Virii reproduce by hijacking a cell and turning it into a virus factory.
It’s my (possibly mistaken) understanding that this happens because they splice their own genetic information into that of the host cell. (this is exploited to make genetic engineering possible isn’t it?)
So, is it theoretically possible that a virus might infect person A, then, in the process of reproducing in A’s system, pick up a chunk of A’s own genetic material (as excess baggage) and when person B catches the virus from A, they also receive a chunk of A’s genetic material.
If this also happened to infect the germ cells in B, is it then concievable(if extremely unlikely) that person B might beget a child which inherits some trait from A, even though there is no direct relationship?
Yes, this is theoretically possible. The degree of likelihood is disputed … I’ll have to hunt down the reference tonight at home, but it’s either in Dawkin’s The Blind Watchmaker or in Dan Dennet’s Darwin’s Dangerous Idea that there’s mention of a researcher who thought she’d found evidence of this actually having happened to a pair of insect species in recent decades. More details to follow …
Some viruses work by integrating their DNA into the host cell’s DNA, but some don’t. They don’t have to be integrated to reproduce. The integrated forms, called proviruses, are fairly inactive until they remove themselves from the host DNA and start reproducing.
Anyway, it has been shown in bacteria that viruses like that do sometimes carry extra DNA around with them when they travel, and they are used for genetic manipulation. I think over the course of hundreds of millions of years that a lot of gene shuffling has happened in bacteria because of this.
I don’t know any specific examples of this happening in animals, but our genomes have huge numbers of proviruses in them, so I think it’s likely.
When I say the integrated forms are fairly inactive, I mean that they aren’t reproducing fast enough to lyse the cell, but they’re not necessarily completely inactive.
HIV is an example of a virus that is fully active even while integrated into host DNA, and that never excises because it’s a retrovirus.
Proviruses do end up getting established in animals’ genomes, even though I agree with you that viruses don’t often infect germ cells. The human genome has a whole lot of provirus sequences in it.
The key word is ‘extremely unlikely’; it boggles my mind to think of the odds of what you’re talking about–a phenomenom called viral transduction–causing a child to inherit some gene like that.
Transduction is a well-established mechanism that can tranfer genes from one bacteria to another via virii. Say, a gene for antibiotic restistance. The problem with this in eukaryotes (organisms like people) is that our genes may contain stretches of DNA that don’t code for anything; let’s call these DNA stretches introns.
Virii are size-limited in the amount of DNA they can transduce into another genome (and that is a rare occurance itself). You can’t fit a car into your mail box.
I don’t have a viral genetics background, but functional genes in people are a lot larger than bacterial genes; for a virus to transduce an entire functional gene from one person to another in agerm cell strikes me as very unlikely. Maybe I’m wrong; let me know.
And for a virus to target germ cells–I second Smeg.
If any Doper knows of a virus that does this, sure it’s possible, but let us/me know–not my area.
Bobscene–a good read on viral life cycles is Mark Ptashne’s “A Genetic Switch” (1992; 2nd Edition; Cell Press…)
From this I gather that a virus ‘either/or’ decides on lysing the cell. If things are good it integrates and becomes a provirus; if things are bad (no food for the bacterial host) the virus becomes reproductive (rats leaving a sinking ship).
I basically agree with you, but I’m confused when you say the Virii aren’t “reproducing fast enough to lyse the cell”.
I don’t know virii, but Ptashne makes a convincing ‘either/or’ arguement about lysogeny. A virus will either integrate and become a provirus, or be infective and lyze the cell. At least with phage lambda. HIV or other virii may be very different; they have/can have a eukaryotic host.
I guess I should clarify the I have some familarity with bacterial defence mechanisms. Methylation et al; after all, this was how restriction enzymes were discovered.
I realize that bacterial defences against virii is a big topic and I don’t expect a definitive answer here. I’m off to search PubMed for reviews.
I took a lot of courses in or involving virology in college and did some lab work with viruses and never heard anyone say “virii.” It isn’t even in my dictionary.
Anyway, there are viruses that reproduce slowly and don’t necessarily lyse the host cell, like f1 in E. coli. But the point I was trying to make is that if lambda integrates, it isn’t totally inactive. It still has genes that are being expressed, but it isn’t reproducing any faster than the host DNA.
My computer science roommate said “virii” was the correct word and all his programing buddies agreed. None of the biology people I’ve talked to use this word. They say viruses.
As to Virii vs Viruses, I’m not sure of the plural, and I really don’t care. Virii may very well be incorrect, I was under the impression that it was Latin for the plural. But I’ve seen used it before, maybe incorrectly.
Bobscene–“Anyway, there are viruses that reproduce slowly and don’t necessarily lyse the host cell, like f1 in E. coli. But the point I was trying to make is that if lambda integrates, it isn’t totally inactive. It still has genes that are being expressed, but it isn’t reproducing any faster than the host DNA”
I’m not disagreeing with you, in fact, phage lambda does cause the active transcription of its own repressor if the virus is in a state of lysogeny. The active expression of this viral repressor is what maintains the lambda phage as a provirus integrated in the genomic DNA. When cell conditions permit other transcription factors (cro?) to outcompete the repressor, the virus reproduces and lyzes the cell.
Of course this is bacteria, mechanisms for higher organisms are different. Phage lambda is a ‘simple’ model. The amount of active transcrition by a provirus is too complex for a debate here. The OP asked about transduction in people, basically.
Whoops! Found my cite, and it wasn’t a virus that was messing up inter-species DNA, but a parasitical mite. The theory is that a mite had happened to penetrate the germ cells of two consecutive hosts that were two related species of fruit fly, and caused some foreign DNA to be replicated when the germ cell was fertilized. Some scientists think this whole idea is stupid, of course … In any case, all agree that this type of ‘mutation’ is not evolutionarily significant, because (a) it’s too unlikely, and (b) the size of the mutation makes it virtually certain to be maladaptive (as it is in the case under consideration). It’s in the Dennett book, BTW, ‘Darwin’s Dangerous Idea’, pp. 141-142. He cites Houck, et.al., “Possible Horizontal Transfer of Drosophila Genes by the Mite Proctolaelaps Regalis”, Science, vol. 253, pp. 1125-29; 1991. So, there you go-closest related situation I know of.