One of my first lab “projects” as a graduate student—assigned to me by my PhD advisor Jack Blazyk—was to clean and organize the lab. This assignment wasn’t out of the ordinary. It is something commonly asked of first-year graduate student plebs. As part of my task, Jack asked me to go through every drawer in the lab, clean them out, and organize the contents. 

One of the drawers held equipment for an ultra-microcentrifuge. Among the rotors, microcentrifuge tubes, tools, and other centrifuge parts were several straws that had been cut into pieces. I couldn’t imagine why anyone would put straw pieces in a lab drawer. So, I threw them away. As it turns out, those straw pieces were parts for the pipettes designed to deliver samples to the centrifuge tubes. Oops.

Fortunately, the straw pieces were easily replaced. 

Straws aren’t junk. They are designed to make it easier for people to consume beverages. From my perspective, however, the straw pieces in the lab drawer must have been trash, because they were in an unfamiliar and unexpected context. If I saw them in a restaurant I would know of their use immediately. But in a laboratory drawer? Yet when I learned more about how the ultra-microcentrifuge worked, I discovered that the straw pieces weren’t junk at all. 

Scientists studying genomes are learning the same lesson I learned all those years ago as a budding graduate student. Sometimes things that appear to be junk are there for a reason. Biologists have long thought that many of the sequence elements in genomes, such as endogenous retroviruses (ERVs), are nothing more than useless junk—the vestiges of an evolutionary history—because they occur in an unfamiliar and unexpected context. 

ERVs bear strong sequence similarity to retroviruses, but biologists initially deemed ERVs junk because they are found in genomes, instead of in viral capsids. Yet, life scientists have come to discover that ERVs serve several vital roles, as recent research from Japan attests.1

This insight has important scientific implications because it gives us a deeper understanding about genome biology. It also has important ramifications for those of us who view the human genome (and all genomes) from a design/creation model perspective because it further justifies our position.

But first a quick primer on retroviruses and ERVs for those who need it. If not, feel free to skip ahead to: Can the Occurrence of ERVs Be Explained from a Creation Model Perspective?

Retroviruses
Like all viruses, retroviruses consist of genetic material surrounded by a protein capsid. Retroviruses infect organisms by invading specific cell types of the host organism. After the retroviruses attach to the target cell’s surface, the targeted cell engulfs them. Once engulfed, the viral genetic material exploits the host cell’s machinery to produce copies of the viral genetic material and viral proteins. These biomolecules then assemble into new viral particles. When the newly formed viruses escape from the invaded cell, the infection cycle repeats.

Because the genetic material of retroviruses is RNA, it must be converted into DNA before the infectious cycle can proceed. This conversion is carried out by an enzyme called reverse transcriptase, which is delivered to the target cell along with the retroviral RNA. The enzyme uses the retroviral RNA to make DNA. This newly made DNA can then use the invaded cell’s biosynthetic pathways to direct the production of new retroviral particles. The DNA copy of the retroviral genetic material can also become incorporated into the host cell’s genome. When this insertion takes place, the retroviral DNA becomes part of the host cell’s genome. This process is called endogenization.

Endogenous Retroviruses (ERVs)
Once retroviral DNA becomes incorporated into an organism’s genome it is called an endogenous retrovirus (in contradistinction to exogenous retroviruses, which exist independent of genomes). The endogenous retrovirus can still produce retroviral particles, if its DNA is transcribed by the host cell’s biochemical machinery. 

If the ERV infects a germ line cell (a sperm cell or an egg cell), it can be inherited and transmitted from generation to generation as a permanent feature of the genome. If the ERV DNA experiences severe mutations, it becomes disabled and remains in the genome as nonfunctional, junk DNA. 

Endogenous Retroviruses and the Case for Human Evolution
Many human ERVs are also found in the genomes of chimpanzees, bonobos, gorillas, and orangutans. Not only do these ERVs share many of the same sequence patterns, but they also appear in corresponding locations in the genomes. Evolutionary biologists view these patterns as evidence for a shared evolutionary history among humans and the great apes. Accordingly, the shared ancestor (of, say, humans and chimpanzees) became infected by a specific retrovirus that became endogenized. Later, the endogenized retroviruses experienced mutations that disabled them in the ancestor’s genome. The ERV sequences were retained in the genomes of humans and chimpanzees as their separate evolutionary lineages diverged from the common ancestor. According to the model, the endogenous retroviruses shared by humans and chimpanzees represent the molecular artifacts of infections that occurred millions of years ago and left their imprint on contemporary genomes via their shared ancestry. 

Can the Occurrence of ERVs Be Explained from a Creation Model Perspective?
For those who advocate for ID or a creation model approach to biology, troubling questions arise: Why would the Creator introduce the same nonfunctional sequence elements in the same locations within the genomes of organisms that naturally group together (based on other biological features)? And why would he create these shared sequence elements to bear such strong similarity to retroviruses?

For many people, the presence and distribution of ERV sequences in genomes provide indisputable evidence for human evolution and our shared ancestry with the great apes. Is it possible, however, to account for ERVs from an intelligent design/creation model perspective?

To do so, at minimum those who advocate for a design/creation must:

• demonstrate that ERVs are functional,
• account for the sequence similarity between ERVs and retroviruses, and
• explain their shared distribution in the genomes of organisms that naturally cluster together.

Toward this end, life scientists have recently identified several roles played by ERVs, including providing a defense against retroviral infections. (See Resources for articles detailing some of these functions.)

ERVs Protect Vulnerable Early-Stage Embryos from Viruses 
In 2015, researchers from Stanford University showed that a class of ERVs in the human genome (HERV-K) becomes transcriptionally active during the 8-cell stage of human embryos. This activity ceases once the embryo reaches the epiblast stage. During this window of time, the researchers detected gag and rec proteins (encoded by the ERVs) in the blastomeres’ cytoplasm.2 After this stage, the expression of the HERV-K sequences becomes silenced through methylation of their LTR sequences.

The researchers demonstrated that ERV expression affords blastomeres protection against the H1N1 virus by hampering its interaction with the cell membrane and disrupting the early stages of the viral invasion. The production of gag proteins and the ERV RNA also inhibits the retroviral life cycle through competitive inhibition, a process that disrupts the assembly of newly made retroviral virions.

Regulation of ERV Expression Is Fine-Tuned
Work by the Japanese research team builds upon this earlier finding. They discovered that the transcription factor SOX-2 regulates ERV expression by binding to promoter sequences in the LTR sequences of HERV-K sequences. This transcription factor is active during the earliest stages of embryonic development. It maintains the blastomeres in a pluripotent state, in which the cells replicate without differentiating. 

By the epiblast stage of embryonic development, SOX-2 expression is shut down. This event allows the embryonic cells to begin the process of differentiation. It also leads to the cessation of ERV transcription. This cessation is important. If ERV expression continues unchecked, then a process called retrotranspositioning occurs, in which the ERV sequences copy themselves continuously and insert randomly throughout the genome. When ERV sequences retrotranspose, they cause damage to the genome that can lead to cancer. Biomedical researchers have discovered that cancer stem cells express SOX-2 at high levels.

As the Japanese team points out, “The strict dependence of HERV-K on SOX-2 has allowed HERV-K to protect early embryos during evolution while limiting the potentially harmful effects of HERV-K retrotransposition on host genome integrity in these early embryos.”3

ERVs in a Creation Model
The results from this study—and others (see the Resources section)—satisfy two of the three criteria required to justifiably interpret the presence of ERVs in genomes from a creation model perspective by (1) demonstrating the functional role of these sequences, and (2) accounting for their close similarity to retroviral genetic material.

But what about the distribution of ERVs in the genomes of organisms that naturally cluster together into nested hierarchies?

It is true that most life scientists regard shared biological features—including DNA sequences—as evidence for their shared evolutionary ancestry. Yet an alternative explanation for biological similarities can be advanced. Following after the ideas of biologist Sir Richard Owen, shared biological features can be interpreted as manifestations of a common blueprint—an archetype that arises out of the Creator’s mind.

In other words, from a creation model perspective, the Creator intentionally introduced the genetic similarities in the genomes of humans and the great apes. This includes junk DNA sequences, such as ERVs. Accordingly, the corresponding sequence similarities and locations for junk DNA sequences among organisms that naturally group reflect functional considerations.

Even though many biologists can’t imagine why a Creator would add ERV sequences into genomes, deeper insight into ERV biology offers an unexpected explanation.

Resources

Thinking about Evolution: 25 Questions Christians Want Answered by Anjeanette Roberts, Fazale Rana, Sue Dykes, and Mark Perez (book)

Who Was Adam? A Creation Model Approach to the Origin of Humanity, 2nd exp. ed., by Fazale Rana with Hugh Ross (book)

The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)

Endogenous Retroviruses Have Function

“Koala Endogenous Retroviruses (ERVs) Protect against Retroviral Infections” by Fazale Rana (article)

“SARS2CoV Gives Insight into the Role of ERVs in the Human Genome” by Fazale Rana (article)

“Endogenous Retroviruses (ERVs) Protect Early-Stage Human Embryos” by Fazale Rana (article)

“Endogenous Viral Elements (EVEs) Help Wasps to Parasitize” by Fazale Rana (article)

“Endogenous Retroviruses Help Fight Tumors” by Fazale Rana (article)

“Questioning Evolutionary Presuppositions about Endogenous Retroviruses” by Anjeanette Roberts (article)

“A Common Design View of ERVs Encourages Scientific Investigation” by Anjeanette Roberts (article)

The Historical and Philosophical Case for Common Design

“Archetype or Ancestor? Sir Richard Owen and the Case for Design” by Fazale Rana (article)

“Duck-Billed Platypus Venom: Designed for Discovery” by Fazale Rana (article)

“Does Old-Earth Creationism Make God Deceptive?” by Fazale Rana (article)

The Negative Impact of the Junk DNA Concept on Scientific Advance

“Does the Evolutionary Paradigm Stymie Scientific Advance?” by Fazale Rana (article)

“Evolution’s Flawed Approach to Science” by Fazale Rana (article)

“Does Evolutionary Bias Create Unhealthy Stereotypes about Pseudogenes?” by Fazale Rana (article)

Check out more from Reasons to Believe @Reasons.org

Endnotes

1. Kazuaki Monde et al., “Movements of Ancient Endogenous Retroviruses Detected in SOX-2-Expressing Cells,” Journal of Virology 96 (April 14, 2022): e00356-22, doi:10.1128/jvi.00356-22.
2. Edward J. Grow et al., “Intrinsic Retroviral Reactivation in Human Preimplantation Embryos and Pluripotent Cells,” Nature 522 (June 11, 2015): 221–25; doi:10.1038/nature14308.
3. Monde et al., “Movements of Ancient Endogenous Retroviruses.”