Features of retroviruses.
  • Retroviruses reproduce by integrating themselves with the DNA of the cells of their hosts.
  • Within the cell, they reverse-transcribe their RNA genomes into DNA versions, and integrate the resulting DNA (the provirus) into the DNA of the host cell.
  • The provirus is then transcribed and translated like any other part of the DNA. This results in the production of new virions which exit the cell to infect new cells, either in the same host organism or another.
  • Retroviruses target particular types of cells.
  • All retroviruses share a distinctive structure, coding for all the requirements for invading a cell, reverse-transcribing the genome, integrating it into the host DNA and forming new virions.
  • All retroviruses exhibit the distinctive viral codon bias.
  • The site of integration is highly variable, and the resulting provirus is also variable, reverse transcription being an error-prone process.

We find, in the genomes of organisms, including ourselves, structures virtually identical to retroviral proviruses, but with certain features that differ from them. The differences and similarities are highly informative.

Features of ERVs
  • There is no sign of active retroviruses that can be associated with ERVs.
  • There are many thousands or ERVs in a typical genome.
  • Each ERV is to be found in every single cell of any given organism, in exactly the same location. The contents of any given ERV are uniform, going from cell to cell.
  • ERVs have the same structure as retroviral proviruses, but they are incapable of producing virions.
  • ERVs have the same distinctive codon bias as retroviral proviruses.
  • Most ERVs are to be found in every member of a given species, always in the same location.

The 'viral hypothesis' is that ERVs are inherited from ancestors who acquired them via retroviral integration into germ line cells.

Here are the advantages of the viral hypothesis
  • It explains their presence in the absence of active retroviruses.
  • It explains their high numbers. All ancestors are potential bequeathers of ERVs.
  • It explains why they are in every cell, in the same location, and why they are uniform. They got there by normal mitosis, which is a high fidelity duplication process.
  • It explains why they have the same structure as proviruses (they are copies of proviruses) and it explains why they are so inactive as proviruses - only inactive (failed) proviruses allow their hosts to bequeath their DNA to their descendants.
  • It explains the viral codon bias. Again, they are copies of proviruses.
  • It explains their universality in the population. Genetic drift will eventually ensure that any given ERV will either become fixed in the population, or will disappear.

Additional support for the viral hypothesis

  • The Phoenix virus was resurrected from the multiple instances of an ERV which is to be found in each human cell. Each instance is a 'failed' retrovirus, but when a 'majority vote' for each base was taken, the resulting DNA produced, "viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny."
  • Some retroviruses perform functions within the body, but where they do, it is only part of the ERV that does anything. Other ERVs do nothing, and yet others are implicated in late-onset diseases such as cancers. A 'designer' hypothesis that 'explains' positive function and no function and detrimental function points to a very strange designer.
  • A retrovirus has been caught in the act of becoming endogenized: The koala retrovirus KoRV. Not a single designer in sight.
  • Retroviruses leave a telltale trace of integration in the form of a repeated host sequence either side of the integrated provirus. This is also evident in ERVs. From Virology Blog: Retroviral Integration and the XMRV Provirus, "The image below shows some of the characteristic features of retroviral integration. A the top is the unintegrated linear DNA of avian sarcoma/leukosis virus produced by reverse transcription. Upon completion of integration, two base pairs (AA•TT) are lost from both termini, and a 6-bp target site in host DNA (pink) is duplicated on either side of the proviral DNA. This target site varies in length from 4 to 6 bp among different retroviruses. The proviral DNA (middle) ends with the conserved 5′-T G…C A-3′ sequence. The provirus serves as a template for the production of the viral RNA genome (bottom)."
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