Intelligent Design, the best explanation of Origins

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Intelligent Design, the best explanation of Origins » Intelligent Design » Viruses: Essential Agents of Life

Viruses: Essential Agents of Life

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1 Viruses: Essential Agents of Life on Fri Jul 17, 2015 11:45 am


Viruses: Essential Agents of Life

Did God make pathogenic viruses?

Viruses do not undergo metabolism, growth, responsiveness to the environment or movement. Viruses do not even replicate themselves directly. They are rogue bits of genetic code that reprogram cells to act in strange ways, which include creating more virus particles. But the viruses themselves do not have the characteristics of living things.

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2 The empires and domains of life on Mon Nov 23, 2015 12:16 pm


from the book: The Logic of Chance: The Nature and Origin of Biological Evolution
By Eugene V. Koonin

The empires and domains of life

Probably an even more fundamental departure from the three-domain schema is the discovery of the Virus World, with its unanticipated, astonishing expanse and the equally surprising evolutionary connectedness. As discussed in Chapter 10, virus-like parasites inevitably emerge in any replicator systems, so there is no exaggeration in the statement that there is no life without viruses. Moreover, it seems almost inevitable that the precellular evolution of life went through a virus-like state. And in quite a meaningful sense, not only viruses taken together, but also major groups of viruses seem to be no less (if not more) fundamentally distinct as the three (or two) domains of cellular life forms, given that viruses employ different replication-expression cycles, unlike cellular life forms which, in this respect, are all the same

Viruses are essential to life. Viruses however depend on life to exist. Without life, no viruses. So the question is like the chicken and egg problem: What came first, Viruses, or life ?

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3 Re: Viruses: Essential Agents of Life on Thu Jun 22, 2017 6:05 am


The Syncytin Gene: Viruses Responsible for Human Life  1

Many individuals think of viruses as harmful organisms that invade, infect and even kill. But the reality is very different as a virus has now been credited with making human life possible.

According to an article in Discover Magazine, Boston-based scientists made an incredible discovery in 2000 (published in Nature).

Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis
Here we describe the opposite situation, where a viral gene has been sequestered to serve an important function in the physiology of a mammalian host. This gene, encoding a protein that we have called syncytin, is the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W2. We find that the major sites of syncytin expression are placental syncytiotrophoblasts, multinucleated cells that originate from fetal trophoblasts. We show that expression of recombinant syncytin in a wide variety of cell types induces the formation of giant syncytia, and that fusion of a human trophoblastic cell line expressing endogenous syncytin can be inhibited by an anti-syncytin antiserum. Our data indicate that syncytin may mediate placental cytotrophoblast fusion in vivo, and thus may be important in human placental morphogenesis

While examining the human genome, they encountered a curious gene now known as syncytin. Syncytin serves to encode a protein that is found only in placenta-based cells. The cells that create syncytin are situated in one location: at the point where the uterus and placenta meet and fuse to form a layer of cells known as the syncytiotrophoblast. This cellular layer is critical as it enables the human fetus to obtain nutrients from the mother’s body.  Syncytin is also found in other primates, like gorillas and chimpanzees. This discovery led scientists to conclude that the genetic change that resulted in the formation of syncytin gene must have occurred at an early point in primate evolution, impacting an ancestor that’s common to humans, gorillas and chimpanzees.

The scientists discovered that syncytin is produced as a precursor to the formation of the cellular layer that allows for a fusion of the placenta and uterus. But what makes syncytin even more incredible is the finding that it didn’t arise from a mammalian gene: syncytin arose from a virus. So what originally started as a viral gene designed to produce proteins that would fuse the host’s cells together, thereby allowing the virus to spread with greater ease, now serves to connect mother and child. Quite simply, syncytin is critical and without it, human life could never form.

Viruses have the ability to make changes at the genetic level. Scientists have found that viruses have been invading and shaping what would ultimately become the human genome for millions of years.  Most of these viruses altered the genetic code by invading sperm or eggs. Once inside these cells, the viruses target the DNA and integrate their own viral DNA into the host’s DNA. If the sperm or egg goes on to produce a viable organism, the viral gene can be inherited from one generation to the next. The net effect has been quite significant over time, as it’s believed that a whopping 8 percent of human DNA — over 100,000 known fragments — can be attributed to viruses. And while most think of viruses as harmful organisms, some gave rise to viral genes in our genome that serve to generate proteins. Some of these viral genes, like syncytin, have been found to be essential to human survival.

Model of the Syncytin 2 protein

Following the 2000 discovery of syncytin, French virologist Thierry Heidmann went on to discover another syncytin gene. Called syncytin 2, this viral gene serves to suppress the mother’s immune system to prevent her body from attacking and rejecting her baby’s tissues as it would a foreign body. Heidmann’s discoveries didn’t end there. His team of researchers discovered that, contrary to the initial findings, syncytin is not just found in the Great Apes, but is present in other mammals, including mice and rabbits. Like humans and primates, the mouse was found to have two varieties of syncytin, called syncytin A and syncytin B. An additional variety of syncytin, called syncytin-Ory1, was discovered in rabbits in 2009. In one study, the syncytin A gene was disabled in a mouse and the embryo died in a matter of days due to its inability to form a syncytiotrophoblast. This served to further emphasize the important role of viruses in shaping the mammalian genome.

Heidmann’s studies into the syncytin gene didn’t end with the rabbits. The virologist ultimately discovered that the carnivoran group of mammals — including dogs, cats, hyenas, tigers, panda bears and seals — all possess a variety of syncytin called syncytin-Car1. 

This led Heidmann to conclude that the virus altered the carnivoran genome sometime after the carnivorans split from other mammal groups approximately 85 million years ago. Over time, it’s believed a process of natural selection occurred and ultimately, syncytin became essential.

Its remarkable how new scientific discoveries are tried to be pressed always into a evolutionary framework by making superficial pseudo scientific assertions. How do they know that syncytin was not essential right from the beginning, and so the viruses, that provide the genetic change ? 

Heidmann’s discoveries paint an incredible story, as these findings have some interesting implications. It appears that on six different occasions, the virus responsible for the syncytin gene infected different mammals. Six slightly different versions of syncytin gene arose, and all six would prove to have a critical role in the reproductive process. The research continues into other mammals, as scientists attempt to determine whether they also have a variant of the syncytin gene.

The Case of Syncytin 2

A second example is the fusogenic syncytin proteins that fuse placental cells together to form the syncytiotrophoblast and which are known to be essential for placental formation. These proteins are coded for by the envelope (env) gene of an endogenous retroviral insert. These proteins are absolutely critical for placental development in humans and mice. The different kinds of Syncytin protein are called "syncytin-A" and "syncytin-B" (found in mice); "syncytin-1? and "syncytin-2" (found in humans). Interestingly, although serving exactly the same function, syncytin-A and syncytin-B are not related to syncytin-1 and syncytin-2. Syncytin protein plays the same function in rabbits (syncytin-ory1). But rabbit syncytin is not related to either the mouse or human form. These ERVs are not even on the same chromosome. Syncytin-1 is on chromosome 7; syncytin-2 is on chromosome 6; syncytin-A is on chromosome 5; and syncytin-B is on chromosome 14. For some reviews of this topic, see Dunlap et al. (2006);Dupressoir et al. (2005); and Harris (1998).
Now, target-site duplication is the hallmark of insertion by integrase (as a consequence of the repair by the host cell's DNA repair proteins of single-strand gaps at each end of the inserted sequence formed upon element insertion). We can use this to infer that these elements are indeed inserts: They are not intrinsic to the genome. So, in this case, an ERV has acquired function subsequent to its insertion, and has apparently been later rendered essential. Could this serve as a counter to irreducible complexity? Here is the question to ask: Did the system function before the insertion of the retrovirus? If the molecular machinery in which the syncytin proteins are functioning is determined to be irreducibly complex, then the theory of intelligent design would predict that it did not function -- unless of course some other protein was fulfilling the role and was subsequently replaced by the syncytin, as per the previous scenario regarding ZipA and FtsA.

Revisiting an Old Chestnut: Retroviruses and Common Descent (Updated) 


One particularly remarkable incidence of functionality with regards these sequences is the involvement of the highly fusogenic retroviral envelope proteins (the syncytins) which are known to be crucially involved in the formation of the placenta syncytiotrophoblast layer generated by trophoblast cell fusion. These proteins are absolutely critical for placental development in humans and mice. The different kinds of Syncytin protein are called "syncytin-A" and "syncytin-B" (found in mice); "syncytin-1" and "syncytin-2" (found in humans). But here's the remarkable thing: Although serving exactly the same function, syncytin-A and syncytin-B are not related to syncytin-1 and syncytin-2. Syncytin protein also plays the same function in rabbits (syncytin-ory1). But rabbit syncytin is not related to either the mouse or the human form. These ERVs are not even on the same chromosome. Syncytin-1 is on chromosome 7; syncytin-2 is on chromosome 6; syncytin-A is on chromosome 5; and syncytin-B is on chromosome 14.
Indeed, Dupressoir et al. (2005) report that

Together, these data strongly argue for a critical role of syncytin-A and -B in murine syncytiotrophoblast formation, thus unraveling a rather unique situation where two pairs of endogenous retroviruses,independently acquired by the primate and rodent lineages, would have been positively selected for a convergent physiological role. [emphasis added]

This is a remarkable case of convergent evolution, of a kind which is highly unlikely to have occurred by Darwinian means.
But be that as it may. Briefly, the argument made in the cited article is this: In addition to the placement of ERV sequences in orthologous loci (and its pertinent nested hierarchical pattern), the article's assessment also takes into consideration the shared mutations among orthologous ERVs which, we are told, also fall into very similar nested hierarchies. Since mutation and ERV placement are independent factors, it is argued that this only makes sense when viewed in the light of descent. Moreover, the comparative degrees of LTR-LTR discontinuity among orthologous ERVs are argued to be implicative of the common descent model. The long-terminal-repeat (LTR) sequences must be identical upon insertion -- copies of retroviral promoters are polymerised during reverse transcription (the retroviral promoter is not transcribed into mRNA, so the ERV would otherwise lose its promoter). There are identical repeats on either terminus of the retroviral genome. During reverse transcription, the tRNA primer detaches and the DNA repeat hybridizes with the remaining RNA repeat at the genome's 3' terminus. These repeats need to be identical, otherwise they cannot hybridise. A copy of the 3' unique and 5' unique sections is polymerised on the opposite terminus. This is what forms the long-terminal-repeats (LTRs), which also have to be identical at the time of integration. Since LTRs are identical upon reverse transcription and integration, greater mutational divergence (common ancestry being true) ought to correlate with an older insertion.


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