Endogenous retroviruses confirm common descent

[BarryDesborough]

Retroviruses such as HIV get replicated by invading the cells of host organisms and hijacking their replication chemistry. They attach to host cells by means of a surface protein, called the envelope or env protein.

Retroviruses store their genomes in RNA, but when they invade a host cell, they transcribe their RNA into DNA, using the cell's resources, under control of their own enzyme, which is called reverse transcriptase. "Reverse", because normally, DNA is transcribed into RNA within a normal cell.

The DNA version of the retroviral genome is then inserted (integrated, in the jargon) into the host DNA. The integrated DNA is called a provirus.

The host cell then dutifully "reads" this provirus resulting in the production of new retroviruses which escape the cell to go on and infect other cells.

Retroviruses do not infect every cell in an organism, and they do not integrate into the host cell in any regular position.

In the genomes of creatures such as ourselves, we find thousands of proviral-like structures, containing (usually broken) versions of the genes for the retroviral enzymes described above, each one in an identical position, comparing cell to cell, and existing in every single cell. This is unlike direct infection. The only reasonable explanation is that these structures are inherent in the genome - IOW they are endogenous. We call them endogenous retroviruses, or ERVs. They can only have entered the genome via the route of infecting ancestral germ-line cells.

The fact that you and I share thousands of ERVs is due to the fact that we share thousands of ancestors.

The fact that you and I and all humans and all chimps and gorillas share thousands of ERVs is due to the fact that we all share thousands of ancestors.

Yes, parts of certain ERVs have a function, even a vital one in some species, but there is no reason why they should be accompanied by all the other paraphernalia of a provirus, other than the fact that they are descended from proviruses. Yes, we have found one ERV which is fixed (ubiquitous) in chimps and gorillas, but not in humans. But remember, each ERV starts out as a single infected germ-line cell. There is no guarantee that it will spread throughout a population. It is no problem for the inheritance account of ERVs, whereas the thousands of ERVs that are shared between chimps, gorillas and human beings cannot be explained in any other way.

Before anyone objects to any of the above, read this article first.

ERVs - Evidence for the Evolutionary Model

If it does not deal with your question, you may then post it here.

 

[Two Thumbs]

What does this have to do with religion or ethics?

 

[BarryDesborough]

What does this have to do with religion or ethics?

People believe (quite wrongly) that evolution opposes religion and that it negates ethics. I know it is infantile, but people will deny the truth of evolution because, they imagine, it has undesirable consequences, rather than because they have an informed opinion that it is false.

This line of evidence cuts through all that garbage and makes it crystal clear that common descent is true. Once that is agreed upon, we can then discuss evolution's implications for religion and ethics.

If you don't want to study and discuss the topic, you do not have to. But please, at least stop posting obscenities in my threads and in reputation comments.

 

[Two Thumbs]

oh wait

You're that anti-free speech guy from yesterday.

Hows the hate working out for you?

 

[BarryDesborough]

Retroviruses such as HIV get replicated by invading the cells of host organisms and hijacking their replication chemistry. They attach to host cells by means of a surface protein, called the envelope or env protein.

Retroviruses store their genomes in RNA, but when they invade a host cell, they transcribe their RNA into DNA, using the cell's resources, under control of their own enzyme, which is called reverse transcriptase. "Reverse", because normally, DNA is transcribed into RNA within a normal cell.

The DNA version of the retroviral genome is then inserted (integrated, in the jargon) into the host DNA. The integrated DNA is called a provirus.

The host cell then dutifully "reads" this provirus resulting in the production of new retroviruses which escape the cell to go on and infect other cells.

Retroviruses do not infect every cell in an organism, and they do not integrate into the host cell in any regular position.

In the genomes of creatures such as ourselves, we find thousands of proviral-like structures, containing (usually broken) versions of the genes for the retroviral enzymes described above, each one in an identical position, comparing cell to cell, and existing in every single cell. This is unlike direct infection. The only reasonable explanation is that these structures are inherent in the genome - IOW they are endogenous. We call them endogenous retroviruses, or ERVs. They can only have entered the genome via the route of infecting ancestral germ-line cells.

The fact that you and I share thousands of ERVs is due to the fact that we share thousands of ancestors.

The fact that you and I and all humans and all chimps and gorillas share thousands of ERVs is due to the fact that we all share thousands of ancestors.

Yes, parts of certain ERVs have a function, even a vital one in some species, but there is no reason why they should be accompanied by all the other paraphernalia of a provirus, other than the fact that they are descended from proviruses. Yes, we have found one ERV which is fixed (ubiquitous) in chimps and gorillas, but not in humans. But remember, each ERV starts out as a single infected germ-line cell. There is no guarantee that it will spread throughout a population. It is no problem for the inheritance account of ERVs, whereas the thousands of ERVs that are shared between chimps, gorillas and human beings cannot be explained in any other way.

Before anyone objects to any of the above, read this article first.

ERVs - Evidence for the Evolutionary Model

If it does not deal with your question, you may then post it here.

Bump.

 

[Youwerecreated]

Retroviruses such as HIV get replicated by invading the cells of host organisms and hijacking their replication chemistry. They attach to host cells by means of a surface protein, called the envelope or env protein.

Retroviruses store their genomes in RNA, but when they invade a host cell, they transcribe their RNA into DNA, using the cell's resources, under control of their own enzyme, which is called reverse transcriptase. "Reverse", because normally, DNA is transcribed into RNA within a normal cell.

The DNA version of the retroviral genome is then inserted (integrated, in the jargon) into the host DNA. The integrated DNA is called a provirus.

The host cell then dutifully "reads" this provirus resulting in the production of new retroviruses which escape the cell to go on and infect other cells.

Retroviruses do not infect every cell in an organism, and they do not integrate into the host cell in any regular position.

In the genomes of creatures such as ourselves, we find thousands of proviral-like structures, containing (usually broken) versions of the genes for the retroviral enzymes described above, each one in an identical position, comparing cell to cell, and existing in every single cell. This is unlike direct infection. The only reasonable explanation is that these structures are inherent in the genome - IOW they are endogenous. We call them endogenous retroviruses, or ERVs. They can only have entered the genome via the route of infecting ancestral germ-line cells.

The fact that you and I share thousands of ERVs is due to the fact that we share thousands of ancestors.

The fact that you and I and all humans and all chimps and gorillas share thousands of ERVs is due to the fact that we all share thousands of ancestors.

Yes, parts of certain ERVs have a function, even a vital one in some species, but there is no reason why they should be accompanied by all the other paraphernalia of a provirus, other than the fact that they are descended from proviruses. Yes, we have found one ERV which is fixed (ubiquitous) in chimps and gorillas, but not in humans. But remember, each ERV starts out as a single infected germ-line cell. There is no guarantee that it will spread throughout a population. It is no problem for the inheritance account of ERVs, whereas the thousands of ERVs that are shared between chimps, gorillas and human beings cannot be explained in any other way.

Before anyone objects to any of the above, read this article first.

ERVs - Evidence for the Evolutionary Model

If it does not deal with your question, you may then post it here.

Response to your article.

Revisiting an Old Chestnut: Retroviruses and Common Descent (Updated) - Evolution News & Views

 

[BarryDesborough]

Retroviruses such as HIV get replicated by invading the cells of host organisms and hijacking their replication chemistry. They attach to host cells by means of a surface protein, called the envelope or env protein.

Retroviruses store their genomes in RNA, but when they invade a host cell, they transcribe their RNA into DNA, using the cell's resources, under control of their own enzyme, which is called reverse transcriptase. "Reverse", because normally, DNA is transcribed into RNA within a normal cell.

The DNA version of the retroviral genome is then inserted (integrated, in the jargon) into the host DNA. The integrated DNA is called a provirus.

The host cell then dutifully "reads" this provirus resulting in the production of new retroviruses which escape the cell to go on and infect other cells.

Retroviruses do not infect every cell in an organism, and they do not integrate into the host cell in any regular position.

In the genomes of creatures such as ourselves, we find thousands of proviral-like structures, containing (usually broken) versions of the genes for the retroviral enzymes described above, each one in an identical position, comparing cell to cell, and existing in every single cell. This is unlike direct infection. The only reasonable explanation is that these structures are inherent in the genome - IOW they are endogenous. We call them endogenous retroviruses, or ERVs. They can only have entered the genome via the route of infecting ancestral germ-line cells.

The fact that you and I share thousands of ERVs is due to the fact that we share thousands of ancestors.

The fact that you and I and all humans and all chimps and gorillas share thousands of ERVs is due to the fact that we all share thousands of ancestors.

Yes, parts of certain ERVs have a function, even a vital one in some species, but there is no reason why they should be accompanied by all the other paraphernalia of a provirus, other than the fact that they are descended from proviruses. Yes, we have found one ERV which is fixed (ubiquitous) in chimps and gorillas, but not in humans. But remember, each ERV starts out as a single infected germ-line cell. There is no guarantee that it will spread throughout a population. It is no problem for the inheritance account of ERVs, whereas the thousands of ERVs that are shared between chimps, gorillas and human beings cannot be explained in any other way.

Before anyone objects to any of the above, read this article first.

ERVs - Evidence for the Evolutionary Model

If it does not deal with your question, you may then post it here.

Response to your article.

Revisiting an Old Chestnut: Retroviruses and Common Descent (Updated) - Evolution News & Views

Jonathan M, a contributor to such sites as evolutionnews.org and uncommondescent.com, has recently responded to my formulation of the ERV argument for common ancestry. He announced in this blog post on the Discovery Institute's “Evolution News & Views” site that he intended on addressing each one of the three “layers of ERV evidence,” over the course of additional blog posts. His first post regards layer 1, and his second post regards layers 2 & 3. Here, I have responded to each of his two subsequent posts.

Evolution News - Evidence for the Evolutionary Model

 

[BarryDesborough]

Retroviruses such as HIV get replicated by invading the cells of host organisms and hijacking their replication chemistry. They attach to host cells by means of a surface protein, called the envelope or env protein.

Retroviruses store their genomes in RNA, but when they invade a host cell, they transcribe their RNA into DNA, using the cell's resources, under control of their own enzyme, which is called reverse transcriptase. "Reverse", because normally, DNA is transcribed into RNA within a normal cell.

The DNA version of the retroviral genome is then inserted (integrated, in the jargon) into the host DNA. The integrated DNA is called a provirus.

The host cell then dutifully "reads" this provirus resulting in the production of new retroviruses which escape the cell to go on and infect other cells.

Retroviruses do not infect every cell in an organism, and they do not integrate into the host cell in any regular position.

In the genomes of creatures such as ourselves, we find thousands of proviral-like structures, containing (usually broken) versions of the genes for the retroviral enzymes described above, each one in an identical position, comparing cell to cell, and existing in every single cell. This is unlike direct infection. The only reasonable explanation is that these structures are inherent in the genome - IOW they are endogenous. We call them endogenous retroviruses, or ERVs. They can only have entered the genome via the route of infecting ancestral germ-line cells.

The fact that you and I share thousands of ERVs is due to the fact that we share thousands of ancestors.

The fact that you and I and all humans and all chimps and gorillas share thousands of ERVs is due to the fact that we all share thousands of ancestors.

Yes, parts of certain ERVs have a function, even a vital one in some species, but there is no reason why they should be accompanied by all the other paraphernalia of a provirus, other than the fact that they are descended from proviruses. Yes, we have found one ERV which is fixed (ubiquitous) in chimps and gorillas, but not in humans. But remember, each ERV starts out as a single infected germ-line cell. There is no guarantee that it will spread throughout a population. It is no problem for the inheritance account of ERVs, whereas the thousands of ERVs that are shared between chimps, gorillas and human beings cannot be explained in any other way.

Before anyone objects to any of the above, read this article first.

ERVs - Evidence for the Evolutionary Model

If it does not deal with your question, you may then post it here.

And rebump.

 

[BarryDesborough]

http://www.the-scientist.com//?articles.view/articleNo/36481/title/Gene-Therapy-Coming-of-Age-/

Ex vivo gene therapy could potentially be used to treat a range of diseases, but until recently clinical application of the approach has been held back by problems with gene-transfer efficiency and safety. One major concern with gene therapy has been its propensity to cause cancer. The reason is that viruses integrate their genetic material almost at random in the host genome, so promoter sequences introduced alongside therapeutic genes can sometimes activate a nearby cancer-causing gene.

To overcome these obstacles, researchers have instead turned to vectors based on lentiviruses, which they have modified not only to improve the efficiency of gene transfer, but also to avoid the activation of cancer-causing genes by loading the vector with self-inactivating promoter sequences that exclusively induce the expression of the therapeutic gene.

In 2009, Aubourg and colleagues published results from a pioneering trial in which they used lentiviral-based gene therapy on HSCs for the first time to treat X-linked adrenoleukodystrophy (ALD), a neurodegenerative disease that affects young males. Roughly 2 years after the treatment, many of the patients’ immune cells carried the corrected the gene, and disease progression had stopped entirely. What’s more, the researchers observed a diverse range of gene integration locations in the cells—a sign that cancer-causing genes had not been activated. If they had, the cancerous cells would have out-proliferated the others, meaning the insertion location that switched on the oncogene would show up in a majority of the modified cells.

“That was a significant advance over prior methods because it showed more efficient and safer gene transfer,” said Naldini. But more demonstrations were needed to move ex vivo gene therapy from the lab to the clinic, he added.

In the latest studies, Naldini and colleagues show that further improvements to lentiviral-vector design increase the number of genetically modified cells. In the first trial, a team led by TIGET’s Allesandra Biffi treated three children with a rare lyosomal storage disorder called metachromatic leukodystrophy (MLD)—a neurodegenerative disease caused by mutations in the gene that produces the enzyme arylsulfatase A (ARSA). There is currently no successful treatment for MLD and patients usually die within a few years.

The researchers transferred a functional ARSA gene into HSCs taken from nine pre-symptomatic MLD patients. Analyses performed 2 years after treatment with the modified HSCs in one patient, and after 18 months in another two patients, revealed that 45–80 percent of the blood cells carried the functional gene. The enzyme was present at normal, healthy levels in these cells and in the cerebro-spinal fluid, where it was completely lacking before. What’s more, long after the symptoms would usually have manifested, the progression of the disease had been stopped in its tracks. “At this stage the patient normally have brain damage or are dead,” said Naldini, “but instead they are alive and thriving.”

In a separate study, a group led by TIGET’s Allesandro Aiuti used the same approach to treat three children with Wiskott-Aldrich Syndrome (WAS), a rare immunodeficiency disorder caused by mutations in the gene encoding a protein called WASP. Analyses carried out 20–32 months after the treatment showed that 20–25 percent of targeted blood cells were genetically corrected; the immune system had largely been restored in all three patients; and symptoms, such as recurring infections of eczema, were reduced or had disappeared altogether.

Crucially, in both studies, molecular analyses of the gene integration patterns in HSC progeny showed no evidence that the vector was activating oncogenes. “These lentiviral vectors don’t appear to have the same problem we saw with retroviral vectors; this is good evidence that they are safer,” said Naldini, though he emphasized that further follow-ups and larger-scale trials are needed.

Paper - Lentiviral Hematopoietic Stem Cell Gene Therapy Benefits Metachromatic Leukodystrophy