ERV FAQ: ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?

1. See Abbie Smith's blog entry, "More syncytia sweetness". Primates, mice and sheep each use a different syncytin gene, from the env region of a different ERV, in a different chromosome, in order to build an essential syncytia in the placentas of their respective lineages. (A syncytium is a cell that contains many cell nuclei, as opposed to normal nuclear cells, which usually contain only one nucleus.) Why different syncytins from different ERVs? Different designs, different designers? Hardly. And why embed the syncytins in ERVS in the first place? What's all the other ERV baggage for?
2. It turns out that syncytia formation is a native trick of retroviruses. HIV will deal with attacking T-cells by absorbing them into the cells it has already infected. How? By attaching them to itself and joining with them, using the very same env proteins it used to enter the original cell! Clever trick. It avoids all the tedious business of invading every T-cell in order to neutralize them.
3. Note that the different syncytia belong to different lineages - further proof of evolution. We can even trace their evolution through their respective family trees. See also, https://www.nationalgeographic.com/science/article/mammals-made-by-viruses Why on earth would a designer take such pains to mimic the the sort of thing we expect from evolution - for no sensible reason? Why did it not mix things up a bit? Why did it never choose to produce any evidence contrary to what we would expect of evolution? See also, Gauger's Gaffe!
4. Still think ERVs are not of retroviral origin? If so, you must have answers to these questions: If ERVs are not retroviral in origin, why do they have reverse transcriptase? What do they have integrase? Why do they have LTR promoters? Why did the Phoenix virus experiment work? Why do ERVs have host DNA repetition on either side of the integration site? Why do koalas have KoRV in both exogenous and endogenous form? Why do ERVs have the same codon bias as retroviruses? See also, The Koala's Tale.
5. It always amazes me when people say, look! These endogenous promoters or genes do something. It _proves_ they are designed! Bits and bobs of some ERVs. Never a whole working ERV (which would likely kill you). If we don't accept that eyes were designed, just because they are useful, why would we conclude that ERVs are designed, just because the odd component has been scavenged from them?
6. When we look at the human/chimp syncytin gene, and consider it's origin, there are two possibilities.

designer or designers inserted it in the genome of both species, in exactly corresponding locations in the DNA (unnecessarily), the syncytin gene being embedded in an elaborately detailed structure that precisely, and pointlessly mimics a retroviral insertion. (See "Why do virologists and geneticists think that ERVs come from retroviruses?") A designer or designers also inserted a different syncytin, in a different location, in a different chromosome, precisely and pointlessly mimicking a different retroviral insertion in mice. And a completely different one again in sheep. The supposed designer(s) didn't bother with Elephants. Or Manatees. Or heteromyid rodents. They were designed to get along without a placental syncytiotrophoblast layer, relying instead on a layer consisting of discrete nuclear cells (cells with a single nucleus each).

• A common ancestor of chimps and humans, its species happily reproducing like elephants, acquired a retroviral infection in a germ-line cell. When it came to reproduce, one of the retroviral genes woke up and affected the development of certain placental cells, having the effect of merging them into a single multi-nucleus cell (a syncytium) just as the corresponding gene in HIV does with T-cells today. This aided reproduction, giving an advantage in the reproductive stakes, such that more and more individuals inherited the trick, and it eventually became a ubiquitous (fixed) feature in the species. At the same time it was spreading through the population, older genes for placental development that were no longer needed mutated into uselessness, rendering the new retroviral gene (but not the rest of its accompanying retroviral baggage) essential. The same thing happened, but with a different retrovirus, in mice. And again, independently, with a different retrovirus in sheep. It did not happen in pigs, or in horses.
• Which of the above two scenarios best explains the retroviral-like structure that is to be found at the site of the human/chimp syncytin gene?
  

See also, True facts about marsupials. and https://barryhisblog.blogspot.com/p/is-placenta-problem-no-ann-no.html

• Someone in FaceBookLand asked, Barry Desborough, Well give me the scientific explanation, detail by detail, as to how an ERV magically turns into one of the most important sequences in the entire genome -- building brains, placentas, and embryos, please. It is a fact, that life will cease at the 4 cell stage if the ERV sequences are knocked out. So --- ball is in your court to tell the world this mystery 

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  I replied,

  A good question. Creationists often express incredulity that evolution can produce new useful genes from scratch. It can, but that's another matter. How much more likely is it that an existing retroviral gene can get modified and "exapted" to serve a useful function for the organism that carries it? Reverse transcriptase has no error correction, and a useful modification (mutation) to a retroviral gene is a more likely happening than a useful gene being formed from scratch. Take syncytins - genes used in helping create placentae. They are found in ERVs in exactly the same loci as you find "env" genes in fully functioning retroviruses. There, they have the action of fusing the targetted host cell with the virus itself, and they induce more host cells to fuse together in a multi-nucleated mass, exactly like the syncytial layer of a placenta. HIV does this, fusing immune system T-cells together, all the better to counter them. HIV is not known to have endogenized. An env gene is a normal part of a retrovirus' own replication equipment and strategy. Syncytin genes have been found in many different ERVs in different chromosomes in different lineages. This indicates that they provide very important adaptive advantages, and their exaptation has occurred many times in the history of the evolution of placental mammals. If you think this is so unlikely and far-fetched, consider that viral replication happens on a vast scale at an enormous rate. People have hit the jackpot multiple times, remember.