Viruses are a mystery: No one knows where they originate. As a virologist, I’ve always thought of viruses as incomplete components of once functionally reproducing cells. As a Christian, I’ve often linked viruses to the fall because of their association with disease and suffering. Although evolutionists certainly wouldn’t agree with my second line of reasoning, many do support an escaped gene theory to explain the origin of viruses. In other words, the vast array and diversity of viruses in nature may originate from sets of genes that have escaped from once living cells.
One virus familiar to most people is human immunodeficiency virus (HIV). HIV is a type of virus known as a retrovirus. All retroviruses encode proteins that transcribe their viral RNA genomes into DNA prior to integration into a host cell’s genome. Transcribing from RNA to DNA is contrary to the vast majority of transcription in biological organisms where DNA serves as the template for RNA transcription. This unique characteristic of going from RNA to DNA is the source of the name retro-virus.
Endogenous retroviral elements (ERVs) are similar to retroviruses in some ways and not like retroviruses in other ways. ERVs are embedded retrovirus-like sequences found in the genomes of many different kinds of animals (hence their name). However, almost all ERVs are unable to form infectious viral particles. They lack certain genes that are necessary for virus assembly and replication. The prevailing theory is that ERVs originated from ancient retroviral infections. And like many others, I find the existence of shared ERVs in the human genome and in the genomes of other nonhuman primates (NHPs) to be some of the strongest evidence in support of common descent (macroevolutionary theory).
However, the longer I think about ERVs and viral origins, and as I observe scientific reports identifying various critical functions associated with ERVs and other repetitive genomic elements, I believe it may be profitable for driving scientific inquiry to question some of the underlying assumptions that support ERVs as inarguable signs of common descent.
Do ERVs Indicate Random Insertion Events?
Despite early findings in vitro, retroviral insertion sites are not always selected randomly. Various retroviruses have varying degrees of insertion site preferences. Some show site bias, and others demonstrate integration specificity at the primary sequence level. Much of the insertion site selection is dependent on interactions between viral proteins and host cell proteins, and these vary from virus to virus and host to host—and possibly even at points of physiological development or activity in a given host. If ERVs arose from ancient retroviral infections of gametes or early stage blastocysts, it is possible that those ancient retroviruses had even greater specificity for insertion site selection than retroviruses tested and observed to date. If true, then at least some shared ERVs might have resulted from independent infection events.
Shared ERV sites are not always identical at first glance. To indicate this, researchers often refer to orthologous sites. In general genomic terms, orthologous sites indicate common descent and refer to relative positions within chromosomes and gene clusters. Orthologous positions would be expected if ERVs originated from ancestral heredity via common descent. But they would also be expected if these elements reflect common design where similar proximity of elements for particular functions are required in the different species according to a common design creation model.
Do Missing ERV Sequences Contradict Common Descent Predictions?
Despite persuasive arguments for the heritability of ERVs, the absence of specific shared ERV sequences in some NHP genomes challenges the common descent paradigm. Some elements are found in chimps, bonobos, and gorillas, but are absent in humans.1 Others are present in chimps and great apes but not in humans and orangutans.2 These findings are surprising, countering expectations from within a common descent model. Their absence undermines the notion that ancient infections of an ancestral primate lineage occurred prior to divergence of the great apes. According to phylogenetic analyses of species, great apes (including humans) share a common ancestor with Old World monkeys; therefore, shared ERVs should parallel this same phylogenetic relationship.3 Additionally, divergence of long terminal repeat sequences (components of ERVs) sometimes varies significantly from one species to another at shared sites, even when normalized for mutation rates. An article in Retrovirology highlighted an example of this that points to a much more recent integration event in humans and a relatively earlier integration event in chimps at a shared ERV insertion site.4
Though these findings contradict common descent theory predictions, naturalistic arguments can be (and are) constructed to accommodate the varying normalized sequence divergence rates and the absence of shared ERVs in some species. These explicit findings, however, present no direct challenge to a common design interpretation. In fact, a common design interpretation of the data suggests these differences are worthy targets for further study as they may directly point to variations in functions within different species.
To assume the egg comes before the chicken when considering retrovirus infections and genomic ERV sequences is to lock in a particular view of relationship that is not set in stone. This is especially true since the origin of viruses is unknown. Perhaps ERV-like sequences are sources of escaped genes that contribute to the genesis of retroviruses. Perhaps retroviruses precede the establishment of ERVs, as is observed today. Perhaps both are true in different instances.
Locking ourselves into one position or the other while we are just beginning to unravel the complexity of the human genome isn’t wise—in fact, it actually hinders scientific exploration. When interpreting data, it is prudent to remember that conclusions drawn from inferences will sometimes be biased or even wrong. Alternative interpretations of data, like that offered by a common design interpretation, actually drive research forward rather than allowing it to stagnate in a particular paradigm.
Further study of both the book of nature and the book of Scripture will lead to greater integration and understanding of what they have to say about human uniqueness and our ultimate purpose in life. We should leave the door open for further inquiry. If common design explanations, grounded in Scripture, help drive research forward, we should at least welcome this perspective in dialogue.
To read more on the subject of ERVs and common design, see AJ’s more comprehensive article, “Questioning Evolutionary Presuppositions about Endogenous Retroviruses.”
- Nehmé Saksouk, Elisabeth Simboeck, and Jérôme Déjardin, “Constitutive Heterochromatin Formation and Transcription in Mammals,” Epigenetics & Chromatin 8 (January 2015), doi:10.1186/1756-8935-8-3.
- In humans, this includes centromeric alpha satellite regions (mega-base scale, high-order repetitive sequences), unique pericentric sequences not represented in human genome drafts, and telomeric and ribosomal regions.
- The PacBio RS II system allows very large fragments of DNA to be sequenced (up to 10,000 bp) which can provide nonheterologous sequences at the ends of long, highly repetitive sequences, which helps in fitting these segments of the human genome into the proper gaps. It can also help determine specific copy number variations which differ from human to human and from chromosome to chromosome, even in an individual. However, it also requires relatively large amounts of high-quality DNA so is not applicable for ancient-DNA sequencing.
- Megan E. Aldrup-MacDonald and Beth A. Sullivan, “The Past, Present, and Future of Human Centromere Genomics,” Genes 5 (January 2014): 33–50, doi:10.3390/genes5010033; Glenn A. Maston, Sara K. Evans, and Michael R. Green, “Transcriptional Regulatory Elements in the Human Genome,” Annual Review of Genomics and Human Genetics 7 (September 2006): 29–59, doi:10.1146/annurev.genom.7.080505.115623.
By Anjeanette Roberts, PhD
Dr. Anjeanette “AJ” Roberts received her PhD in cell and molecular biology from the University of Pennsylvania in 1996, and currently serves as a Visiting Fellow with the Rivendell Institute at Yale University in New Haven, CT.