an ancestors of both the wild and the inbred mice acquired the ERVs because the viruses could infect them.

  • [quote]
  • (4) Essential beneficial functions of some ERVs and irreducibly complex coordination between ERVs and host DNA sequences argue against the possibility of historical acquisition of ERVs followed by positive selection (see below).[/quote]

Certain parts of certain ERVs perform essential functions, but the puzzle remains - why do these parts appear embedded in a proviral structure, the rest of which does not perform any beneficial function? Evolutionary theory would lead us to expect that features that can be easily adapted to perform a beneficial function by relatively minor modification will be likely to arise and be positively selected and improved.

The cooption of env genes to act as syncytins is a classic example of this phenomenon. The fact that there are numerous different examples of syncyins based on env genes from different ERVs strengthens the argument for cooption as opposed to that of design.

The 'beneficial function' design argument conveniently ignores the non-functional and the detrimental 'designs'. Why should beneficial features be significant, while neutral and detrimental ones not be?

And this assertion that these systems are irreducibly complex (which is unsupported by any evidence) is a particularly poor one. Irreducible complexity is the notion that a system cannot evolve because it is too improbable that each of its components can arise by variation and selection in the absence of the others. Apart from irreducible complexity being flawed as a basic concept, in this case, it is applied inappropriately even under its own terms. The ERV component does not appear in the host DNA by means of mutation, but by infection. Thus, a major component of this 'irreducibly complex' system appears, almost ready made, in one fell swoop. In fact, this example does illustrate the flaw in the irreducible complexity notion. A component of an 'irreducibly complex' system is not initially required to be a part of the system the observer is scratching his head over. It is sufficient that it performs a function. In this case, that function was that of the env environment protein, i.e. to attach, not placental cells to those of the uterus, but the viruses to the target cells' protein coats.

Consider that, for an ENV that is no longer replication-competent via the viral re-infection route, it is still replication-competent via host organism reproduction. The ERV is 'in the same boat' as the rest of the host's DNA, and the selection pressure on the ERV will be pressure to cooperate with the host DNA.

  • [quote]
  • (5) The existence of numerous solo LTRs in genomes suggests retroviral deletions, which may account for frequency polymorphism of some ERVs among populations. In other words, frequency polymorphism is a sign that the sequences are being lost, instead of being added on through endogenization.[/quote]

Deletions are evidence of the negative selection and loss by genetic drift of non-beneficial ERV DNA. However, as we have seen, novel ERVs are acquired as well as lost. It is hard to see what Liu finds so mysterious about this.

To be continued.