Let us go on to the next section in Liu's piece,

[quote]
  • Retroviruses: exogenous and endogenous

  • The main beneficial role of viruses known to date is the ecological role of horizontal gene transfer (DNA transduction) by bacteriophages. These viruses enable bacteria to share advantageous traits such as antibiotic resistance.[/quote]

It is easy to gain an inaccurate impression from this, that transduction is a purely beneficial process. Bacteriophages can transfer any bacterial DNA. It may be advantageous to the bacterium, neutral or detrimental. And antibiotic resistance? What benefits from the transference of resistance? Certainly not humans infected by bacteria with resistance to multiple antibiotics! Beneficial DNA (beneficial to the bacteria) becomes more common in a population of bacteria by simple evolutionary principles – heritable traits, however acquired, will increase in frequency in a population if they confer a survival-to-reproduction advantage.

  • [quote]
  • The only family of viruses that are known to transduce genes among eukaryotic organisms (such as vertebrates) is that of the retroviruses. Retroviruses are viruses that have RNA as their genome but make DNA copies of it in the infected cell. They are similar to some bacteriophages (temperate phages) in that both insert their genetic material (DNA provirus) into host cell chromosome(s). This integration of viral and cellular DNA increases the chances of transduction of cellular genes adjacent to a provirus. Some retroviruses are known to transduce tumor genes (oncogenes) into the new host, which, while promoting the proliferation of the infected cell, often bring disaster to the organism.[/quote]

This underlines the point I made above. DNA transduction by retroviruses does not 'care' what cellular DNA it transfers, nor where it is re-inserted. Such DNA may be beneficial, neutral or detrimental to the infected cell and organism. They can, indeed transduce oncogenes. See Mechanism of transduction by retroviruses - A Swain and JM Coffin. It hardly argues for a 'creator' of retroviruses when the results of his design are indistinguishable from pure happenstance.

  • [quote]
  • While temperate phages only insert a single copy of the provirus into the host chromosome, retroviruses are allowed to insert multiple copies of proviruses into different sites of the same host genome. Integration of proviruses into the host’s germline cells (cells that give rise to eggs or sperm) will result in inherited retroviruses.[/quote]

Temperate phages do not insert proviruses into host chromosomes. They insert prophages. But what does this have to do with retroviruses? Retroviruses do indeed integrate into germline cells, where they become heritable. This is what an endogenous retrovirus is – the remnants of a provirus in a specific location in the genetic inheritance of a creature. Any two creatures sharing multiple ERVs in corresponding locations in their genomes are therefore necessarily related by common ancestry – the ancestors being those who acquired the germline integrations in the first place.

  • [quote]
  • On the other hand, the genomes of all vertebrates and humans harbor multiple copies of endogenous retroviruses (ERVs), DNA sequences that have genes and gene organizations homologous to those of retroviruses. Indeed, ERVs constitute about 8% of the human genome, a proportion much larger than the sum of all single-copy genes. While some ERVs are expressed and some even assembled into intracellular viral particles, most of them are deficient and are rarely transmitted horizontally. In view of this, retroviruses that are normally absent in healthy hosts are called exogenous retroviruses. Are ERVs degenerated germline copies of exogenous viruses which infected the host’s ancestors in history?[/quote]

After stating that integration of proviruses into germline cells results in inherited retroviruses, Liu now wonders if inherited retroviruses are the result of the integration of proviruses into germline cells! As if to ponder this question, Liu goes on to describe the evidence for the endogenization theory, that the source of heritable endogenous retroviruses is indeed the integration of exogenous retroviruses.

  • [quote]Evidences supporting the endogenization theory for the origin of ERVs include the following.

  • (1) Modern exogenous viruses can infect the germline and be inherited like the host’s own genes.

  • (2) Some endogenous viruses are replication-competent and infectious. When isolated murine leukemia viruses (MuLV, an endogenous mouse retrovirus) were inoculated into a new host, their proviruses were able to colonize the recipient genome.

  • (3) Polymorphism (variation) of the chromosomal positions of an ERV among individuals of the same species suggests independent endogenization events. For instance, proviruses of the Koala retrovirus (KoRV) are found in different loci in different animals.

  • (4) Allelic frequency polymorphism (variation in the frequency of finding a DNA sequence among populations) indicates recent endogenization. KoRV is present in koala in northern Australia, but absent in some animals in southern Australia.6 Similarly, HERV-K113, a provirus located on human chromosome 19p13.11, is rare among Caucasians and more prevalent among Africans, Asians, and Polynesians.

  • (5) Negative correlation between degrees of positional polymorphism and sequence polymorphism conforms to the endogenization-degeneration hypothesis. ERVs with fixed chromosomal positions (less positional polymorphism) often demonstrate more sequence polymorphism with deleterious mutations and differences between the 5’ and 3’ long terminal repeats (LTRs), consistently pointing to the hypothesis that the virus infected an early ancestor and degenerated during its long history, while proviruses with varied locations such as KoRV are often intact and infectious, indicating recent or ongoing endogenization.[/quote]

All Liu is trying to say here in (5) is that ERVs in varied locations such as KoRV are relatively recent, with few mutations, while ERVs in less varied or in singular locations exhibit a greater number of mutations. (Positional polymorphism is when an ERV appears in more than one position in the chromosomes. This may be in more than one position in an individual's DNA, or in the genome of a species, or in the genome of a group of species. Each instance of an ERV in a particular position, however, will be fixed in the sense that it will always be inherited in that position. When we say an ERV is fixed in a population, that means something different. When a genetic feature is fixed in a population, it means that every individual possesses it. Sequence polymorphism means variation in form in a population for a given feature.)

Liu has not listed certain other evidences for the theory that ERVs are the result of germline infections. I'll add to his list here:-

  • (6) The curious case of the phoenix virus. This is a working virus resurrected from inactive ERVs. Why should this experiment have worked if the ERVs were not degenerate proviruses?

  • (7) Viral codon bias. A codon is a triplet of DNA or RNA bases. In translating RNA into a protein, each triplet is translated into a specific amino acid. But the interesting thing is that nearly every such amino acid can be translated from more than one triplet. Now certain types of life forms 'prefer' certain codons over others, and virus' 'preferences' are different. ERVs exhibit the same codon preference, or bias, as exogenous viruses.

  • (8) The phylogenetic evidence from the types of ERVs. Humans, for example, share most of their ERVs with chimpanzees, then, in order of the number of shared ERVs, they share the next highest number with other great apes, then with gibbons, then with old world monkeys and then with new world monkeys. ERVS unique to each species tend to bear the evidence that they are the most recently acquired. The ERVs that are shared among primates are shared in a pattern called a nested hierarchy or tree. A nested hierarchy is a necessary consequence of descent with modification, which is consistent with the 'endogenization theory'. An intelligent designer is not constrained to produce a nested hierarchy of this sort, and where such a hierarchy is maintained in unnecessary detail, as it is, this would make such a hypothetical intelligent designer a bit of a prankster.

  • (9) The phylogenetic evidence from differences in long terminal repeats and from other mutations to ERV genes. Long terminal repeats (LTRs) are sections of DNA at either end of a retroviral insertion. They must be identical at the time of insertion. However, LTRs and ERV contents gradually acquire mutations and begin to differ from one another. Drawing up tables of differences and similarities between orthogolous ERVs in different species produces a nested hierarchy once again.

  • (10) The agreement between (8) and (9), despite the nested hierarchies being derived from different effects - integration in the case of (8) and mutation in the case of (9).

To be continued.