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ERV FAQ: ERVs promote the transcription of host DNA. Doesn't this prove they are designed?

(Return to the ERV FAQ)
Recombined LTR remnant functioning as a native gene promoter.
  1. Integrated retroviruses have two identical regions, one at each end of the integration, called long terminal repeats (LTRs). These perform two functions, the first to promote the transcription of retroviral genes within the host cell and also to cause transcription back into RNA of all the non-protein coding parts of the provirus, without either of which functions, the retrovirus would not get replicated. This latter task is particularly tricky and complicated, and the LTR promoters must have specific features to fulfill it. A promoter that was designed to promote "native" DNA would not need these retroviral-specific features.
  2. As mentioned above, promoters are essential for getting retroviral genes transcribed. Retroviruses don't "care" if an incidental by-product of dropping a promoter into the genome is to promote some "native" genetics as well. Drop a promoter into a genome, more or less at random, and there is a god chance that it will promote something or other. Natural selection will "decide" whether that promotion activity is bad news, or not.
  3. Not all ERV LTRs promote transcription, not by a long way and among those that do, many of the the resulting transcripts either serve no identifiable purpose or are implicated in late-onset diseases.
  4. (Summary) The main thing that LTRs do, when they do anything, is to promote transcription. That does not mean that all the transcripts do anything useful. Some will. Some won't. Some are implicated in late-onset diseases. The structure of an LTR in a retrovirus is specific to a tricky problem retroviruses face in getting transcribed once again. That structure makes no sense as a designed promoter for native genes. It makes no sense to have useful, useless and dangerous transcripts lying about. It makes no sense to scatter the genome with ERVs, only some of which provide promoters that promote anything. It makes no sense to attach to those promoters sets of genes that pertain solely to the retroviral replication cycle - namely reverse transcriptase and integrase.
    If I wanted to argue that some aspect of the human genome was designed, I would not point to ERVs. They make no sense whatsoever as designed features.

(Return to the ERV FAQ)

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