Evidence for God from Science

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Jbuza wrote:
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B cells produce antibodies, antibodies are like markers which attach to proteins. The receptor end of an antibody can take multiple forms simply because of the ability of transposons. Transposons are not endogeneous retroviruses.

So your contention is that antibodies take on the appropriate shape because they can? That is kind of silly isn't it?

No the immune responce is a little mor intracate than that.
http://www.cehs.siu.edu/fix/medmicro/genimm.htm

Jbuza wrote:My point is that there is information contained within "retroids" that "tell" the antibodies what the appropriate shape is.

What are retriods?
The antigen is what causes B cells to produce antibodies.

Jbuza wrote:There must be a mechanism that lets the antibodies know what the nature of the problem is, and that is information in the genome.

No the antibodies are a result of B cells interacting with antigens.
http://www.biology.arizona.edu/IMMUNOLO ... cture.html

Jbuza wrote: ------------
bgood
The information you posted above shows an interesting relationship between mammal evolution and retrovirus evolution. But you focus on one aspect and disregard the rest. Why?

ARE you asking me why I don't just believe everything I read without judgement?

Don't you want to look at the data before making a judgement?
Don't you want to understand what an endogeneous retrovirus is before making andy declarative statements?

Jbuza wrote:Hey don't sweat it. I think then it boils down to your belief that indogenous retroviruses are hharmful remnants of virul infections in eons gone by, and that my belief that the human with his intact DNA is a marvelous creation.

That is the crux of the issue, isn't it?

So now that we have that settled, I am totally open to learning about HERVs, but I am not going to accept the assumption that they are harmful, or that they are cuasal simply because they are present with a disease.

Studies are done with those who posess a HERV and those who do not. Then the course of the disease if followed and the results published.

Jbuza wrote:How can you demonstrate that the HERVs make the disease worse? Can you show the course of the disease in the abscense of the HERV?

Of course, otherwise it wouldn't be a scientific study, it would be an anecdotal study! There must be a control group who lacks the HERV in order to distinguish what may be agravated by the HERV.

Jbuza wrote:I think that very little is known and that it is exceedingly difficult to demonstrate most of the claims that I have found, including the ones I have made.

The first question one might ask is, how do we identify an endogenous retorvirus.

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Jbuza wrote:

The first question one might ask is, how do we identify an endogenous retorvirus.

I agree that would be best, do you know of these types of studies having been done?

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many endogenous retroviruses play important roles in host biology, such as control of gene transcription, cell fusion during placental development in the course of the germination of an embryo, and resistance to exogenous retroviral infection. Endogenous retroviruses have also received special attention in the research of immunology-related pathologies, such as autoimmune diseases such as multiple sclerosis, although endogenous retroviruses have not yet been proven to play any causal role in this class of disease.

http://en.wikipedia.org/wiki/Retrovirus

This is from wikipediea!
Here the original study.
http://www.retrovirology.com/content/2/1/19
The gene expressed by this retrovirus has been incorporated into primate genomes. As I stated before genes expressed will create proteins whether or not the cell requires it. In this case it would seem this particular protein became integrated into primate placental biology.
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Jbuza wrote:Retroviruses are RNA viruses found in all vertebrates. The retrovirus reproduces by reverse transcribing (copying) its RNA into DNA that is then integrated into the host-cell genome to be transcribed into viruses. Many retroviral sequences have become permanently integrated into the human genome as human endogenous retroviruses, or HERVs. The human genome (indeed all genomes) also contains retrovirus-like retrotransposons, mobile elements that multiply by making RNA copies that are reverse transcribed into DNA and integrated into new sites in the genome. The main difference between a retrovirus and a retrotransposon is that the latter lacks an envelope.

http://www.i-sis.org.uk/ERCD.php

Yes, I am familiar with this.
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Jbuza wrote: I wonder if mammals were unable to reproduce in the view of evolution until they were infected with viruses that gave them the sequences that protect the placenta from the mothers immuns system.

The syncytiotrophoblast allows the embrio access to nutrients.
http://www.med.mun.ca/anatomyts/embryo/emb2.htm
These endogenous retroviral proteins are not found in all mammals.
The experiment above notes how they discovered the genes. The properties of one of the genes is it causes cells to fuse together, in the process of placenta formation. The action of this particular protein is weak.

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Jbuza wrote:Is there any actual evidence to demonstrate that these sections of our DNA is from viral activity, because I have been doing a great deal of reading, and I haven't been able to find a single source that has been able to demonstrate this.

Quit focusing on the implications for a moment. I don't care to argue about evolution any more.

A retrovirus is a type of virus. It contains a siongle strand of RNA. Once it enters a cell it uses a proces called reverse transcription to produce a adouble stranded DNA, which then is inserted into the host cells genetic code. From there the host cells own machinery produces the proteins to create new virus particles.
http://www.whfreeman.com/kuby/content/anm/kb03an01.htm

Now how do we identify it? Well all retroviruses have a comonality.
http://users.rcn.com/jkimball.ma.ultran ... ruses.html
They all possess genes for producing the envelopes which contain the RNA strand. These proteins are named env, gag, and pol.

As stated before the function of a protein is based on its shape, which is a result of the genetic code. A eukaryotic cell does not need reverse transcriptase, which is exactly what pol encodes.

Many of the HERV's are inactive. How do we know? Because the mechanism by which the eukaryotic cells read the genetic code requires a specific sequence to begin. This is known as a start codon. There are also stop codons. The transcription begins and ends where ever the codon is found.
http://users.rcn.com/jkimball.ma.ultran ... odons.html

HERV's are identified by finding sections of code which encode for the gag, env and pol proteins.
In most cases these proteins have been deactivated by a change in the sequence(mutation) A single frameshift will turn off the start codon.

For instance AUG AUA AAG CCU GAG UAA is an example of functioning code.
AUG is the codon to begin transcription.
UAA is the codon which signals an end.

A frameshift leads to UGA UAA AGC CUG AGU
The sequence is still identifyable but the gene has been inactivated.

A frameshift can occur from an insertion or a deletion.
There are of course other ways the viral genes have been deactivated.

What is the basis for identifying these strings of code as retroviral in origin?
http://mbe.oxfordjournals.org/cgi/conte ... t/msi088v1
As stated above retroviruses do this. This is how a cold and HIV works. This is how H5N1 Influenza works. The virus inserts it's own genetic code into an organism.

So to find HERV's we look for the same sequence found in retroviruses in the human genome.
http://www.retrovirology.com/content/1/1/32

Jbuza wrote:Perhaps it is just the result of the presupposition of evolution actually having occoured. All the Junk DNA and remnants of the past shrink year by year as more and more functioning is found.

I'm not here to espouse one idea or another, if you think there is a grand conspiracy, I no longer feel that I can change your mind. The functioning found in the junk DNA is something refered to as selfish genes, it is not the functioning anyone had imagined, but I will not get into that.

Jbuza wrote:CAn you demonstrate this is so, or do you just buy into the party line. If the only evidence is that evolution took place so it must be so, than you have nothing, and only the amorphous mass of circular reasonings that evolution has become.

I am not trying to prove evolution, I just don't want you to dismiss a whole area of study just because you feel it threatens your beleifs. There is no party line.

Genetic sequence of HERV-K pol gene
http://www.ncbi.nlm.nih.gov/entrez/view ... val=300006

Another HERV-K pol protein including chemical properties. This one shows amino acid sequence not genetic sequence.
(Every three letters in the genetic code correspond to one amino acid)
http://harvester.embl.de/harvester/Q9WJ/Q9WJR5.htm

Genetic sequence of HERV-FRD
http://www.ncbi.nlm.nih.gov/entrez/view ... l=46485772

HIV pol gene showing long terminating A's and T's
http://www.ncbi.nlm.nih.gov/entrez/view ... l=12004606

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Jbuza wrote:Great post Bgood, I will have to reread it and check your sources, because I find the area interesting. I do want to make a couple of quick comments though.

I don't feel there is a conspiracy per se, but it isn't suprising to see it interpreted from an evolutionary standpoint, thaat was my point. Mainstream science presupposes evolution to be LAW.

It was not originally interpreted from an evolutionary standpoint.
When ERV's were first discovered it was thought to have occurred from active viral infections during life. Then it was found to be inherited.

ERV's in humans were then also found in other primates. In analogous locations with nearly identical sequences.

Jbuza wrote:Secondly my beliefs aside I have seen no evidence that would place evolution above a defunct hypothesis.

I will try and get back to your post and absorb some of the information.

Again thanks for the information.

Jon

Whatever you want to beleive, the facts are there. You can interpret them any way you want.

=)