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cockswain's avatar

Technical virology questions about ERVs and RNA vs. DNA viral rates of mutation?

Asked by cockswain (15276points) October 14th, 2010

This is stemming from a sidebar from two other threads as to not hijack them. I have two questions. The first is about endogenous retroviruses (ERVs). I understand they are compelling evidence of human evolution as their viral DNA is inserted in multiple places across hominoid ancestors. How does a virus insert itself into genomic DNA?

The second question is somewhat related. RNA viruses mutate/adapt faster than DNA viruses. The extent of my knowledge currently is that the DNA virus undergoes a “proof-reading” mechanism and the RNA is able to circumvent. What is this “proof-reading” mechanism, and what is the general mode of translation for each of these types of viruses?

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6 Answers

Rarebear's avatar

You’re going to make me dig out my old biochemistry texts for this one. Don’t have time now but I’ll do it when I get home from work.

cockswain's avatar

@Rarebear Don’t knock yourself out, I could research this myself to get the answers. I like using Fluther, and can ask follow-up questions to experts.

shilolo's avatar

Most retroviruses express an integrase protein that acts to facilitate viral end joining to host DNA.

As to your second question, it has more to do with the fact that the retroviral reverse transcriptase (which reads RNA and makes DNA) is very error prone.

cockswain's avatar

@shilolo Perfect. As it turned out, a PhD biochemist was happening by my cube and I asked him these questions a couple hours ago. What you are both saying is identical.

Next question(s): How does the cell shut off a DNA virus over time? I’m assuming the viral DNA in our genome is no longer active. I’m also guessing the viral DNA has its own promoter encoded as well. Does the cell evolve an enzyme to halt the promoter (or something)? Also, are you aware of any cases of someone lacking the enzyme to stop the viral DNA expression, and thus they have a problem?

I could be making bad assumptions; correct any flawed thinking please.

shilolo's avatar

Good questions. Not so simple to answer concisely. One major mechanism used by multicellular organisms (such as humans) is the expression of cytokines by immune cells to signal to infected cells to shut of viral replication. The very first such cytokine discovered was a type I interferon. Interferons do a number of things, but in virally infected cells, they signal the cells to express antiviral mechanisms such as downregulating protein synthesis, expression of RNAses and DNAses to degrade nucleic acids, induction of host cell death (kill the vehicle) and expression of MHC molecules so that a more robust immune response can ensue. Virally infected cells are also targets of host natural killer cells and CD8+ cytotoxic T-cells that seek out and destroy infected cells.

With respect to the integrated viruses, many are only quiescent (such as HIV), and can reactivate later after being induced by unknown factors. Much of what we know about viral replication has also been learned from studying viruses of bacteria known as phages.

cockswain's avatar

Fascinating. Amazing how these processes have evolved on this planet. After I peruse the links I may have more questions, but will probably forge on my own for a bit. Thanks for the info.

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