What Are Endogenous Retroviruses?

Endogenous retroviruses (ERVs) are viral gene sequences that have become integrated into the genome of a host organism. These genetic elements originated from ancient retroviral infections of germ cells. When a retrovirus infects an organism, it converts its RNA genome into DNA and integrates this DNA into the host cell's genome. If this integration occurs in a germ cell (egg or sperm), the viral sequence can be passed on to offspring.

Over time, these viral sequences became fixed in the host genome and were passed down to offspring. ERVs typically no longer produce infectious viruses but remain as "genomic fossils," providing a record of previous viral infections.

ERVs as Evidence for Evolution

ERVs provide multiple lines of evidence that support evolutionary theory:

1. Shared ERVs at Identical Locations

Humans and chimpanzees share over 200,000 ERV insertions at identical locations in their genomes. This pattern can only be reasonably explained by inheritance from a common ancestor.

2. Hierarchical Distribution

The pattern of shared ERVs across different species forms a nested hierarchy that perfectly matches the evolutionary tree derived from other evidence. For example, some ERVs are found in all primates, others only in great apes, and others only in humans and chimpanzees.

3. Sequence Degradation

ERVs accumulate mutations over time. The degree of sequence divergence in ERVs can be used as a "molecular clock" to estimate the time of species divergence, and these estimates align with other dating methods.

4. Co-option for Host Functions

Some ERVs have been repurposed for important biological functions, illustrating how natural selection can adapt existing genetic material for new purposes.

Examples of Repurposed ERVs

ERV-Derived Gene Function Species
Syncytin-1 (from HERV-W) Critical for placenta formation Humans and other primates
Syncytin-2 (from HERV-FRD) Placental development and immunosuppression Humans and other primates
Syncytin-A and Syncytin-B Placental development Mice and other rodents
Syncytin-Car1 Placental development Carnivores (cats, dogs)
HERV-K elements Early embryonic development Humans

Each of these ERV-derived genes was independently co-opted in different mammalian lineages, demonstrating convergent evolution. Different mammal groups have repurposed different viral elements for similar functions, exactly as evolution would predict.

The Mathematical Improbability of Shared ERVs

The shared presence of ERV insertions in humans and chimpanzees at identical genomic locations poses a significant challenge to non-evolutionary models. Let's examine this mathematically.

Key Facts:

  • Human genome size: ~3 billion base pairs
  • Shared ERV insertions between humans and chimps: >200,000
  • Not all genomic locations are suitable for insertion. Let's conservatively estimate that 1% of the genome is insertable.

Calculation:

  1. Probability of a single ERV inserting at a specific location:

    \[ P(\text{insertion}) = \frac{1}{3 \times 10^9 \times 0.01} = \frac{1}{3 \times 10^7} \approx \frac{1}{30,000,000} \]

  2. Probability of the same ERV inserting at the same location in both species independently:

    \[ P(\text{shared insertion}) = P(\text{insertion})^2 = \left(\frac{1}{30,000,000}\right)^2 \approx \frac{1}{900,000,000,000,000} \]

  3. Probability of 200,000 shared insertions occurring independently:

    \[ P(\text{200,000 shared insertions}) = \left(\frac{1}{900,000,000,000,000}\right)^{200,000} \approx \frac{1}{10^{3000000}} \]

Interpretation:

This probability is so astronomically small that it's effectively zero—far smaller than the probability of randomly selecting the same atom from the observable universe multiple times in succession. For comparison:

  • Number of atoms in the observable universe: \(~10^{80}\)
  • Probability of randomly selecting the same atom from the universe 37 times in a row: \(~\frac{1}{10^{2960}}\)

The Evolutionary Explanation

The evolutionary model explains these shared insertions simply:

  1. ERVs inserted into the genome of a common ancestor of humans and chimpanzees.
  2. These insertions were inherited by both lineages after their evolutionary split.

This explanation requires no statistically improbable events and aligns with all other genetic and fossil evidence.

Example: The Koala ERV

The koala retrovirus (KoRV) provides a fascinating contemporary example of a retrovirus in the process of becoming endogenous. This case offers a real-time window into the evolutionary process that produced the ERVs we observe in human and other mammalian genomes.

The Koala Retrovirus

KoRV is currently in the process of endogenization in the koala population. Key observations include:

  • Northern Australian koala populations have KoRV integrated into their germline (i.e., it's endogenous)
  • Southern populations have varying degrees of endogenization
  • KoRV is both endogenous (inherited) and exogenous (infectious) in many koalas
  • The virus appears to have entered the koala germline less than 200 years ago

ERVs and Disease

While most ERVs in the human genome are inactive, some can influence disease processes:

ERV Type Associated Condition Mechanism
HERV-W Multiple Sclerosis Activation of HERV-W envelope protein (MSRV) triggers inflammatory responses
HERV-K Amyotrophic Lateral Sclerosis Expression of HERV-K proteins may contribute to neurodegeneration
Various HERVs Autoimmune diseases Molecular mimicry between HERV proteins and self-antigens
HERV-K Certain cancers Activation of normally silent HERV sequences

These disease associations represent an ongoing cost of carrying viral sequences in our genome, a trade-off that has developed over evolutionary time.

Objections

"God designed ERVs to serve a functional purpose."

While some ERVs have been co-opted for functional roles, the vast majority (>99%) show signs of degradation consistent with being genomic fossils. Additionally, different mammal lineages have independently co-opted different viral elements for similar functions, which aligns with evolution but not with design.

"ERVs can only insert in predetermined locations."

While retroviruses do have integration site preferences, these preferences are nowhere near specific enough to explain the observed patterns. The mathematical calculations above account for potential integration site preferences. Further, we observe that related species share both functional and non-functional ERVs at identical positions, exactly as common ancestry would predict.

"ERVs could be the result of horizontal gene transfer, not inheritance."

The pattern of ERV sharing precisely matches the independently derived evolutionary tree. For horizontal transfer to explain this pattern would require hundreds of thousands of independent transfers that somehow exactly mimic the expected pattern of common descent. This is statistically impossible.

Conclusion

Endogenous retroviruses provide some of the most compelling molecular evidence for evolution and common ancestry. The shared patterns of ERV insertions in human and other genomes create a clear record of our evolutionary history that cannot be reasonably explained by any non-evolutionary model.

The evidence from ERVs aligns perfectly with multiple independent lines of evidence from comparative anatomy, the fossil record, biogeography, and other genetic markers. Together, they form an overwhelming scientific case for the common ancestry of life on Earth.

Further Reading