Naturalism is the belief that the existence of the Universe can be explained solely through some sort of natural evolutionary process, rather than a supernatural origin. Naturalism, and by implication atheism, necessarily contradict themselves. One cannot be a naturalist and not contradict himself. How so?
If one is a naturalist, he must believe that the Universe is an effect with no cause. The evidence from nature, however, is that all material effects must have a cause.
If one is a naturalist, he must believe that the rules/laws that govern the physical Universe “wrote” themselves. The evidence from nature, however, is that laws do not create themselves.
If one is a naturalist, he must believe that matter and energy could either create themselves or exist forever. The evidence from nature, however, is that matter and energy could not create itself (First Law of Thermodynamics), nor could it exist forever (Second Law of Thermodynamics).
If one is a naturalist, he must believe that at some point(s) in the past, non-living matter gave rise to living matter: life came from non-life. The evidence from nature, however, is that life only comes from life.
If one is a naturalist, he must believe that one kind of creature can morph into or give birth to a totally different kind of creature over time: macroevolution occurred. The evidence from nature, however, is that life produces according to its kind, not according to another kind.
A naturalist contradicts himself because he must believe in phenomena which do not occur in nature. Causeless effects, laws without law makers, the spontaneous generation of matter/energy and life, and evolution across phylogenic boundaries do not occur in nature.If one chooses to believe that such things could happen in nature, he is no longer a naturalist. He believes in unnatural—supernatural—phenomena. The naturalist is, in actuality, a supernaturalist under the guise of a naturalist. We can, at least, agree with the naturalist on one thing, even if he would not wish to concede it: the origin of the Universe requires supernatural activity. “The heavens declare the glory of God” (Psalm 19:1). Choosing not to believe in Him is “without excuse” (Romans 1:20).
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“Vestigial” organs are parts of the human body that, in many cases, were once thought by many evolutionists to be virtually useless leftovers from previous species in the human evolutionary ancestry that have yet to be eliminated from the body.1 In 1895, German anatomist Robert Wiedersheim made a list of 86 organs that he considered “wholly” or at least “in part functionless,”2 which have subsequently been shown to be useful as more study has been conducted on those organs over the decades. The Theory of Evolution predicts that such vestigial organs should exist, and yet not one organ has been found on the human body that does not have a legitimate function, effectively falsifying evolution.
Vestigial organs are still listed among the alleged evidences for evolution in most textbooks, even though the examples given (e.g., wisdom teeth, the tonsils, the coccyx, the appendix, the parathyroid, hair, and the male nipple) have, long ago, been shown to be useful components of the human body.
Some have, thankfully, given up on the vestigial organ argument but, unfortunately, have “updated” it with a more “modern” version: the vestigial gene argument. As evolutionary geneticist of the University of Chicago Jerry Coyne explained,
[W]hen a trait is no longer used, or becomes reduced, the genes that make it don’t instantly disappear from the genome: Evolution stops their action by inactivating them, not snipping them out of the DNA. From this we can make a prediction. We expect to find, in the genomes of many species, silenced, or “dead,” genes: genes that once were useful but are no longer intact or expressed. In other words, there should be vestigial genes.3
He, and many others, believe that is exactly what we see in the human genome: vestigial genes, “pseudogenes,” or “Junk DNA.” Creationists argue that all DNA serves a purpose (even if we do not yet fully understand it), having been created by God. The only exceptions would, perhaps, be in those rare cases where genetic entropy or mutations have, over the centuries, harmed the original DNA as God designed it, affecting its function.4
Don’t miss an important point in Coyne’s statement: according to Coyne, evolution would “predict” that junk DNA exists. In a scientific context, a “prediction” is a technical term. When a scientific theory is developed, if it is a legitimate scientific theory, it should have the ability to make predictions that can be verified or falsified upon further study (i.e., “If theory X is true, then we will find Y.”).
If the predictions are verified, it does not necessarily “prove” the theory. Instead, it gathers support for the theory and shows it to have greater “explanatory power”—the ability to explain more evidence. While verified predictions do not necessarily prove a theory, if the predictions are found to be false upon examination of the evidence, the theoryis falsified (at least, that version of the theory).5
Unfortunately for evolutionists, as with vestigial organs, as scientists further examine the human genome, they are discovering that evolutionists, once again, have been too rash in claiming they have found evidence for evolution. A growing arsenal of evidence is overwhelmingly falsifying an evolutionary prediction.
Jonathan Wells is a molecular and cell biologist of the Center for Science and Culture at the Discovery Institute in Seattle. In his 2011 book, The Myth of Junk DNA, he cites several prominent evolutionists who use the “Junk DNA” argument. He responded:
The arguments by Dawkins, Miller, Shermer, Collins, Kitcher, Coyne and Avise rest on the premise that most non-protein-coding DNA is junk, without any significant biological function. Yet a virtual flood of recent evidence shows that they are mistaken: Much of the DNA they claim to be “junk” actually performs important functions in living cells. The following chapters cite hundreds of scientific articles…that testify to those functions—and those articles are only a small sample of a large and growing body of literature on the subject.6
The evidence against the Junk DNA argument was already growing by leaps and bounds years ago and has continued over the decade since.7
As a case in point, consider an article released by New Scientist in July of last year.8 The writer, Michael Marshall, explains that the “new, more complete version of the human genome” that was released in May of 2021 “has uncovered enormous amounts of genetic variation between people that we couldn’t detect before…. Other studies have suggested that the new genome will finally reveal the functions of seemingly useless, repetitive sequences of ‘Junk DNA.’” Marshall explains that previous technology that was used to sequence the human genome made scientists “blind” to the fact that such sequences are, in fact, useful.
After studying sections of the sequence that have DNA that repeat “over and over without interruption,” geneticist of the University of Connecticut Rachel O’Neill said, “Most surprising is the number of repeats and the types of complex repeats…. They’re not just random repeated sequences, they have structure, and that structure can impact the organization of our genome.” Marshall explains, “Many geneticists have long argued that much of this repetitive DNA has no function and is ‘junk.’ However, some parts do seem to play roles—for instance, in regulating the activity of genes.”
As scientists study the evidence, the Junk DNA argument has been steadily dismantled, falsifying an evolutionary prediction and verifying creationist predictions. As is always the case, the more we learn about the Universe, the more we are struck by the fact that even its most microscopic, seemingly pointless characteristics have been intricately designed with specific purposes in mind.
Endnotes
1 Other vestigial organs are thought to have a diminished or changed, rather than non-existent, function. If they have a function at all, however, regardless of how important those functions may seem to scientists today, they are not evidence of poor design or pointless, evolutionary leftovers. The existence of organs that are apparently not as important/essential in function today compared to other organs does not prove that those organs were once more functional than they are now. They may have always had the same functionality they do today. For example, while a “pinkie” finger may not be as “useful” or essential as a heart, that does not mean that the pinkie is unimportant or proof of diminished function. Does the fact that carpet in the floorboard of a car is not as useful/important as a car motor mean that floorboard carpet has a diminished function compared to an alleged evolutionary ancestor? Or, rather, is floorboard carpet evidence that engineers include non-essential components in their designs that are still useful for other purposes (e.g., aesthetics, comfort, convenience, etc.)? See also Endnote 4.
2 Robert Wiedersheim (1895), The Structure of Man: An Index To His Past History (London: Macmillan), pp. 200-203.
3 Jerry A. Coyne (2009), Why Evolution is True (New York: Viking), pp. 66-67.
4 Note that genetic degeneration of the human body has not caused humans to be non-humans or non-humans to be humans. Such evolutionary examples are examples of “microevolutionary” rather than “macroevolutionary”/Darwinian change. Note also that such examples would be examples of de-evolution, rather than the progressive evolution espoused by Darwinists. Also, besides a consideration of the effect that genetic entropy would have had on the human body over the millennia, it is also possible that the pre-Flood world was so different from the post-Flood world that some features of the human body or genome do not function in the way they were originally designed to function due to an environment change. In other words, some aspects of the human body may be corrupted remnants of original humans, not evolutionary ancestors.
5 As a simple (silly) example, if a theory was presented that stated that humans are bi-pedal, a prediction of that theory would be that normal humans will have two legs everywhere they are examined. While each verification of that prediction does not prove the theory (but only adds support for it), the discovery of an unmutated tri-pedal human would directly falsify the bi-pedal theory.
6 Jonathan Wells (2011), The Myth of Junk DNA (Seattle, WA: Discovery Institute in Seattle), Kindle file, Chapter 2.
7 E.g., Yusuf Tutar (2012), “Pseudogenes,” Comparative and Functional Genomics, 2012:424526; S.W. Cheetham, G.J. Faulkner, and M.E. Dinger (2020), “Overcoming Challenges and Dogmas to Understand the Functions of Pseudogenes,” Nature Reviews Genetics, 21:191-201; R.K. Singh, D. Singh, A. Yadava, et al. (2020), “Molecular Fossils ‘Pseudogenes’ as Functional Signature in Biological System,” Genes & Genomics, 42:619-630; Evgeniy S. Balakiriv and Francisco J. Ayala (2003), “Pseudogenes: Are They ‘Junk’ or Functional DNA?” Annual Review of Genetics, 37:123-151.
8 Michael Marshall (2021), “Full Human Genome Put to Work,” New Scientist, 251[3345]:12, emp. added.
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EDITOR’S NOTE: The following article was written by A.P. auxiliary staff scientist Dr. Deweese who holds a Ph.D. in Biochemistry from Vanderbilt University and serves as Professor of Biochemisty and Director of Undergraduate Research at Freed-Hardeman University.
Introduction
For the past two and a half years, the world has been given a front-row seat to the process of science as the pandemic of SARS-CoV-2 has made its way around the world and back again. This article examines the virus and its components with a goal to understand how the virus works and how it is changing over time. Further, we will seek to consider the implications of viral evolution and step back to think about how viruses fit into a biblical worldview. [For a more extensive study of the nature of SARS-CoV-2, see the online version of this article.]
Before January of 2020, relatively few individuals used the term “coronavirus” in everyday language, much less understood its implications. While there are a few different coronaviruses that cause things like the common cold, prior to SARS-CoV-2, only two had caused major problems in humans: severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV).
An outbreak of SARS-CoV occurred in 2002-2004, which infected over 8,000 people and killed nearly 10% of those infected.1 MERS-CoV was associated with the Arabian Peninsula and occurred from 2012-2015 with about a 30% death rate, but a very low transmission rate.2 As of October, 2021, there have been a total of 2,578 cases with 888 reported deaths (34.4%) since 2012.3
By contrast, SARS-CoV-2 has spread globally in just over two years with over 419 million cases worldwide and over 5.8 million deaths (~1.4% of those infected) so far according to the Johns Hopkins Coronavirus Resource Center.4 Unfortunately, these numbers do not clarify for us the difference between people who died from the effects of COVID versus those who died of other causes but had COVID.
In general, SARS-CoV and MERS-CoV are naturally found in rodents and/or bats but have undergone “zoonotic transmission” to infect humans.5 Zoonosis is a term used to describe a disease that has undergone “spillover” from vertebrate animals to humans.6 As you might guess, there are barriers and challenges that prevent many diseases from infecting different organisms. However, some barriers are not insurmountable. Many questions still surround how and what changes took place to give us SARS-CoV-2—were they natural mutations in animal populations or were they part of experimental efforts perhaps aiming to thwart an epidemic? There are those on various sides of these issues.7
This article is not intended to settle the question of the origin of the virus or to take a particular side. Instead, we want to ask more fundamental questions: what is different between SARS-CoV-2 and previous deadly coronaviruses? Why does it spread so quickly? What will happen moving forward? And what are the apologetic implications of the coronavirus?
What Do We Learn About Mutations and Natural Selection from SARS-CoV-2 Variants?
One way to study viruses is to see how the sequences vary from other known viruses. Interestingly, SARS-CoV-2 is only 79% similar to SARS-CoV.8 This means that both viruses share about 79% of the same sequence information. The closest sequences to SARS-CoV-2 are viruses isolated from bats found in Yunnan province 1000+ km from Wuhan, denoted RaTG13 and RmYN02.9 RaTG13 is the closest, sharing 96.2% identify, while the RmYN02 shares 93.3% identity with SARS-CoV-2 reference sequence (note that the reference sequence is the first sequence that was released by Chinese researchers before the variants).
In this context, nucleotide “identity” means that two sequences are identical at that percentage of sites. Thus, 100% identity would mean that they have the same nucleotides at all possible sites. In a 30,000-nucleotide sequence, a 90% identity means that 27,000 sites match between two sequences.10
Throughout the pandemic, researchers have tracked the changes occurring in the genome of SARS-CoV-2 using advanced DNA sequencing technologies. As a result, there are now over four million SARS-CoV-2 viral sequences for us to compare in the public NCBI Virus Variation database.11 This is a bit of a unique situation because we’ve never had such a large pandemic occur while we have had the ability to sequence the genetic information of the virus in real-time worldwide. This massive effort has provided a way to track genomic changes (i.e., mutations in the virus) over time to see what types of changes are occurring and what types of changes are not occurring.
In general, we observe the changes typically seen in any organism: deletion, insertion, and single nucleotide changes. Single nucleotide changes are by far the most common. At this point, perhaps you are wondering how many changes are in the variants when compared to the reference sequence. In even the most extreme cases—like the Omicron variant—the total number of nucleotide changes (including insertions and deletions) is around 100 (less than 1%). Thus, for over 99% of the sequence there are no changes.
As of this writing, 10 variants are considered “Variants Being Monitored” (VBM) by the Centers for Disease Control, while two are listed as “Variants of Concern” (VOC): delta and omicron.12 In reviewing mutation data on these variants, most of the mutations tend to occur in the Spike protein-coding region with additional mutations in the ORF1ab region and some variants showing mutations in the nucleocapsid (N) protein-coding region.13 Mutations in the Spike protein tend to be focused within the amino terminal domain (the first part of the protein) or the RBD, as noted above. These are the regions that antibodies typically bind, especially those formed through vaccination with the mRNA vaccines.
As seen in Figure 1, Spike protein point mutation sites are mapped onto a three-dimensional model of the protein for the Omicron variant. The mutation sites are highlighted as red spheres. The region in red is the Receptor Binding Domain (RBD). The concentration of red spheres in this area underscores the importance of understanding how this region is changing and what impact that has on viral transmission and treatability. Mutations in this region can result in evasion of antibodies that target Spike protein.14 In other words, some of these mutations in the Spike protein make this region less able to be bound by antibodies from vaccination and/or prior infection. It is also worth noting that in addition to antibodies, T-cells also respond to SARS-CoV-2 and T-cell response includes binding to Spike (or other viral proteins). Notably, T-cell response in vaccinated and/or prior infected individuals still mostly retain the ability to recognize Omicron.15
Figure 1: Structure of Spike Protein Showing Region of Receptor Binding Domain. The image is a ribbon diagram of a structure generated using cryo-electron microscopy (PDB ID 6zGG). Spike protein is a trimer (three monomers) shown in blue, green, and orange. The receptor binding domain of the green monomer is colored red and spheres represent sites mutated in Omicron (Some sites are also mutated in other variants).
What can we learn from this? There are a few key takeaways for us to consider. First, mutations in SARS-CoV-2 are still rare in the sense that we do not see widespread mutation throughout the viral genome. This is due to the error correction mechanism and apparently a low tolerance of genetic change. The mutations that are occurring are enabling the virus to survive and spread more readily while causing more mild symptoms in general. Thus, you could argue that natural selection is filtering out mutations that do not benefit the virus. As noted by Dutch botanist and geneticist Hugo de Vries, however, “Natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest.”16 Natural selection does not provide the mechanism for the origin of new information, which is necessary for the evolution of new viruses and organisms.17
Second, the types of changes we are seeing fall into the basic categories of insertions, deletions, and single-nucleotide changes. The largest insertion in the sequences examined was nine nucleotides. Interestingly, this sequence is not found anywhere in the virus or in any of the variants examined except Omicron. There is a similar sequence in the genome (about 4,000 nucleotides away) that is off by one nucleotide, but the author has not seen a lot of speculation around this sequence.
There are some limitations to this brief study. For instance, there are 10s to 100s of thousands of sequences for some of these variants. So, there will undoubtedly be variability among the various samples. Yet, even with such variability, the general themes noted above remain: no novel sets of information have been generated by the DNA changes observed. More specifically, no new proteins or enzymatic functions have been observed. Instead, mutation and selection appear to be at work on the existing protein-coding genes, which is why we see most mutations focused on regions like the Spike protein-coding sequence. In order for new features to develop as in the Neo-Darwinian model of evolution, new genetic information is needed, but we do not observe this occurring.18
SARS-CoV-2 is mutating, but it is also clear that it is still SARS-CoV-2 (i.e., we do not see new functions arising though we do see modification of functions). We are seeing first-hand what types of mutations are possible. Note that this does not necessarily mean that we know what is possible in a living organism—viral growth and mutation have unique constraints. Other studies have argued that mutations tend to modify or break existing features rather than build new ones.19 This appears to hold true in SARS-CoV-2.
Are Viruses a Form of “Natural Evil” that Support a Case Against God?
In considering the SARS-CoV-2 virus and its cost on our world, it is worth asking, why do we have viruses anyway? From a human perspective, it can often seem like all viruses are “bad.” Are viruses a “natural evil” created by God to plague the world? After all, the only time the media (or society more generally) tends to focus on viruses is in the context of the seasonal flu or in the case of an outbreak of some deadly virus—like MERS or SARS. In fact, the word “virus” originated from the Latin term for poison.20 Our language has clear implications for how we view viruses. Do viruses represent a “bad” design on the part of the Creator?
As a little exercise in considering the roles and purposes of viruses, let’s first ask: how many types of viruses are there? Current taxonomy of viral species by the International Committee on the Taxonomy of Viruses lists 10,434 species.21 It seems generally agreed that this is an under-representation of the total number of viruses in nature, as additional viruses continue to be discovered year by year. In support of this idea, it has been stated that there are ~1031 bacterial viruses (called bacteriophages) in the biosphere, which exceeds the estimate of the number of stars in the universe!22 Interestingly, only approximately 219 viruses have been found to infect humans. Of these viruses, relatively few cause disease or death in humans.23 Far fewer have been found to cause epidemics or pandemics.24 Yet, as humans, we generally focus on these few cases that cause disease rather than on the thousands of viruses (perhaps hundreds of thousands or millions?) that exist throughout nature.25
To be clear, the 1918 Spanish flu, HIV, SARS, MERS, and SARS-CoV-2 have all had a major impact on our world. Many lives were lost or dramatically changed because of these viruses and their associated epidemics or pandemics. Yet, the integral role of viruses in nature has not been all negative as will be pointed out below.
Second, if there are so many different viruses, what do they do? Are there natural and ecological functions and roles for viruses? The answer to that is yes. In fact, there are many functions and roles for viruses in nature. For example, bacteriophages, mentioned above, help control bacterial populations.26 In addition, bacteriophages can aid in transfer of genes between bacteria, serve as a nutrient repository, and defend bacteria against other bacteria.27
Further, viruses may also play similar roles in eukaryotes and higher organisms including symbiotic relationships.28 In humans, infection with GB-virus C has been associated with slowed progression of HIV infection, suggesting that this virus helps block HIV from infecting host cells.29 Some have argued that the roles of viruses worldwide are so important that life as we know it would not exist without viruses.30
So, does coronavirus have a natural role in bats or pangolins? This is a harder question to answer as few people are looking at this question—the general starting assumption is that viruses are “poison” or “pathogens.”31 Interestingly, this assumption, based upon evolutionary presuppositions, may be impeding our understanding of the roles of viruses in nature. Additional research will be needed to identify and explore such roles.
Consider for a moment: why would God allow viruses? Again, recall that most viruses do not cause problems and disease in humans, and it is reasonable to consider that many viruses have useful roles in nature. Could viruses be originally created entities that perhaps have also decayed since the Fall like our own genomes?32 If viruses were originally created by God to serve specific roles in nature, then it is possible that the nature and roles of viruses have been corrupted over time by genetic mutation.33 The biochemical components in viruses are highly sophisticated—for example, reverse transcriptase (making DNA from RNA), error-correction, self-assembly, etc. These complex systems are best explained in a design model.
This perspective on viruses being designed entities has proved to be a fruitful research endeavor.34 In fact, understanding the original design of viruses may help us identify the roles of viruses and how those roles have become corrupted over time. This may help us understand virulence and the ability of a virus to spread and mutate, which may help us predict future pandemic threats.
What can we expect moving forward? As we move forward, we can expect that SARS-CoV-2 will remain present continuing to change. The rate of change may slow since the virus is infecting fewer individuals than when it was spreading at its peak. Changes in the virus may enable it to continue to spread and possibly even cause new outbreaks, but the changes also seem to reduce the ability of the virus to cause serious illness in most people. Note that serious illness is still happening, especially in individuals with multiple risk factors, and we need to be serious about looking after those who are most at risk. The good news is that new treatments and approaches are becoming available to help minimize the health impact where possible.
Conclusion
SARS-CoV-2 has spread around the world over the last two and a half years and caused major loss of life. Though the virus has mutated during that time, no new genetic information has been generated nor have novel features developed as needed by a Neo-Darwinian model. Further, while the origin of this strain of the virus may remain contentious and debated, it is clear that viruses as a whole are designed entities fulfilling important roles in nature. It may be hard for us to identify those roles in the present time due to the genetic changes that have taken place in those viruses since the Fall in Genesis 3. Nevertheless, viewing viruses as designed entities that have experienced genetic change and decay since the Fall has served as a valuable framework for research in this area. In addition, this view helps remind us of God’s power in creation and of the consequences of sin that have been building since the Fall.
Endnotes
1 “Revised U.S. Surveillance Case Definition for Severe Acute Respiratory Syndrome (Sars) and Update on Sars Cases—United States and Worldwide, December 2003,” (2003), MMWR: Morbidity and Mortality Weekly Report, 52[49]:1202-1206.
2 B. Rha, J. Rudd, et al. (2015), “Update on the Epidemiology of Middle East Respiratory Syndrome Coronavirus (Mers-Cov) Infection, and Guidance for the Public, Clinicians, and Public Health Authorities—January 2015,” MMWR: Morbidity and Mortality Weekly Report, 64[3]:61-62.
6 K.G. Andersen, A. Rambaut, et al. (2020), “The Proximal Origin of Sars-Cov-2,” Nature Medicine, 26[4]:450-452; Y. Deigin, and R. Segreto (2021), “Sars-Cov-2’s Claimed Natural Origin Is Undermined by Issues with Genome Sequences of Its Relative Strains: Coronavirus Sequences Ratg13, Mp789 and Rmyn02 Raise Multiple Questions to Be Critically Addressed by the Scientific Community,” Bioessays, 43[7]:e2100015; M. Seyran, D. Pizzol, et al. (2021), “Questions Concerning the Proximal Origin of Sars-Cov-2” Journal of Medical Virology, 93[3]:1204-1206; J. van Helden, C.D. Butler, et al. (2021), “An Appeal for an Objective, Open, and Transparent Scientific Debate About the Origin of Sars-Cov-2,” Lancet, 398[10309]:1402-1404.
7 G.A. Rossi, O. Sacco, et al. (2020), “Differences and Similarities between Sars-Cov and Sars-Cov-2: Spike Receptor-Binding Domain Recognition and Host Cell Infection with Support of Cellular Serine Proteases,” Infection, 48[5]:665-669.
8 Hong Zhou, Xing Chen, et al. (2020), “A Novel Bat Coronavirus Closely Related to Sars-Cov-2 Contains Natural Insertions at the S1/S2 Cleavage Site of the Spike Protein,” Current Biology, 30[11]:2196-2203, e2193; Peng Zhou, Xing-Lou Yang, et al. (2020), “A Pneumonia Outbreak Associated with a New Coronavirus of Probable Bat Origin,” Nature, 579[7798]:270-273.
9 See the extended version of this article for a more technical discussion, https://apologeticspress.org/going-viral-exploring-virus-mutations-and-evolution-extended/.
10 E.L. Hatcher, S.A. Zhdanov, et al. (2017), “Virus Variation Resource-Improved Response to Emergent Viral Outbreaks,” Nucleic Acids Research, 45[D1]:D482-d490.
12 O’Toole, V. Hill, et al. (2022), “Tracking the International Spread of Sars-Cov-2 Lineages B.1.1.7 and B.1.351/501y-V2 [Version 1; Peer Review: 3 Approved],” Welcome Open Res, 6[121].
13 Chakraborty, A.R. Sharma, et al. (2022), “A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of Sars-Cov-2 and Their Emerging Variants with Escape Mutations,” Frontiers in Immunology, 13:801522.
14 V. Naranbhai, A. Nathan, et al. (2022), “T Cell Reactivity to the Sars-Cov-2 Omicron Variant Is Preserved in Most but Not All Individuals,” Cell, 185[6]:1041-1051.e1046.
15 Hugo de Vries and Daniel Trembly MacDougal (1905), Species and Varieties, Their Origin by Mutation; Lectures Delivered at the University of California (Chicago, IL: The Open Court Publishing Company).
16 J.C. Sanford (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications).
17 Ibid.; Michael J. Behe (2019), Darwin Devolves : The New Science About DNA That Challenges Evolution (New York: Harper Collins).
18 Behe, 2019; M.J. Behe (2010), “Experimental Evolution, Loss-of-Function Mutations, and ‘the First Rule of Adaptive Evolution,’” Quarterly Review of Biology, 85[4]:419-445.
19 Harald Brüssow (2021), “On the Role of Viruses in Nature and What This Means for the Covid-19 Pandemic,” Microbial Biotechnology, 14[1]:79-81.
20 Peter J. Walker, Stuart G. Siddell, et al. (2020), “Changes to Virus Taxonomy and the Statutes Ratified by the International Committee on Taxonomy of Viruses (2020),” Archives of Virology, 165[11]:2737-2748.
21 F. Rohwer and R. Edwards (2002), “The Phage Proteomic Tree: A Genome-Based Taxonomy for Phage,” Journal of Bacteriology, 184[16]:4529-4535; Georgia Purdom and Joe Francis (2009), “More Abundant Than Stars,” Answers Research Journal, 2:85-95.
22 Mark Woolhouse, Fiona Scott, et al. (2012), “Human Viruses: Discovery and Emergence,” Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 367[1604]:2864-2871.
24 Ibid.; M.E. Woolhouse, R. Howey, et al. (2008), “Temporal Trends in the Discovery of Human Viruses,” Proceedings: Biological Sciences, 275[1647]:2111-2115.
26 Z. Naureen, A. Dautaj, et al. (2020), “Bacteriophages Presence in Nature and Their Role in the Natural Selection of Bacterial Populations,” Acta Bio-Medica: Atenei Parmensis, 91[13-S]:e2020024.
28 M.J. Roossinck (2015), “Move over, Bacteria! Viruses Make Their Mark as Mutualistic Microbial Symbionts,” Journal of Virology, 89[13]:6532-6535; Marilyn J. Roossinck (2011), “The Good Viruses: Viral Mutualistic Symbioses,” Nature Reviews Microbiology, 9[2]:99-108.
29 Nirjal Bhattarai and Jack T. Stapleton (2012), “Gb Virus C: The Good Boy Virus?” Trends in Microbiology, 20[3]:124-130.
