URL @ https://barryhisblog.blogspot.com/p/what-is-case-for-common-descent-from.html
Here is a brief overview. Much more detail can be found here,
https://web.archive.org/web/20230531193743/http://www.evolutionarymodel.com/ervs.htm
Here is a brief overview. Much more detail can be found here,
https://web.archive.org/web/20230531193743/http://www.evolutionarymodel.com/ervs.htm
Further FAQ entries go into into the following points in more depth and answer common questions about them.
1. Retroviruses replicate by invading the cells of host organisms, converting their RNA genomes into DNA, and inserting (integrating, in the jargon) the DNA into the DNA of the host cell. The integrated DNA is called a "provirus". The host cell then "reads" the provirus, converting it back into RNA, resulting in the production of more viruses.
2. Retroviruses tend to target certain types of cells. Their "envelope" proteins tend to be specialized to attach to the surfaces of these cells.
3. The integration into the host's DNA is made by a retroviral enzyme called integrase. While certain retroviruses can show a general tendency to integrate their DNA in certain types of regions in a host cell's DNA, they do not target specific points (loci). This means that in an infected individual, not all cells will be infected, and in those that are, the retroviral integration will be in a different locus or loci in the DNA of each cell.
4. We find, in the genomes of creatures such as ourselves and chimpanzees, inherited structures that cannot be anything but the remnants of retroviral integrations. Some are more complete than others, but many have the full set of genes that would be necessary for a complete retrovirus, were they not faulty. We call these structures endogenous retroviruses (ERVs). Unlike the case where each cell is individually infected, they appear in the exact same loci in the DNA of every single nuclear cell (cells with nuclei containing DNA).
5. Although certain components of some ERVs perform functions in the host, some even being essential in many cases, no complete ERVs are functional. Design, as an explanation for ERVs, does not make any sense. A designer would have no need to include specifically retroviral genes in its designs, which now do nothing, or may even cause harm. There would also be no need to design in non-functional traces of the action of integrase, traces of which are present in ERVs.
6. The only explanation that makes any sense is that ERVs are the result of retroviral integrations with germ-line DNA - the DNA of egg cells or sperm cells, followed by reproduction and consequent cell division. Cell division will duplicate the ERVs in the same loci in the DNA of every cell. Separate, parallel infection would not infect every cell, and the proviruses would end up in different loci, comparing one infected cell with another.
7. All human beings have some 200,000+ ERV and ERV fragments in the DNA of every one of their cells. Most of them are in identical DNA loci going from cell to cell, and person to person. This means that we all share common ancestors - the ancestors that first acquired each of the germ-line retroviral integrations.
8. All human beings and chimpanzees have some 200,000+ ERV and ERV fragments in the DNA of every one of their cells. Most of them are in precisely corresponding DNA loci going from cell to cell, and individual to individual. This means that we all share common ancestors - the ancestors that first acquired each of the germ-line retroviral infections. See https://web.archive.org/web/20230531193743/http://www.evolutionarymodel.com/ervs.htm#Amount_of_Shared_ERVs
ChatGPT says, about https://barryhisblog.blogspot.com/2025/01/url-here-is-brief-overview.html
ReplyDelete"The post lays out an explanation for how endogenous retroviruses (ERVs) serve as evidence for common descent. It describes the process by which retroviruses integrate into a host’s genome and then, if they infect germ-line cells, become inherited across generations. This results in the same viral “fossils” appearing at the same genomic locations in related species—a pattern that strongly supports shared ancestry.
In many ways, the explanation is consistent with mainstream evolutionary biology. The discussion covers how random integration events (mediated by retroviral enzymes like integrase) end up being fixed in populations and then observed as shared features in species like humans and chimpanzees. This is a well-accepted line of evidence in evolutionary genetics.
However, a few points are worth noting:
Perspective and Tone: The blog is written in a style that is both informative and opinionated. The author engages with alternative hypotheses (such as the “VIGEs-first hypothesis”) and critiques them in a way that can seem dismissive. While this reflects the author's strong views, it means that readers should also consult peer-reviewed sources for a balanced perspective.
Context of Debate: The post is part of a broader debate, as evidenced by the lengthy comment thread. Many of the responses focus on disagreements over the interpretation of the data. It’s useful to remember that while the shared ERV pattern is a powerful indicator of common descent, the scientific community continues to explore and debate the finer details of viral evolution.
Verification with Peer-Reviewed Research: Although the post does cite several sources (and even links to an archived page with more details), it’s always a good idea to cross-check such discussions with current, peer-reviewed research articles or trusted scientific reviews.
Overall, I think the post provides a detailed and generally accurate explanation of how ERVs support the case for common descent. At the same time, its polemical tone and engagement in online debates mean it represents one perspective within a larger scientific discussion. For a well-rounded understanding, it would be beneficial to compare its claims with additional sources from the broader scientific literature."