Mass Extinctions, Evolutionary Leaps, and the Virus-Information Connection


FOTCM Member
This article:

Links to an open paper:
Cambrian comb jellies from Utah illuminate the early evolution of nervous and sensory systems in ctenophores

Could that be the one being referred to?
I think it is one.

we describe two ctenophore species from the Cambrian of Utah [fossils], which
illuminate the early evolution of nervous and sensory features in the phylum.
Thalassostaphylos elegans has 16 comb rows, an oral skirt, and an apical organ
with polar fields. Ctenorhabdotus campanelliformis has 24 comb rows, an oral
skirt, an apical organ enclosed by a capsule and neurological tissues preserved
as carbonaceous films. These are concentrated around the apical organ and
ciliated furrows, which connect to a circumoral nerve ring via longitudinal
axons. C. campanelliformis deviates from the neuroanatomy of living ctenophores
and demonstrates a substantial complexity in the nervous system of
Cambrian ctenophores.


  • Cambrian comb jellies from Utah.pdf
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Chapter 8: Saltationism vs Darwinism​

The previous chapter provided abundant examples of evolutionary leaps following mass extinctions. When one zooms out over past eons, one can see each that geologic period mark the apparition of new life forms that are distinctly more evolved than the life forms belonging to the preceding period.

This notion of evolution was far from foreign to past thinkers. Already, more than two millennia ago, Greek philosopher Anaximander[1] established a surprisingly sound theory of evolution:

Anaximander believed that life began in the sea, and that by some type of adaptation to the environment, animals evolved into what they are today. He believed that the human species must have been born out of other animals[2]

Notice that Anaximander’s theory was not baseless speculation, since fossils, their origin and their meaning were already known in ancient Greece.[3] Evolution concepts similar to Anaximander’s can be found in Roman times, in Lucrecius’ writings for example:

Lucretius claimed that a type of natural selection caused monster-like creatures to die-off, and that the creatures which survived did so due to their capacity for strength, speed, or intelligence. Lucretius parted with Anaximander by claiming that a land animal could not evolve from a creature of the sea, and he was skeptical that one species could evolve out of another.[4]

The conception of evolution was still much alive centuries, as testified by this excerpt of the Muqaddimah[5]:

One should then take a look at the world of creation. It started out from the minerals and progressed, in an ingenious, gradual manner, to plants and animals. The last stage of minerals is connected with the first stage of plants, such as herbs and seedless plants. The last stage of plants, such as palms and vines, is connected with the first stage of animals, such as snails and shellfish which have only the power of touch. The word 'connection' with regard to these created things means that the last stage of each group is fully prepared to become the first stage of the newest group. The animal world then widens, its species become numerous, and, in a gradual process of creation, it finally leads to man, who is able to think and reflect. The higher stage of man is reached from the world of monkeys, in which both sagacity and perception are found, but which has not reached the stage of actual reflection and thinking. At this point we come to the first stage of man. This is as far as our (physical) observation extends[6]

Belon Bird Skeleton.jpg

© Public Domain
Comparison between bird and human skeleton by Pierre Bellon (1555 AD)

Likewise during the enlightenment period, almost two centuries before Charles Darwin, the notion of evolution was widely theorized by thinkers like Pierre Louis Maupertius[7] or John Ray[8]. But notice that like Lucrecius, Ray didn’t believe in a progressive evolution from one species to another:

Animals likewise that differ specifically preserve their distinct species permanently; one species never springs from the seed of another nor vice versa[9]

The above shows that during the 24 centuries that separate Anaximander from Charles Darwin, evolution was known, researched and theorized[10].

Decades prior to Charles Darwin, evolution was well established as exemplified by the work of Jean-Baptiste Lamarck[11], Étienne Geoffroy Saint-Hilaire[12] or Lorenz Oken[13], who developed detailed theories of evolution, which like most other theories of evolution of these times were saltationists. Saltation comes from the latin “saltus” meaning "leap". For virtually all scientists of the time, evolution proceeded by sudden and large change.

Consequently Charles Darwin didn’t invent evolution theory whatsoever; he just replaced complexity-driven evolutionary leaps by random incremental changes. To put it bluntly, Darwin replaced a truth by a lie.

Darwinism is built on two foundations: random mutations effecting small changes. Both these foundations are falsified by facts. About randomness, here are the probabilities that random mutations led to various life forms in 5 billion years of random evolution:

Thus in 5.109 years the probability of random synthesis of the about 103 enzymes of the simplest cell was evaluated to ~ 10-40,000; and the probability of ~ 10-24,000,000 for the advent of man[14]

The probability of 10-24,000,000 is quite commensurable. It is equal to 0.XXX1 % where XXX represents 24 million zeros. If the probability of winning the lottery is 1 in 14 millions[15], 10-24,000,000 is the probability of winning the lottery 10 times each second of lifetime. That’s probably one of the reasons why all experiments attempting to re-create even the simplest lifeforms failed[16].

The second tenet of Darwinism, postulates small incremental changes. This should lead to continuous fossils record displaying life forms shifting very progressively from one species to another. The problem is that the fossil records tell a whole different story:

Darwin's central dogma emphasizing "small steps" (Darwin 1859,1871) is in fact completely refuted by the fossil record, as eukaryotic evolution generally proceeds in quantum leaps in the absence of intermediary forms (Eldredge and Gould 1972; Gould 2002; Hoyle and Wickramasinghe 1984).[17]

Actually Darwin himself was painfully aware of the abyssal gap between his gradual theory of evolution and the bouncy nature of fossil records:

Charles Darwin viewed the fossil record more as an embarrassment than as an aid to his theory. Why, he asked (1859, p. 310), do we not find the "infinitely numerous transitional links that would illustrate the slow and steady operation of natural selection? "Why then is not every geological formation and every stratum full of such intermediate links? Geology assuredly does not reveal any such finely graduated organic chain; and this, perhaps, is the gravest objection which can be urged against my theory" (1859, p. 280).[18]

Darwin’s doubts were confirmed by modern research based on ever increasing fossil records and new paleontology technics. Recent research papers including one extensive meta-studies show that evolutionary leaps are the rule rather than exception:

More modern studies, including a meta-analysis examining 58 published studies on speciation patterns in the fossil record showed that 71% of species exhibited stasis, and 63% were associated with punctuated patterns of evolutionary change. According to Michael Benton, "it seems clear then that stasis is common, and that had not been predicted from modern genetic studies." A paramount example of evolutionary stasis is the fern Osmunda claytoniana. Based on paleontological evidence it has remained unchanged, even at the level of fossilized nuclei and chromosomes, for at least 180 million years.[19]

The example of Osmunda claytoniana is not isolated. As previously mentioned[20] tardigrades appeared during the Cambrian explosion ca. 540 Mya and are still extant with little or no evolution during half a billion year of existence.

As shown in the quote above, not only most species experience evolutionary leap but then most species experience long periods of total stagnation (stasis). This succession of sudden leaps and long period of stagnation is totally contrary to the concept a gradual change.

Notice also that the studies quoted above only deal with species. The apparition and demise of whole families, clades and even phila - as exemplified by the Cambrian explosion[21] with the sudden apparition of more than 90% of modern phyla, some of them staying virtually unchanged for more than 500 million years - is even less linear than the pattern exhibited by species.

Despite the consecration in the 19th and 20th Century of Darwin’s postulate as the inalterable truth Saltationism survived. The chasm between Darwinism and fossil reality became so wide that saltationism has been experiencing a revival since the 1960’s:

MacGillavry (1968, p. 70) has written that "many species do not show any evolutionary change at all." MacGillavry points out that, although gradual change might be expected on a theoretical basis, it is rarely encountered, and that such a situation is not an artifact of the fossilization process. Another of the rare statements to this effect was made by Kurten (1965, p.345): "The situation suggests that new species arose comparatively rapidly, but once established, tended to continue without any change."[22]

And, in the 1970’s, a modern alternative to Darwin’s theory was conceptualized thanks to the works of Niles Eldredge[23], Harry Whittington[24] and Stephen Jay Gould[25]:

While differing significantly in details, both Whittington and Gould proposed that all modern animal phyla had appeared almost simultaneously in a rather short span of geological period. This view led to the modernization of Darwin's tree of life and the theory of punctuated equilibrium, which Eldredge and Gould developed in the early 1970s and which views evolution as long intervals of near-stasis (evolutionary stagnation) "punctuated" by short periods of rapid change[26]

The diagram below illustrates the fundamental differences between the smooth Darwinian evolution line (light grey) and the jagged saltationist curve (black) alternating long period of stasis (horizontal sections of the curve) with sudden evolutionary leaps (vertical sections of the curve):

life forms complexity vs time.jpg
Life forms complexity VS. Number of specie

Notice that, in the diagram above, the cyclicity of mass extinctions/life explosions is idealized over the 27 My cycle. In reality and in addition to the 27 My cometary cycle that is in sync with more than half the documented mass extinctions[27] , there are also other cometary cycle or isolated (non-cyclical) cometary events that account for other mass extinctions.

Notice also that the biodiversity as shown by the number of species or higher taxa remains constant over long periods of time:

Sepkoski (1978) constructed an explicit defense of the use of higher taxa (e.g., families or orders) as a surrogate for species diversity, and employed ordinal diversity to infer that the numbers of extant marine species had been constant since the late Ordovician (~440 Ma). [28]

So there is a clear de-correlation between complexity and diversity. While the latter increases by leaps, the former remains overall constant.
After the brief interlude about the history of evolution theory, let’s go back to our investigation of the causes of the above described evolutionary leaps.

[1] Anaximander ca. 610 – ca. 546 BC was a pre-Socratic Greek philosopher who lived in Miletus, a city of Ionia. He belonged to the Milesian school and learned the teachings of his master Thales. He succeeded Thales and became the second master of that school where he counted Anaximenes and, arguably, Pythagoras amongst his pupils.
See: Wikipedia contributors. (2021). “Anaximander”. Wikipedia, The Free Encyclopedia
[2] Jacob Bell (2019) “Evolutionary Theory in Ancient Greece & Rome” Classical Wisdom
[3] University of Berkeley editors (1996) “Evolution and Paleontology in the Ancient World”. University of Berkeley
[4] Jacob Bell (2019) “Evolutionary Theory in Ancient Greece & Rome” Classical Wisdom
[5] book written by the Arab historian Ibn Khaldun in 1377 AD
[6] Khaldun, ibn. (1377) "The Muqaddimah" Translated by Franz Rosenthal
[7] French mathematician and philosopher (1698 – 1759)
[8] English naturalist (1627 - 1705)
[9] Ray, (1686) “History of Plants”, translated by E. Silk.
[10] Osborn, Henry Fairfield (1894). “From the Greeks to Darwin: An outline of the development of the evolution idea”. Macmillan and Co
[11] French biologist and naturalist (1744 – 1829)
[12] French naturalist (1772 – 1844)
[13] German naturalist, botanist, biologist and ornithologist (1779 – 1851)
[14] Preoteasa, E., & Apostol, M. (2008) “Collective dynamics of water in the living cell and in bulk liquid. New physical models and biological inferences”. arXiv: Biological Physics
[15] Wikipedia contributors (2021) “Lottery mathematics” Wikipedia
[16] Steele EJ, et al. (2018) “Cause of Cambrian Explosion - Terrestrial or Cosmic?” Prog Biophys Mol Biol. 136:3-23
[17] Merill Singer et al. (2011) “Extinctions: History, Origins, Causes & Future of Mass Extinctions” Cosmology Science Publishers
[18] Niles Eldredge & Stephen Jay Gould (1972) “Punctuated Equilibria: An Alternative to Phyletic Gradualism” In “Models in Paleobiology”. Freeman Cooper. pp. 82-115
[19] Wikipedia contributors (2021) “Punctuated equilibrium”. Wikipedia
[20] See Part II, chapter “the Cambrian Explosion”
[21] See previous Chapter “The Cambrian Life Explosion”
[22] Eldredge, N. (1971) “The Allopatric Model And Phylogeny In Paleozoic Invertebrates” Evolution 25: 156-167
[23] American biologist and paleontologist (1943-)
[24] American paleontologist (1916–2010)
[25] American paleontologist, evolutionary biologist, and historian of science (1941 – 2002)
[26] Wikipedia contributors (2021) “Cambrian explosion” Wikipedia
[27] See Part I, Chapter 3
[28] Philip W. Signor (1994) “Biodiversity in Geological Time”. American Zoologist, Volume 34, Issue 1, Pages 23–32


Dagobah Resident
FOTCM Member


Dagobah Resident
FOTCM Member
Thank you for sharing your work here, Pierre! I'm following your posting with bated breath :-)

So there is a clear de-correlation between complexity and diversity. While the latter increases by leaps, the former remains overall constant.
Just a small correction here. I think the order in the second sentence should be swapped: While the former increases by leaps, the latter remains overall constant.


Jedi Council Member
FOTCM Member
This book is excellent, @Pierre and appreciate you sharing it on the forum. Just reading through the chapters, one can observe the way life has evolved from 1D to 3D on the planet Earth and continues to evolve further. Interestingly, we had Kantek with fully evolved 3D life and Mars was on its way to becoming a 2D planet before Earth stole its water. That proves that that there is plenty of life out there in other Solar systems with some type of life being seeded on all types of planets and in turn, terraforming them via natural processes. As the C's have said and I am paraphrasing that STO works within the natural order of Universe and the end result is incredibly beautiful.


The Living Force
FOTCM Member
Un Grand MERCI Pierre pour le Chapitre 8 toujours aussi passionnant, quel plaisir de pouvoir le lire en Français...
MERCI Channa pour le PDF très utile...

A big THANK YOU Pierre for the Chapter 8 always so fascinating, what a pleasure to be able to read it in French...
THANK YOU Channa for the very useful PDF...


FOTCM Member

Part III: Viruses are the Drivers of Life​

influenza virus.jpeg

© Adobe StockGraphic
Representation of an Influenza virus

Chapter 9: The Enigma of Speciation​

We concluded the chapter titled “Other life explosion” with the following statement: the above suggests that major cometary impacts are not only destructive acts through the removal of obsolete lifeforms during mass extinctions but also creative acts through the introduction of more elaborate lifeforms. But what is the mechanism beyond these sudden life explosions?

Surprisingly, for a long time, this peculiarity didn’t attract much attention from the scientific community:

[…] the extinction of the dinosaurs and many other groups of animals at the Cretaceous-Tertiary (K-T) boundary was the last of the six major mass extinction episodes identified around 1960 from the fossil record, the earlier ones (in chronological order) being near or at the end of the Cambrian, Ordovician, Devonian, Permian and Triassic Periods. However, very few evolutionary biologists or palaeontologists (investigators of fossils) saw any reason to think a special explanation was required for these events. By this time, the Modern Synthesis, blending traditional Darwinism with population genetics, had become the overwhelmingly-dominant evolutionary paradigm, and it was believed that the entire course of life on Earth could be explained through the mechanism of adaptive mutation. [1]

Darwinists tentatively explain the evolutionary leaps by the vacancy of ecological niches enabling the apparition of new species. This theoretical process is called adaptive radiation[2]. It claims that the release from competition induced by mass extinction allows the ensuing evolutionary leaps.

If reduced competition was indeed the driver of evolutionary leaps, the most severe the mass extinction was, the lower the competition became and, consequently, the greater the evolutionary leap should be. But it is not the case at all:

[T]here is no apparent relationship between the magnitude of an extinction and its ecological or evolutionary impact.[3]

Actually paleontologists’ data show that competition or lack thereof plays no role in the origination of new species or the extinction of existing ones:

The deep-sea record shows that species originations and extinctions are individual events unrelated to other species in the same environment. Competitive replacement (a fitter species leaking out of a marginal environment and outcompeting an established species) is generally not observed.[4]

One can leave a bacterium in any environment as long as one wants; competition or not, it won’t lead to a trilobite. This point is further illustrated by the previously mentioned ridiculously low probability[5] of the advent of even the simplest cell. Vacant ecological space can’t account for the sudden apparition of new and more complex species, whom, at least in some cases, are devoid of any known ancestors. While competitive replacement might play a marginal role in some instances, it is not enough, there’s obviously something missing.

According to recent research, mass extinctions do enable the subsequent evolutionary leaps:

There is no denying the profound evolutionary impetus mass extinctions have provided to the history of life. Mass extinctions create new evolutionary opportunities and redirect the course of evolution. [6]

But how can mass extinctions (an act of destruction) enable life explosion (an act of creation) if not through the Darwinian competitive replacement? According to English biochemist and evolutionist Trevor Palmer, the answer lies in genetics:

[…] developments in genetics have suggested that mass extinctions may do more than create vacant ecological space for the radiation of new species. It seems clear that stress can give rise to hypermutations and also to epigenetic changes, so it must be considered possible that a catastrophic mass extinction episode could give rise to a range of variants beyond what was likely to have occurred during normal times[7]

What could be the cause of the above-mentioned “hypermutations” and “epigenetic changes” that lead to the apparition of new species?

By the way, the evolutionary leaps observed after mass extinctions require not only “hypermutations” as stated in the above quote but beneficial hypermutations enabling the sudden appearance of not only new but also more complex, more organized lifeforms. What could cause these fundamental and beneficial changes?

The apparition of new and more complex species after cometary-induced mass extinctions is a recurring pattern. This emergence of new species is called “speciation”, a process that has been observed in real time, only once in animals[8]: Australian rock wallabies.

rock wallaby -Petrogale_xanthopus_-_Monarto_1.JPG

© Periptus
Yellow-footed rock wallaby (Petrogale xanthopus) at Monarto Zoo, Australia

Currently, the reorganizing of retroviruses in the genomes of is leading to the birth of a new species:

In 2001, O'Neill and her colleagues showed how retroviruses inhabiting the centromeres of the chromosomes of hybrid Australian rock wallabies are creating new species by wholesale juggling of chromosomal fragments. [9]

This viral speciation hypothesis exposed in the above quote fits with Trevor Palmer’s thesis according to which speciation is driven by “hypermutation” and “epigenetics changes”. Indeed, viruses are known to play a major role in epigenetics:

Viruses infecting animal cells are thought to play central roles in shaping the epigenetic scenario of infected cells. In this context it has become obvious that knowing the impact that viral infections have on the epigenetic control of their host cells will certainly lead to a better understanding of the interplay viruses have with animal cells.[10]

Likewise, viruses are a major cause of “hypermutations” in hosts’ genomes through at least three processes:

1/ The integration of the viral genome in the host’s genome, a phenomenon also known as viral genome integration. This integration is a necessary step[11] for all retroviruses and it occurs also for other viruses, including some as common as hepatitis B[12], human herpes[13] (HHV-6) or Epstein Barr[14] viruses.

Let’s illustrate the viral genome integration with an example. A given animal is exposed to a new virus, carried by air, water or other lifeforms. At this point in time, for this animal, the virus is an exogenous virus. If the viral infection and integration occurs in the germline of this host, the virus sequence will become part of its progeny’s DNA, the exogenous virus has become an endogenous virus, and from now on it is a hereditary viral sequence integrated in the host descendants’ genomes. This integration of viral genetic sequences into a host’s DNA modifies it de facto as shown in the following illustration:

Integration viral.jpg
© Yoder Lab
viral integration into host genome

2/ once the virus is integrated, it can further alter the host’s genome through a number of modifications amongst which duplication[15], deletion[16], replication[17] and recombination hotspots[18].

3/ viral sequences inserted in a host’s genome modify the expression of this genome, in other terms they turn on and off the existing genes[19] of the host’s genome. This point will be developed in the next pages.

Actually, the virus-induced modifications of the host’s genome are so deep that it can lead to fundamentally opposite results: death on one hand, evolution on the other one, depending on the host. This duality is reminiscent of recurring mass extinctions scenarios where the obsolete species face death while the sparred ones evolve:

Upon cell infection, some viruses integrate their genome into the host chromosome, either as part of their life cycle (such as retroviruses), or incidentally. While possibly promoting long-term persistence of the virus into the cell, viral genome integration may also lead to drastic consequences for the host cell, including gene disruption, insertional mutagenesis and cell death, as well as contributing to species evolution.[20]

The ongoing speciation among Wallaby is not the only case of apparition of new lifeforms induced by viral sequences. The very apparition of the genus homo (humans) is also associated with viral activity:

Humans share about 99% of their genomic DNA with chimpanzees and bonobos; thus, the differences between these species are unlikely to be in gene content but could be caused by inherited changes in regulatory systems. Endogenous retroviruses (ERVs) comprise ∼ 5% of the human genome. The LTRs of ERVs contain many regulatory sequences, such as promoters, enhancers, polyadenylation signals and factor-binding sites. Thus, they can influence the expression of nearby human genes. […] It is likely that some of these ERVs could have integrated into regulatory regions of the human genome, and therefore could have had an impact on the expression of adjacent genes, which have consequently contributed to human evolution[21]

In the quote above, the author makes a distinction between coding genes (i.e. that create proteins) and non-coding genes - that don’t create protein but instead regulate the activity of the coding regions.

To use an analogy, coding genes are like musicians who, instead of producing sound, produce proteins, which are the fundamental building-blocks of lifeforms. Non-coding genes play an even more fundamental role; they are like an orchestra director who, instead of directing musicians, directs[22] the expression of coding genes.

coding region.jpg
© Jeffrey Zheng
Non-coding regions vs coding regions

As shown in the illustration above, coincidentally or not, most viral sequences are integrated[23] in our non-coding genes, while they are very rare in coding regions[24].

Now that we know a bit more about coding and non-coding regions, let’s go back to the apparition of humans and clarify the reason why viruses are the probable cause of the divergence between humans and other hominids (great apes).

- The genome difference between human and chimpanzees is only 0.5% in active coding regions[25]. So the morphologic (also known as phenotypic) differences must come from non-coding regions.
- In the non-coding regions (the orchestra directors), the most active[26] DNA sequences are called LTR (Long Terminal Repeat) and they are of viral origin[27].
- Out 19 LTRs presence tested in human and other great apes genomes, 17 (~90%) were human specific.[28]

The three points developed above show that the main genetic difference between humans and chimpanzees lies in viral LTRs, which are therefore the probable genetic cause of the obvious morphologic differences.

Notice that the influence of viruses on the human genome and its expression didn’t stop with the divergence between humans from other great apes. Since then, viruses have been markedly shaping human DNA:

[…] an astonishing 30 percent of all protein adaptations since humans' divergence with chimpanzees have been driven by viruses.[29]

Not only viruses are considered as the cause of the apparition of humans (genus homo) but the apparition of the whole taxonomic family (hominids) - to which they belong along with seven other extant species of great apes[30] - is also attributed to viruses:

Hughes and Coffin used phylogenetic and sequence analysis to suggest that human endogenous retroviruses may have induced large-scale deletions, duplications and chromosome reshuffling in human genomic evolution. In the opinion of the geneticist Eugene Sverdlov, these viruses played a significant role in the evolution and divergence of the hominids.[31]

One of the evidence provided by Sverdlov to correlate the hominids divergence with retrovirus activity is the conspicuous apparition of retroviruses in hosts’ genomes at the time great apes (hominids) diverged from other apes:

Some HERVs emerged in the genome over 30 MY ago, while others have appeared rather recently, at about the time of hominid and ape lineages divergence.[32] [33]

The apparition of placental mammals to which the hominids family belongs is also correlated to the genomic integration of viral sequences[34].

Coincidently or not, the earliest fossil of a placental mammal dates back to 66 Mya, right at the time of the Cretaceous–Paleogene extinction event. The fossil belongs to the species Protungulatum donnae[35].

The taxonomic subclass constituted by placental mammals is by far the most represented of the three subclasses of mammals with nearly 4,000 species[36] offering a broad morphologic diversity from the bat to the whale.

Until the advent of the placentals, reproductive strategies were based on egg-laying. Placentals brought a number of major innovations: placenta and uterus of course, but also the deactivation of the mother’s immune system against the fetus and the protection against infections of the fetus, which is virtually devoid of any immunity. ERVs play a major role in these innovations:

- They are necessary to the morphogenesis of the placenta[37].
- They protect the fetus from infections by related exogenous retroviruses[38]
- They protect the fetus from the mother’s immune system[39]
- They control the expression of the embryo’s genome during its development[40]

The illustration below shows the role played by some ERVs at each step of development from germ cell to fully formed embryo. Keep in mind that not all ERVs in placentals have been identified yet and even less ERVs have been characterized. Despite these limitations, the role played by ERVs is already omnipresent:

erv in embryogenesis.jpg
© Yangquan Xiang
Selective activation of some ERVs during host development

The placental mammals (eutherian) taxonomic subclass belongs to the vertebrate taxonomic subgroup which appeared during the previously described Cambrian explosion[41] and coincides both phylogenetically[42] and temporally with the apparition of retroviruses together with their vertebrate hosts:

[…] recent studies which date the emergence of the complex retroviruses of vertebrate lines at or just before the Cambrian Explosion of ∼500 Ma. Such viruses are known to be plausibly associated with major evolutionary genomic processes.[43]

If we go further back the phylogenetic tree leading to humans, we discover again the prominent role played by ERVs, this time in the creation of cellular nucleus[44] and the apparition of one of the three[45] domains of life, the eukaryotes[46] (organisms whose cells have nucleus): which encompasses virtually all macroscopic lifeforms, including the previously described vertebrates.

To recap, the apparition of our genus (homo), the apparition of the family it belongs to (hominids), the apparition of the subclass it belongs to (eutheria), the subphylum that contains it (vertebrates) and the domain it belongs to (eukaryotes) are each closely associated with the integration of ERVs in the hosts’ genomes.

In the diagram below, from left to right, the light grey arrow shows the apparition of the eukaryotes, the white arrow shows the divergence of the vertebrates from other chordates[47], the medium grey arrow indicates the eutheria divergence, the dark grey arrow shows the great apes (hominids) divergence and the black arrow marks the human (homo) divergence:

phylogeny human2 bw cropped.jpg
Human phylogenic tree

To illustrate further the fundamental role played by viruses in speciation, the example of syncytin is edifying. Syncytin is a protein coded by a human endo-retrovirus called HERW1, involved in the specific development of placental mammals described previously. The role of Syncytin is so cardinal that it is necessary for placental development:

Genetic studies in mice have established that the proteins encoded by syncytin A (Syna) and Synb, which arose independently in the rodent lineage from different ERV copies, are both required for the formation of the bilayered syncytiotrophoblast of the murine placenta.[48]

Now, the unexpected feature of syncytin is that it was acquired by mammals at least seven times, during distinct integration of distinct viruses and each time this integration is correlated with the aftermath of a speciation event:

[…] syncytin acquisition from distinct viruses has occurred independently at least seven times, each event happening after the divergence of the mammalian orders in which they are found.[49]

In addition, paleovirological analyses established that syncytin-1 that is found in human that is around 30 million years old[50], coeval with the end-Eocene extinction.

Protein_HERV-FRD_PDB_ syncytin2.png
© commons.wikimedia
Structure of the syncytin protein

The paradox raised by virtually identical genomes leading to different morphology is not limited to the above mentioned example of homo vs chimpanzees. Actually, when compared to one another, most lifeforms exhibit the same contradiction. It is a thorny issue for Darwinists, according to whom evolution proceeds through incremental genetic changes, which lead to incremental morphologic changes. It is obviously not the case:

Results of recent research in evolutionary developmental biology is that the diversity of body plans and morphology in organisms across many phyla are not necessarily reflected in diversity at the level of the sequences of genes, including those of the developmental genetic toolkit and other genes involved in development. Indeed, as John Gerhart and Marc Kirschner have noted, there is an apparent paradox: "where we most expect to find variation, we find conservation, a lack of change". So, if the observed morphological novelty between different clades does not come from changes in gene sequences (such as by mutation), where does it come from? Novelty may arise by mutation-driven changes in gene regulation.[51]

As detailed in the human-chimpanzee divergence and applicable to virtually any lifeforms, viral sequences can and do cause different expressions of virtually identical genomes[52], which solves the paradox exposed in the quote above.

There are a sheer number[53] of viruses integrated in various hosts’ genomes, but their integration is not systematically dated. Nonetheless the examination of the scientific literature reveals four dates for the integration of three different virus families into mammals’ genomes:

- the integration of bornaviridae ca. 93 Mya
- the integration of circoviridae ca. 68 Mya
- the integration of filoviridae and parvoviridae, which are both dated to 30 Mya:

dating integration of viruses in hosts.jpg
© Holmes et al.
Dating of the integration of viruses in hosts’ genomes

Notice that each of these four dating almost perfectly match the timing of some of the most recent mass extinctions:

- The end-Eocene extinction ca. 34 Mya (cometary cycle #2)
- the Cretaceous–Tertiary extinction ca. 66 Mya (cometary cycle #3)
- the Cenomanian-Turonian extinction ca. 93 Mya (cometary cycle #4)

Beside the apparition of new families of viruses seems to be also associated with time of comet-induced mass extinctions. It is for example the case of the viral family baculoviruses that contains 85 species of viruses[54] and mostly infect insects[55]. Baculoviruses are thought to have appeared ca. 310 Mya[56], which is the time of the Carboniferous-Permian extinction.

In this chapter, we’ve observed three strong correlations:

1/ ERVs and new taxa: ERVs are associated with the apparition of whole new taxa; species like humans or wallabies, family like hominids, subphylum like vertebrates and even the taxonomic domain eukaryotes.

2/ ERVs and mass extinctions: The integration of new viral families (bornaviridae, circoviridae, filoviridae and baculoviridae) and new viruses (the viral gene of syncytin-1) in hosts’ genomes is associated with the time of mass extinctions.

3/ New taxa and mass extinctions: the apparition of a number of new taxa is repeatedly associated with mass extinctions as extensively described part II.

correlation mass extinction erv speciation2.jpg
Correlation between new taxa, new viruses and mass extinctions

Are these three associations fortuitous or do comet-induced mass extinctions mark the time when new ERVs are integrated in host genomes AND the time when these genomic integrations lead to the apparition of new lifeforms?

We have already seen two examples where these three associations are part of a single consistent chain of events: a/ the divergence of the placentals, because of the genomic integration of a new virus during the K/T extinction, b/ the emergence of new viruses along with their vertebrate hosts during the Cambrian explosion.

But the examples of the placentals and the vertebrates are not odd exceptions. Scientific literature reveals other instances when the integration of new ERVs was instrumental in the apparition of new species during or soon after a mass extinction:

- Jawed vertebrates appeared in the aftermath of the Ordovician–Silurian extinction. Analysis of their genomes reveals the viral origin of the RAG1 and RAG2 proteins and their pivotal role in the speciation of jawed vertebrates:

The results support the theory that RAG1 and RAG2 were once components of a transposable element [of viral origin[57]], and that the split nature of immunoglobulin and T-cell-receptor genes derives from germline insertion of this element into an ancestral receptor gene soon after the evolutionary divergence of jawed and jawless vertebrates.[58]

- Teleost fishes appeared in the aftermath of the Permian–Triassic extinction and their apparition was, at least partly, caused by viral sequences:

In contrast to mammalian genomes, teleost genomes also contain multiple families of active transposable elements [of viral origin[59]], which might have played a role in speciation by affecting hybrid sterility and viability.[60]

- Lepidoptera: a whole order of insects containing 126 families[61] and 180,000 species including moths, wasps and butterflies. Lepidoptera represents 10% of the species of living organisms[62] and appeared 200 Mya[63] at the time of the Permian-Triassic extinction without clearly identified ancestors[64]. At the same time[65] appeared a new family of viruses: the bracovirus which lives symbiotically in virtually every lepidopterian species[66].

lepidoptera wing fossil bw.jpg
© Van Eldijk
Exquisitely fossilised Lepidoptera wing from the Triassic-Jurassic boundary

The information gathered above - in particular the apparition of the vertebrates, the teleost fishes, the placentals the jawed vertebrates and Lepidoptera all occurring because the integration of new viral sequences around the times of mass extinctions - strongly suggest a causative chain of events involving the following time sequence: comet-induced mass extinctions, apparition of new viruses, integration of viral sequences in hosts’ genomes and finally apparition of new taxa, as depicted in the diagram below:

new virus new species.jpg
Comet → virus → speciation chain of event

[1] Palmer, Trevor (2018) “Perilous Planet Earth Revisited Chronology and Catastrophism” ResearchGate​
[2] Givnish, T.J. (2015) “Adaptive radiation versus ‘radiation’ and ‘explosive diversification’: why conceptual distinctions are fundamental to understanding evolution” New Phytol, 207: 297-30
[3] Douglas H. Erwin (2001) “Lessons from the past: Biotic recoveries from mass extinctions”. PNAS, 98 (10) 5399-5403
[4] Cesare Emiliani (1994). “Evolution--a composite model” Evolutionary Theory, Vol.10, No.6, 299-303
[5] ~ 10-40,000
[6] Erwin, Douglas (2001) “Lessons from the past: Biotic recoveries from mass extinctions” PNAS 98 (10) 5399-5403
[7] Trevor Palmer (2010) “Lamarck – The Man, the Myth and the Legacy”. C&C Review, pp. 40-51
[8] Two other cases of real time speciation are often mentioned. The first if the Central European blackcap, a bird, which “could be on the verge of a speciation event”. The second is the Galapagos finch, whose genome analysis revealed that, after all, it was only a large cactus finch
See: Jennifer Skene (2010) “Evo in the news: Speciation in real time” UC museum of Paleontology
University of Berkeley contributors (2010) “Understanding Evolution: Speciation in real time” University of Berkeley
[9] Ryan, Frank. (2004). “Human endogenous retroviruses in health and disease: a symbiotic perspective”. Journal of the Royal Society of Medicine, 97(12), 560–565.
[10] Silvia C. Galvan et al. (2015).“Epigenetics and animal virus infections”. Editorial. Frontiers in Genetics.
[11] Desfarges, S., Ciuffi, A. (2012) “Viral Integration and Consequences on Host Gene Expression” Viruses: Essential Agents of Life, 147–175
[12] Murakami Y et al. (2005) “Large scaled analysis of hepatitis B virus (HBV) DNA integration in HBV related hepatocellular carcinomas” Gut 54:1162-1168
[13] Pellett PE et al (2011) “Chromosomally integrated human herpesvirus 6: questions and answers”. Rev Med Virol
[14] Gao J, et al. (2006) “Epstein-Barr virus integrates frequently into chromosome 4q, 2q, 1q and 7q of burkitt's lymphoma cell line” J. Virol. Methods 136:193-199
[15] Hughes JF, Coffin JM (2001) "Evidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution" Nature Genetics. 29 (4): 487–89
[16] Campbell, I. et al. (2014) “Human endogenous retroviral elements promote genome instability via non-allelic homologous recombination” BMC biology, 12, 74
[17] Ibid
[18] Mighel, A.J. et al (1997). “Alu sequences” FEBS Lettre 417, 1–5
[19] A gene is a sequence of DNA or RNA
[20] Desfarges, S. et al. (2012) “Viral Integration and Consequences on Host Gene Expression”. Viruses: Essential Agents of Life, 147–175
[21] Khodosevich, K. et al. (2002). “Endogenous retroviruses and human evolution.” Comparative and functional genomics, 3(6), 494–498
[22] Fernandes, J. et al. (2019) “Long Non-Coding RNAs in the Regulation of Gene Expression: Physiology and Disease”. Non-coding RNA, 5(1), 17
[23] De Parseval, N. et al. (2003) “Survey of human genes of retroviral origin: identification and transcriptome of the genes with coding capacity for complete envelope proteins” Journal of virology, 77(19), 10414–10422
[24] De Parseval, 2003
[25] Goodman M. (1999) “The genomic record of humankind’s evolutionary roots”. Am J Hum Genet 64: 31–39
[26] Boeke JD, Stoye JP. (1997). ‘’Retrotransposons, endogenous retroviruses, and the evolution of retroelements” In Retro- viruses, Cold Spring Harbor Laboratory Press 343 – 435
[27] Lower R, et al. (1996) “The viruses in all of us: characteristics and biological significance of human endogenous retrovirus sequences” PNAS 93:5177–5184
[28] Khodosevich, K. et al. (2002) “Endogenous retroviruses and human evolution.” Comparative and functional genomics, 3(6), 494–498
[29] Genetics Society of America (2016) “Viruses revealed to be a major driver of human evolution: Study tracking protein adaptation over millions of years yields insights relevant to fighting today's viruses” ScienceDaily
[30] 3 species of orangoutan, 2 species of gorilla, 1 species of chimpanzee and 1 species of bonobo. See:
Groves, C. P. (2005) “Mammal Species of the World: A Taxonomic and Geographic Reference (3rd ed.)” Johns Hopkins University Press. pp. 181–184
[31] Ryan, Frank (2004) “Human endogenous retroviruses in health and disease: a symbiotic perspective”. Journal of the Royal Society of Medicine, 97(12), 560–565
[32] Sverdlov ED. (2000) “Retroviruses and primate evolution” Bioessays;22(2):161-71
[33] Some of the ERVs that distinguish great apes from other apes are Fc2master and Fc2 env
[34] Chuong E. B. (2013) “Retroviruses facilitate the rapid evolution of the mammalian placenta” BioEssays : news and reviews in molecular, cellular and developmental biology, 35(10), 853–861
[35] O'Leary et al. (2013) "The Placental Mammal Ancestor and the Post–K-Pg Radiation of Placentals" Science. 339 (6120): 662–667
[36] Dave Smith (1994) “Eutheria, the Placental Mammals” University of Berkeley Museum of Paleontology
[37] Mi, S. (2000) “Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis.” Nature 403:785–788
[38] Benit, L. (2001). “Identification, phylogeny, and evolution of retroviral elements based on their envelope genes.” J. Virol. 75:11709–11719
[39] Cianciolo, G. J. et al. (1985). “Inhibition of lymphocyte proliferation by a synthetic peptide homologous to retroviral envelope protein’’. Science 230:453–455
[40] Fu, B., et al. (2019). “Endogenous Retroviruses Function as Gene Expression Regulatory Elements During Mammalian Pre-implantation Embryo Development”. International journal of molecular sciences, 20(3), 790
[41] See Part II: Chapter “The Cambrian Life Explosion”
[42] Aiewsakun, P. et al. (2017) “Marine origin of retroviruses in the early Palaeozoic Era” Nature Communications 8, 13954
[43] Edward J. Steele, et al. (2018). “Cause of Cambrian Explosion - Terrestrial or Cosmic?” Progress in Biophysics and Molecular Biology, Volume 136, Pages 3-23
[44] Takemura M (2001) "Poxviruses and the origin of the eukaryotic nucleus". Journal of Molecular Evolution. 52 (5): 419–425
[45] The two other domains are the prokaryotes (bacteria) and the archaea (single-celled organism)
[46] Yoshikawa G et al. (2019) "Medusavirus, a Novel Large DNA Virus Discovered from Hot Spring Water" Journal of Virology. 93 (8)
[47] Taxonomic phylum including all lifeforms equipped with a backbone amongst other distinctive features
[48] Feschotte, C., Gilbert, C. (2012) “Endogenous viruses: insights into viral evolution and impact on host biology” Nature Review Genetics 13, 283–296
[49] Katzourakis A. (2013) “Paleovirology: inferring viral evolution from host genome sequence data” Philosophical transactions of the Royal Society of London. 368(1626), 20120493
[50] Lavialle, C., et al. (2013) “Paleovirology of 'syncytins', retroviral env genes exapted for a role in placentation” Philosophical transactions of the Royal Society of London. 368(1626), 20120507
[51] Wikipedia contributors (2021) “Evolutionary developmental biology” Wikipedia
[52] Rebollo R, et al. (2012) "Transposable elements: an abundant and natural source of regulatory sequences for host genes" Annual Review of Genetics 46 (1): 21–42
[53] See chapter : anteriority and pervasivness of Viruses
[54] Harrison, RL et al. (2018). "ICTV Virus Taxonomy Profile: Baculoviridae". The Journal of General Virology. 99 (9): 1185–1186
[55] Wang, M., & Hu, Z. (2019) “Cross-talking between baculoviruses and host insects towards a successful infection” Philosophical transactions of the Royal Society of London. 374(1767), 20180324
[56] Theze, J. et al. (2011) "Paleozoic origin of insect large dsDNA viruses". PNAS. 108 (38): 15931–5
[57] Young, G. R., et al. (2012) “Resurrection of endogenous retroviruses in antibody-deficient mice”. Nature, 491(7426), 774–778
[58] Agrawal, A., et al (1998) “Transposition mediated by RAG1 and RAG2 and its implications for the evolution of the immune system” Nature 394, 744–751
[59] Young, G. R. et al. (2012) “Resurrection of endogenous retroviruses in antibody-deficient mice” Nature, 491(7426), 774–778
[60] Volff, JN. (2005) “Genome evolution and biodiversity in teleost fish” Heredity 94, 280–294
[61] Capinera, John L. (2008) "Butterflies and moths" In “Encyclopedia of Entomology”. Springer. pp. 626–672
[62] Mallet, Jim (2007) "Taxonomy of Lepidoptera: the scale of the problem". The Lepidoptera Taxome Project
[63] van Eldijk et al. (2018) "A Triassic-Jurassic window into the evolution of Lepidoptera". Science Advances. 4 (1): e1701568
[64] J.-C. Sohn et al. (2015) “The fossil record and taphonomy of butterflies and moths (Insecta, Lepidoptera): Implications for evolutionary diversity and divergence-time estimates” BMC Evol. Biol. 15, 12
[65] Jennifer Welsh (2011) “Oldest Viruses Infected Insects 300 Million Years Ago” Live Science
[66] Gasmi L, et al. (2015) “Recurrent Domestication by Lepidoptera of Genes from Their Parasites Mediated by Bracoviruses” PLOS Genetics 11(9): e1005470


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FOTCM Member

Chapter 10: Species-Specific Eradication or Enhancement​

Beside their role played in speciation, viruses might also explain a puzzling feature of most mass extinctions: their apparent species discrimination.

Although the mechanical effects of a cometary impact whether mega tsunami, ice Age or induced mass volcanism can and do account for most destruction observed during mass extinctions, it falls short to explain its species-specific dimension: while one given species was eradicated, another closely related species sharing similar habitat, nutrition, physiology was spared:

Twenty-one of the twenty-seven species of lampshells (brachiopods) were completely obliterated at the K-T boundary, only to be suddenly replaced by twenty-four entirely new species.[1]

Why were some species spared and even blossomed while others closely related species were totally obliterated? Was it only a matter of random chance?

This species-specific actions displayed by viruses has been repeatedly proven by modern experiments. For example, the inoculation of the same virus to various species of fruit flies leads to dramatically different results. For some species the viral infection is benign or even asymptomatic while for other closely related fruit fly species, the virus is deadly:

The researchers infected 48 species of fruit fly with an RNA virus, and found that the amount of harm caused by the virus was extremely variable in the new hosts, with some species having relatively benign infections and other species dying rapidly.[2]

This species discrimination revealed by viruses is not limited to insects in laboratory settings. In nature the most evolved mammals, including humans, experience the same species-specific viral action:

The Ebola virus, for example, appears to cause few symptoms in its natural reservoir, the fruit bat, but it is deadly in chimpanzees, gorillas and humans.[3]

Similarly to Ebola, nearly all HERVs have a species-specific action because their binding sites in their hosts are themselves species-specific:

[…] nearly 90% of HERVs exist in the human genome as solitary LTRs and often contain transcription factor binding sites that are species-specific[4]

The same applies to virtually each virus-species interaction:

host species-specific and virus strain-specific interactions of viral molecules with the host innate immune system play a pivotal role in determining virus host range and virulence.[5]

In the same vein, the same species-specific viral action might apply to mass extinctions. For example, despite the eradication of 75% of the species, the K/T extinction, including its epidemics component, seems to have been species-selective:

wide variety of species were spared, or quickly recovered, such as amphibians, birds, crocodiles, ferns, insects, lizards, seed-producing plant, snakes, turtles, and most mammals which quickly diversified and became the dominant land animal[6]

Not only were some species spared while others were decimated, but these two phenomena seem to have been concomitant:

Continuing perturbations will allow at least some groups to accommodate and potentially diversify while other groups may still be declining. Several mass extinction episodes, particularly during the Late Devonian, fall into this category.[7]

During this same K/T event the previously mentioned bornavirus[8] appeared seem to have played a key and species-specific role:

"While studying the genetic history of these EBLs [endogenous bornaviral-like elements] and their locations in the genomes of various species, we concluded that they likely integrated into mammal DNA approximately 70 million years ago,” Wellehan said.
Sixty-six million years ago, the end-Cretaceous extinction led to the disappearance of all non-avian dinosaurs. Although the cataclysm following the Chicxulub meteor impact receives much of the blame for the extinction in popular culture, climate shifts following the volcanic release of carbon dioxide also helped bring about the end of the dinosaur age.
Bornaviruses are in the same order of viruses as Ebola, measles and rabies, all of which are capable of causing significant population-level effects. During the end-Cretaceous extinction, EBLs within mammal genomes may have protected mammals from bornaviruses that affected birds and reptiles, allowing them to step into the ecological niche left by extinct dinosaur species"[9]

© Getty Images
Electron microscopy of bornaviruses

Could bornaviruses have been a novel viruses introduced during the Chicxulub event, subsequently integrated in the pre-mammalian genome providing enhancement in the form of protection from other diseases while contributing to the removal of obsolete life forms, the non-avian dinosaurs?

Are viruses the agent allowing the emergence of new more complex life form and also contributing to the removal of obsolete life forms, along with other mechanical and indiscriminate destruction induced by cometary impacts like mega-tsunamis, induced volcanism or ice age?

According to Chandra Wickramasinghe, viruses target specific hosts inducing enhancement or death depending on the match between the host’s genome and the viral sequence:

the virus acts purposefully, targeting and inserting its RNA or DNA into specific hosts where there is a perfect genetic match. However, when there is a slight mismatch (or due to UV or other genetic damage), errors are introduced into the genome, and the host sickens and may die.[10]

This idea is confirmed by Shawn Joseph for whom both removal of obsolete species and the apparition of new species are directed by the interaction between genomes and the environment:

The interaction between the environment and genetic activity, regulates the emergence of new species and the elimination of yet others--a form of evolutionary-apoptosis.[…] As a form of evolutionary apoptosis, extinction is tightly regulated at the genetic and cellular level, and specific environmental (Lovelock 2006) and biological triggers (Ward 2009), will initiate the mass death and elimination of specific species.
Multicellular organisms which served as a genetic bridge to subsequent species, and which have fulfilled their biological purpose and provide no additional biological/environmental function, are destroyed by biologically/genetically regulated processes (Joseph 2009a).[11]

[1] Felix, Robert (2008) “Magnetic Reversals and Evolutionary Leaps: The True Origin of Species” Sugarhouse Publications P. 33
[2] University of Cambridge (2015) “Emerging diseases likely to be more harmful in similar species” ScienceDaily
[3] Idib
[4] Friedli M., Trono D (2015) “The Developmental Control of Transposable Elements and the Evolution of Higher Species” Annu. Rev. Cell Dev. Boil. 31:429–451
[5] Rothenburg S, Brennan G. (2020) “Species-Specific Host-Virus Interactions: Implications for Viral Host Range and Virulence” Trends Microbiol 28(1):46-56
[6] Singer, Merill (2011) “Extinctions: History, Origins, Causes & Future of Mass Extinctions” Cosmology Science Publishers P.4-26
[7] Budd A F & Johnson K G (1999) Paleobiology 25:188–200
[8] See previous chapter “The Enigma of Speciation”
[9] Hyndman TH et al. (2018) “Divergent bornaviruses from Australian carpet pythons with neurological disease date the origin of extant Bornaviridae prior to the end-Cretaceous extinction” PLOS Pathogens 14(2): e1006881
[10] Wickramasinghe, Chandra et al (2013) “Diseases From Space: Astrobiology, Viruses, Microbiology, Meteors, Comets, Evolution” Cosmology Science Publishers
[11] Joseph, Rhawn (2009) “Extinction, Metamorphosis, Evolutionary Apoptosis, and Genetically Programmed Species Mass Death” Journal of Cosmology
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