Viruses: Originally Created Good?

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This is the title of a very interesting article written by Jerry Bergman, a creationist, in 1999. I provide Dr. Bergman’s main points below and one reason this article is significant is because up until very recently, most people including scientists have viewed viruses as “bad”, as the 2006 Nature article below points out. Bergman, on the other hand, being a creationist, apparently realized the truth of the Biblical statements which affirm that God created all things “good” in the beginning. This is a great example of how the Bible is an excellent source for valid scientific hypotheses, often when the rest of science has it wrong.

Here’s the abstract of Bergman’s article …

A review of the structure, function, and role of viruses in ecology is presented. It is concluded that viruses are non-living entities, similar to seeds and spores whose functions include carrying genes from one plant or animal to another. Viruses are a part of a system that helps to produce the variety that is critical for life and, importantly, they carry resistance to disease from one organism to another. Most viruses live in their host without causing problems. Pathogenesis is evidence of something gone wrong, a mutation or the accidental movement of genes, and not evidence of a system deliberately designed to cause human disease and suffering.

And some points Bergman makes which I think are fascinating …

* Bacteria used to be thought of as mostly “bad”, but now they are known to be essential for life
* Viruses seem to be turning out the same way — once thought of as “bad” — it now appears that they are essential for life on the planet
* Pathogenic viruses probably are so because they are either out of place, or mutated
* We may be able to use viruses to treat bacterial infections much more effectively than with antibiotics
* Viruses are essential for molecular biology research

I don’t know about you, but for me the thought of “Viruses Are Good” was a new thought for me. But come to think about it, the Book of Genesis tells us that ALL things were created “good.” Why not viruses also? Remember, while the Book of Genesis is not a scientific book, it has been shown to be largely accurate in the statements which we can verify, therefore, it is reasonable to use the Book of Genesis as a source for scientific hypotheses.

Apparently, Creationist author Jerry Bergman ran with this idea and began searching the literature for evidence of this. Some people say creationists are anti-progress, but this is nonsense. The truth is that we are often on the cutting edge … we don’t mind talking about controversial things, even when it brings ridicule upon us. And often, given enough time, the rest of science catches on to our “crazy ideas” and they become mainstream. NOTE: There are a few citation errors in Bergman’s article. See Errata at end of this post.

Bergman’s article prompted me to do a little Googling myself and I found some interesting articles …

Here’s a 2006 article in Nature entitled “Virology: The gene weavers” by Nature science writer Garry Hamilton.

Hamilton writes …

In from the cold
Viruses have long been viewed as nature’s outsiders. As parasites that depend on a host cell for survival, they don’t seem to have fully earned the stripes of a living organism. But they are actually far more abundant, diverse and complex than once thought. Recent calculations suggest there may be more undiscovered genes in the viral world — most belonging to phages — than in all other life forms combined. And this vast presence and diversity has profound effects on the rest of life. By shuttling genes into and out of their hosts, viruses seem to be a major driving force in the evolution of higher organisms. Even within our own genome, genes that came from viruses are hard at work. This in turn has led to the realization that viruses probably play a major role in the ecological, biochemical and evolutionary processes that underlie the entire natural world. Rather than being the outsiders, viruses have emerged as perhaps life’s most ubiquitous presence.

And he quotes Luis Villarreal, director of the Center for Virus Research at the University of California, Irvine, [who] even argues that a large portion of what distinguishes humans from chimps is viral DNA.

“I think it’s become apparent that viruses are involved everywhere,” says Villarreal. “I would argue they are the most creative genetic entities that we know.”




Virology: Chimps harbour HIV in wild

Science doi:10.1126/science.1126531 (2006)
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Wild chimpanzees (pictured right) have long been suspected as the source of the human immunodeficiency virus, HIV. Now that theory has been confirmed: evidence from southern Cameroon shows that wild members of the chimpanzee subspecies Pan troglodytes troglodytes harbour the strain of simian immunodeficiency virus (SIV) that is most closely related to pandemic HIV.

Researchers led by Beatrice Hahn of the University of Alabama at Birmingham report the presence of antibodies against the SIV strain in droppings left by wild chimps. This strain had previously only been detected in captive animals.

The virus, which does not seem to cause disease in the chimps, was probably transmitted to humans by exposure to blood during bushmeat hunting or butchery. The location of the discovery also supports the idea that the HIV pandemic had its roots in nearby Kinshasa, in the Democratic Republic of Congo.
Full Nature Article


Science 28 July 2006:
Vol. 313. no. 5786, pp. 523 – 526

Chimpanzee Reservoirs of Pandemic and Nonpandemic HIV-1

Brandon F. Keele,1 Fran Van Heuverswyn,2 Yingying Li,1 Elizabeth Bailes,3 Jun Takehisa,1 Mario L. Santiago,1* Frederic Bibollet-Ruche,1 Yalu Chen,1 Louise V. Wain,3 Florian Liegeois,2 Severin Loul,4 Eitel Mpoudi Ngole,4 Yanga Bienvenue,4 Eric Delaporte,2 John F. Y. Brookfield,3 Paul M. Sharp,3 George M. Shaw,1,5 Martine Peeters,2 Beatrice H. Hahn1{dagger}

Human immunodeficiency virus type 1 (HIV-1), the cause of human acquired immunodeficiency syndrome (AIDS), is a zoonotic infection of staggering proportions and social impact. Yet uncertainty persists regarding its natural reservoir. The virus most closely related to HIV-1 is a simian immunodeficiency virus (SIV) thus far identified only in captive members of the chimpanzee subspecies Pan troglodytes troglodytes. Here we report the detection of SIVcpz antibodies and nucleic acids in fecal samples from wild-living P. t. troglodytes apes in southern Cameroon, where prevalence rates in some communities reached 29 to 35%. By sequence analysis of endemic SIVcpz strains, we could trace the origins of pandemic (group M) and nonpandemic (group N) HIV-1 to distinct, geographically isolated chimpanzee communities. These findings establish P. t. troglodytes as a natural reservoir of HIV-1.

None of 23 P. t. vellerosus or 67 gorilla specimens exhibited detectable Western blot reactivity to any HIV-1 protein (table S1).

The findings presented here, together with prior studies, provide for the first time a clear picture of the origin of HIV-1 and the seeds of the AIDS pandemic.

As for Bergman’s theory of inappropriate contact with apes … well, I think he is speculating there.



A professional virologist over at IIDB says …

OK, I see what you mean by “reshuffling”. But CM and Eric are correct to point out that your quoted passage deals with novel and apparently unusual viruses collected from multiple sources. Not HIV which was the subject of Bergman’s argument.

I will say though, that recombination plays a role in the generation of novel viruses for certain types of animal retroviruses and this has been amply documented. Animals like mice or chickens can carry endogenous copies related to the infecting viruses and recombinational events between these exogenous and endogenous elements can generate altered viruses, often with new host ranges – these result from the replacement of the viral envelope gene. Rarely, animal retroviruses can also acquire host genes by recombination – in some cases host genes involved in growth regulation. Recombinant viruses with such genes can go on to cause cancer. Google “sarcoma viruses”. (example = Rous sarcoma virus)

There is no evidence that these recombinational events represent some sort of designed process.

I focus now on her last sentence and note that this is not correct. There IS evidence which has been accumulating lately that recombination is under tight cellular control and gives us strong suspicions that it was designed.

Where is this evidence?

Well, I always turn to creationists for such answers first if such are available because, as I said, scientists who have the world view which best describes actual reality (that is, creationism) are logically most likely to have the answers for explaining phenomena in the real world.

So I’m going to introduce you to Chris Ashcraft, a creationist author who works for Eden Bioscience. Chris has a masters in biology from Texas Tech and two years in a PhD program in Genetics at OSU. Now, in case you think that guys without PhD’s aren’t capable, let me just remind you about Gregor Mendel — you know, the Father of Modern Genetics? …

Education and early career.Mendel’s interest in natural science developed early. After two years’ study at the Philosophical Institute at Olmütz (now Olomouc, Czech Republic), he entered the Augustinian monastery at Brünn, Moravia (later Brno, Czech Republic), in 1843, taking the name Gregor. He was ordained a priest in 1847. During the period of his monastic training he taught himself a certain amount of science. From 1849 he acted for a short time as a substitute teacher of Greek and mathematics in the secondary school at Znaim (Znojmo), near Brünn. In 1850 he took the examination for certification as a regular teacher but failed, his lowest marks being given, ironically, in biology and geology.He was then sent by his abbot to the University of Vienna, where he studied physics, chemistry, mathematics, zoology, and botany (1851–53). In 1854 Mendel returned to Brünn and taught natural science in the technical high school there until 1868, although he never succeeded in passing the examination for a teacher’s license. In that year he was elected abbot of his monastery.

Mendel, Gregor. (2007). In Encyclopædia Britannica. Retrieved February 16, 2007, from Encyclopædia Britannica Online: Full text

So please … don’t tell me how you need this or that degree from this or that university in order to be on the cutting edge of science. That’s just a myth.

Back to Chris Ashcraft …

In 2004 Answers In Genesis published a very interesting article of his in their technical journal, entitled “Genetic Variability by Design.” You should read the whole thing. It soundly refutes the notion that “there is no evidence that these recombinational events represent some sort of designed process.”

On the contrary, there is a growing body of evidence for just that. I will snip some quotes from this article — heavily documented from the science literature — with the hope that you will be tantalized to actually read it. I read the papers that I am given and you should also read the papers that I give you. I promise that your time will not be wasted.

Browsing through the article, we have …

There are two potential sources for changes to gene sequence; mutations and recombination. The cell recombines DNA for various reasons including the purposeful generation of diversity. Mutations on the other hand are changes resulting from of exposures to foreign mutagens, or the result of errors during biochemical reactions such as DNA replication. Changes to genes are almost universally attributed to the latter, however, replication attempts to copy the genome verbatim, while recombination is intentionally making alterations in a largely uncharacterized manner. Therefore, any changes found should be automatically assumed the result of recombination. This simple logic has escaped modern philosophers who do not recognize the existence of cellular design behind such variability. Although it is certainly possible for mutations to produce a beneficial change to the genome, finely tuned environmental adaptations are not likely accomplished by randomly altering genetic code.

Naturalism assumes that life and genetic information exist without intent, and therefore, the changes to genes that ultimately drive evolution are presumed to be independent of cellular intent. Darwinian evolution essentially requires mutations as the source of new genetic information to explain the existence of variability before cellular mechanisms developed. Due to this theoretic necessity, cellular reactions have not been adequately sought as a purposeful source of new alleles.

Although changes to gene sequence are still commonly assumed the result of mutations, evidence has surfaced which is helping to demonstrate that new alleles are the result of purposeful genetic recombination.

It is now widely recognized that genetic editions through HR are part of a highly coordinated process involving a cascade of specific macromolecule interactions,7 and controlled by highly organized regulatory systems.8 In particular, the induction of recombination during meiosis is reliant upon several genes, and is regulated by a complex network of cell signaling mechanisms.9

7 Cascades of Non-covalent Protein-protein and Protein-DNA Interactions for Homologous DNA Recombination. Takehiko Shibata. RIKEN Review 46:24-28 (2002)
8 Hierarchic Regulation of Recombination. Kunihiro Ohta. RIKEN Review 41:28-29 (2001)
9 Homologous genetic recombination as an intrinsic dynamic property of a DNA structure induced by RecA/Rad51-family proteins: a possible advantage of DNA over RNA as genomic material. Shibata, T., Nishinaka, et al. Proc. Natl. Acad. Sci. U.S.A. 98(15):8425-8432 (2001)

The specific details or exact sequence homology required for HR remain largely unknown, but the plethora of functions accomplished by these reactions has elevated them to the position of master mechanic responsible for virtually all forms of sequence editing and maintenance.

It has now been thoroughly documented that mitotic recombination via gene conversion is able to create genetically altered cells, and researchers have suggested that this process can generate a gene with novel functions by rearranging various parts of the parental reading frames.16

16 Functions of Homologous DNA Recombination. Takehiko Shibata. RIKEN Review 41:21-23 (2001)

Evolutionists generally assume that new alleles are the result of random mutations that have accumulated gradually over millions of years. However, living populations have been tested only decades following severe genetic bottlenecks to find surprisingly high genetic diversity. This strongly suggests a mechanism for rapidly restoring variability, and the yet this possibility has not yet been adequately explored.18

18 Allozyme evidence for crane systematics and polymorphisms within populations of sandhill, sarus, Siberian and whooping cranes. Dessauer, H. C., G. F. Gee, and J. S. Rogers. Molecular Phylogenetics and Evolution 1:279-288 (1992)

It is becoming increasingly questionable that variability is the result of random mutations as commonly claimed by evolutionists. The following quote adequately validates this assertion. “Adaptive evolution has long been regarded as the result of postmutational sorting by the process of natural selection. Mutations have been postulated to occur at random, producing genetically different individuals that then compete for resources, the result being selection of better adapted genotypes. Molecular biology has demonstrated, however, that the rate and spectrum of mutations is in large part under the control of genetic factors. Because genetic factors are themselves the subject of adaptive evolution, this discovery has brought into question the random nature of mutagenesis. It would be highly adaptive for organisms inhabiting variable environments to modulate mutational dynamics in ways likely to produce necessary adaptive mutations in a timely fashion while limiting the generation of other, probably deleterious, mutations.”24 Evidence for the Adaptive Evolution of Mutation Rates. Minireview by David Metzgar, Christopher Wills (2000) Cell 101, p581.

Note the desire of this author to “enlarge the tent” for the term “mutation.” I noticed this desire at AtBC by “Russell”, an Ohio State microbiology professor during a debate I had there. But this desire counters current teaching in biology. The current (2006) high school Biology text (Prentice Hall, authored by Miller/Levine) restricts the term “mutation” to random events.

The genes of the major histocompatibility complex (MHC) are similarly edited during meiosis through the process of gene conversion using template DNA that resides elsewhere in the genome.24 By editing the genes of the MHC, new alleles are created for each offspring giving the immunity system an ability to recognize its cells apart from any other. As with all known hypervariable genes, MHC editions are not random changes. The frequency of gene conversion events varies greatly from one allele to the next, and is localized to specific areas that are rich in CpG nucleotide dimers.30


It is truly more logical to propose that cells have been designed to perform some level of genetic engineering, than suggest random mutations are responsible for finely tuned adaptations. Atheists must believe that mutations are the ultimate source of new genetic information out of theoretic necessity. However, since Gregor Mendel discovered the basics of genetics, it has remained reasonably obvious that cellular mechanisms are generating the variations of related species that Darwin described. Although Mendelian genetics and selective breeding histories have answered a great portion of the mystery behind genetic diversity, the exact relationship between HR and population variety remains far from understood.

Since random genetic changes will simply not result in an expected sequence, the immunity system provides an excellent example of the seemingly unlimited potential of HR to generate new information. The mechanisms behind this type of gene conversion are not yet understood, but clearly illustrate the ability of the cell to specifically edit genes, and thereby rapidly multiply the number of alleles in a population. Further characterization should prove to be valuable evidence that cellular design governs the production of genetic variability, and adaptive evolution that occurs as a result.

“The ability to induce homologous recombination in response to unfavorable environmental changes would be adaptive for each species, as it would increase genetic diversity and would help to avoid species’ extinction. Homologous recombination would be more efficient for evolution than random mutagenesis or nonhomologous recombination. Although the latter two will mostly disrupt previously existing genes rather than creating new ones, homologous recombination can use previously existing genes as building blocks, thus enabling the creation of new proteins with more complex functions in a step-by-step manner.” 13 Proc. Natl. Acad. Sci. U.S.A. 98(15):8425-8432 (2001)

Read the whole article from this very alert and cutting-edge creationist here …

BERGMAN ARTICLE ERRATA (The journal where this article first appeared is being notified.)
32. Brown, P., How the parasite learnt to Walk, New Scientist 152(2056):32–36, 1996. [Should read “How the parasite learnt to Kill”]

60. Morse, S., 1990. Stirring up Trouble; Environmental Disruption Can Divert Animal Viruses into People. Science. 30(5):20. [Incorrect journal title. Should be “The Sciences.”]

63. Lurier, S.E., Darnell Jr., J. E., Baltimore, D. and Campbell, A., General Virology, John Wiley and Sons, New York, NY. p. 36, 1978. Return to text.
64. Lurier, ref. 63, p. 159. Return to text
65. Lurier, ref. 63, p. 228. Return to text.
[Author’s name is actually “Luria”, not “Lurier”]


3 Responses to “Viruses: Originally Created Good?”

  1. […] previous claims that there are hundreds of such articles. Additionally afdave is trivializing the large number of errors VoxRat is finding in an article by Jerry Bergman, Ph.D. titled “Did God Make […]

  2. Yes, virus are essential for evolution 😀

  3. Oh, how wonderful…viruses as part of “intelligent design”! People, people…virus are escaped bits of genomes, whose only similarities are that they share a lifestyle which involves using cellualr organisms as hosts to provide essential-to-virus functions like protein translation from mRNA.

    And that is their ONLY commonality. Viruses do NOT share the same single origin; they may well co-exist quite well with their hosts BUT are not symbiotic or even commensal in the same way bacteria frequently are. While they have probably contributed significantly to especially mammalian evolution – a retrovirus envelope protein is probably the reason we mammals have placentae, for example – it is far more likely that this is by blind chance than by design.

    Face it: this is a virus planet. There are probably 10exp31 virus particles on it, enough to outnumber all other organisms combined by a factor of 10 or more. And they don’t have enough mind to worry about what we think, or why.

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