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ERV FAQ: Why do virologists and geneticists think that ERVs come from retroviruses? Isn't that just supposition on their part?


Much material in this page has been lifted from Abbie Smith.Hope you don't mind Abbie, :D

Every detail of every full ERV is replete with complex and subtle details attesting to its origin in retroviruses. ERVs have the same structure as retroviral integrations. This is some -10 kilobases of genes specific to the retroviral replication cycle. All retroviruses and complete ERVs include genes we call gag, pol and env. The function of these genes will be gone into in detail in the following notes. In addition, several other features common to retroviral integrations and ERVs only make sense in terms of the requirements of the retroviral replication cycle.

"The gag gene encodes for ‘Gag’ the giant protein, which gets chopped into several smaller proteins, Matrix, Capsid, and Nucleocapsid (and sometimes a few more tiny ones, depending on the retrovirus)."

"Matrix is the structural protein just inside the envelope (the membrane the virus stole from its host cell). It has ‘outside’ functions (targeting the virus assembly to the right kind of cell membrane, keeping the outside protein env, in order) and ‘inside’ functions (targeting the reverse transcribed DNA to the new host cell nucleus). Jack of all trades protein, like lots of retroviral proteins. They run a tight ship."

"Capsid forms the viral ‘core’. Normally when you think of a ‘virus’, you think of this shape, an icosahedron. Retroviral ‘cores’ really look more like a cylinder-cone-thingie, like the bottom pic here. That particular pic is also worth a second look– More protein cuts to Capsid need to take place after a baby virus buds off from its host cell to make an immature virus mature. Blocking this maturation step is what the next family of anti-HIV-1 retrovirals do. *thumbs up*"

"Nucleocapsid is a structural protein that wraps up the retroviral genome to make sure its packaged properly into the Capsid."

Pol codes for all the enzymes a retrovirus needs:"

"Protease– Chomps big proteins into all the little functional proteins, like we saw with Gag getting chomped into Matrix/Capsid/Nucleocapsid. The name ‘protease’ can be a little confusing because all organisms have ‘proteases‘, but only the protease that the retrovirus carries with it is the ‘right‘ protease to cleave in all the ‘right’ spots to get all the ‘right’ proteins in the end. Instead of giving retroviral proteases a special name, they just named it ‘Protease’. heh. Protease inhibitors are a great target for anti-retrovirals."

"Reverse Transcriptase– Another target for anti-retrovirals. Though the process of reverse transcription can be found in you and I (coooool), retroviruses need to carry an enzyme with them to convert viral RNA into DNA on demand. This process not only requires converting an RNA genome into a DNA genome, but also:"

"RNase H– The RT enzyme has (at least) two active sites. One performs the process of reverse transcription. Another active site has RNase activity (chops up RNA, specifically, RNA Hybridized with DNA haha!). RNase H chews up the old RNA template after a single strand of DNA has been made, so the single strand of DNA can be made into double stranded DNA, and subsequently inserted into the host cells genome. This might make more sense if you see this animation. *might* The process of reverse transcription is rather absurd."

"Integrase– Host cells don't come packed with the necessary biochemical machinery to move DNA out of the cytoplasm into the nucleus, to be inserted into the host DNA. So once again, retroviruses need to bring an enzyme capable of performing those activities. Integrase should be a perfect target for antiretrovirals… But we havent figured any out yet…"

Env. See http://scienceblogs.com/erv/2008/07/17/intro-to-ervs-envy-my-env/

LTRs. See this page. RNA polymerase's normal function is to convert nuclear DNA into messenger RNA that makes for proteins. It does not normally make RNA that 'codes" for promoters. Our bodies have no need for them. But retroviruses need their promoters to be converted back to RNA for when the replication cycle begins again. Long terminal repeats (LTRs) cause the RNA polymerase to produce them by a complicated "hack". The point is, that LTRs basic and original function is a part of the replication process of retroviruses. They cannot be part of any supposed original "design" of our genomes. That would not make any sense.

See http://barryhisblog.blogspot.fr/p/ervs-promote-transcription-of-host-dna.html and http://scienceblogs.com/erv/2009/07/16/intro-to-ervs-ltr-gator

Retroviruses exhibit the distinctive viral codon bias.

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." See also The "Phoenix Virus": an explanation of an experiment.

A retrovirus has been caught in the act of becoming endogenized: See The koala retrovirus KoRV and The Koala's Tale.

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)."





(Return to the ERV FAQ)

12 comments:

  1. From my 2013 paper:

    Previously, I have argued that in order to understand the origin of RNA viruses, it is imperative to completely ignore the mainstream view that a major part of our genome is made of the genetic debris of ancient inva-sions of RNA viruses. Instead, I have hypothesized that transposable and transposed elements might have been originally designed to generate variation in offspring and should therefore be renamed variation-and-integrity assuring genetic elements (short: VIGEs). Hence, the major part of genomes contains VIGEs and their degenerate remnants. As mentioned above, ERVs are mobile genetic elementscharacterized by gag and pol genes that closely resemble full-blown RNA viruses, such as influenza and human immunodeficiency viruses. The origin of such RNA viruses can therefore be understood as a transformed ERV. In other words, RNA viruses may form in genomes from ‘gag-pol elements’. Gag-pol elements may trans-mute into RNA viruses through sequential uptake and/or recombination of genomic genes (‘host genes’), which serve to further the virus envelope (to wrap up the RNA molecule derived from the VIGE) and genes that enable them to leave and re-enter host cells. Once such derailed VIGEs become shuttle vectors between different hosts, they have converted into full-blown RNA viruses. This view, the ‘VIGE-first hypothesis’, solves the RNA virus paradox, i.e. the observation that all families of RNA viruses found today “could only have appeared very recently, probably not more than about 50,000 years ago”.(see my paper of 2009). In addition, it provides a plausible explanation for the origin of RNA-virus-driven diseases. Still, a challenge to the ‘VIGE-first hypothesis’ is presented by naturalistic philosophers claiming that novel genes derived their sequence from endogenous retroviruses. An interesting example is provided by syncytin, a protein critically involved in the development of mammalian placenta. The coding sequence of the syncytin gene seems to be made from an endogenous retrovirus envelope gene. The ‘VIGE-first hypothesis’ now says that it must be the other way around, i.e. the syncytin gene was captured by a gag-pol element. [In this paper,] I will argue that the most parsimonious explanation to under-stand the syncytin locus is by assuming the integration of two such elements. This novel vision implies that the functional syncytin gene present in the human genome was not derived from the envelope gene of an ancient RNA virus. Instead, the gag-pol elements that contain a syncytin-like gene (known as HERV-W provirus) are secondary and originated after uptake of the syncytin gene from the genome. Importantly, this vision also indicates that HERV-W may be on its way to become a full-blown RNA virus.

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    1. Speculations require evidence in order to be interesting, Peer. Re. the RNA virus "paradox", I don't need to see your paper of 2009. Here is a paper from 2003, http://jvi.asm.org/content/77/7/3893 which discusses it. Some dishonest commentators have spun this up as being a problem for endogenization, neglecting to mention that retroviruses evolve rapidly. It is no surprise that modern "species" arose recently.

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    2. The whole main stream idea about the genome is full of viruses is speculation. The only way out for the mainstream opinion to solve the RNA virus paradox is to demonstrate gag and pol sequences unrelated to those we currently observe. Since they cannot do so (the do not exist), the paradox stands as a falsification of main stream opinion. The VIGE first predicts that RNA viruses are of recent origin because the eminate from the genome all the time because of exogenization. If you had taken time to read my papers you would now know that the mechanisms to enter the cells use parts of genes present in modern genomes. HIV for instance uses part of an interleukin gene to enter via CCR5. Genomes are not 50% made of viruses. They are made of VIGEs.

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    3. > it is imperative to completely ignore the mainstream view that a major part of our genome is made of the genetic debris of ancient inva-sions of RNA viruses

      Why would we do that when the evidence that most of our ERVs were the result of invasions is overwhelming?

      1. We know exactly how LTRs are formed. They are formed in the process of reverse transcription from RNA to DNA. If an ERV exists and it is flanked by LTRs then it is the result of an invasion.

      2. The same goes for solo LTRs - these sequences once flanked ERVs. Their mere existence indicates that they were once encoded by RNA and that an ERV infection happened at this site.

      3. Many ERVs have Target Site Repeats - another clear indication of an insertion event

      4. Many ERVs are overlapping - unless your argument is that God made people and Chimpanzees and all sorts of other animals with overlapping ERVs then this is also clear evidence that these ERVs weren't always in these locations.

      I could list more reasons but I think these are sufficient enough

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    4. AceofSpades, as I told you before, the evo-community has cause and effect up-side-down:

      1) The genome is littered with isolated LTRs, which might function as recombination sites for ERVs. These spots are in actuality the spots where they integrate and explains why we sometimes see them shared between species.

      2) The isolated LTRs are NOT remnants of ERVs, but these are the docking sites for potential recombination. Here too, the evo-community has swapped cause and effect.

      3) Indeed, these might be the genuine insertions.

      4) Initially, there may have been many overlapping ERVs. This is the mechanism to induce genetic variation in offspring. A designer is free to chose how and where to introduce it in a genome. In fact, the overlap between chimp and man is not huge and this might reflect that the mechanisms was put in place here. [Interestingly, from a biblical view, the ERVs might be the executors of the curse after the fall. Loss of control over ERV activity may have lead to death and diseases, including RNA viruses...]

      As said, Ace, most likely you have cause and effect up-side-down. So, convince me with more arguments.

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    5. Peer, it is disingenuous of you to asked to be convinced by arguments when you have sworn not to be persuaded by anything whatsoever.

      Now try and convince us with some evidence.

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    6. I have not sworn anything. My line of argumentation is different. I did not start from the preconceived idea of (universal) common descent, but from the genetic data, from the information in the genome. Over the past decade, it became increasinly clear that man and chimp are not so similar after all if we look at the genetic contents as a whole. We have now observed 643 human specific and 780 chimp specific protein coding genes, and approx 1000 miRNA genes specific for humans. This shows a common ancestor is highly unlikely. Therefore, the data interpreted as "demonstrating common descent" must be looked at with more caution. I have proposed that we may better understand these data from common mechanisms instead of common descent. It boils down to a frontloading evolutionary process with limited common ancestry.

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    7. Peer Terborg good show! That's good not to swear, best to leave to the un/anti religious, hell bound on imposing their valueless status on all. Biological changes generally used to argue for Evolution are looked at in detail, they turn out to be the precise opposite of what such a process would require... Viruses … steal DNA that they find useful to their success.

      “Many viruses can easily incorporate ready-made genes from other viruses into their genomes,” “This is a possibility anytime a host is infected with two different viral strains.” LiveScience’s editorial director Robert Roy Britt

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    8. Is this supposed to refute the evidence for common descent, Marc? How is that supposed to work?

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  2. Peer, you blog for "Creation Ministries International". Do you subscribe to their statement of faith, or not?

    Here's a project for you. Compare the genomes of creatures of the same "kind" that geneticists say are distantly related. Show that the differences are always smaller than those between chimps and humans. Be sure to use exactly the same criteria in all cases.

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    1. Thanks, Barry, but I have different projects ongoing, which take most of my time. What would your project demonstrate, anyway? Evolution? Common Descent? Selection? Or mere relatedness?

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    2. For the third time of asking, Peer, you blog for "Creation Ministries International". Do you subscribe to their statement of faith, or not?

      What would my project demonstrate? That humans and chimps have far greater genetic differences that any two species representative of a what creationists call "kinds. Or not. I have often suggested to various creationist and intelligent design "research" "institutes", investigations that would test and support (or otherwise) their hypotheses. Strangely, they are never keen. It's almost as if they have no real confidence in the veracity of their notions. I "strangely", but perhaps not. It fits in with their articles of faith that effectively state that evidence is irrelevant. Still, it does make one wonder why they pretend to be sciency. Keeps the contributions coming in, I suppose.

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