posted
I'm curious too. I can't even imagine how one virus could protect its host from the depredations of another virus. How would that work? It could be that the body's immune system bolsters itself to combat virus B, and is incidentally more effective against virus A, but that wouldn't explain why virus A carriers who had virus B and lost it would have a mortality rate so much higher than those who just had virus A to begin with. Hmmm.
I'm going to be very interested to hear more about this as they figure this one out. This could be big.
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posted
Two things, they say they've found it in men, but they haven't said anything about women with HIV/AIDS, and aparently doesn't say anything about any other affects of this second virus. Very interesting indeed. Satyagraha
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posted
I thought they were reasearching it specifically in that male population because it was where they had the most historical documentation.
But it would be interesting to see female numbers as well. This is an area that I highly doubt gender makes a difference. The symptoms of the virus are basically the same in both males and females.
posted
One way could be that Virus A creates/releases proteins that block certain receptors on cell membranes so that Virus B cannot successfully infiltrate the cells.
Was that intentional? My best puns are often unintentional. My subconscious is much funnier than I am.
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Viruses can't infect viruses, it wouldn't work.
Although it could be that they share the same receptor site on the cell surface, so virus B effectively blocks HIV while it's present.
Viruses don't tend to produce proteins other than those necessary for their own reproduction, those being coding for heads and tails and packaging. For it to have picked up the DNA to produce a protein to block the receptors for HIV they would have had to have picked it up from some other human host. Which is, I suppose, possible. But viral genomes are so tiny it wouldn't take long to sequence them. Only the protein that's blocking the receptor site would contain the required code to exit the cell, so it'd be pretty easy to locate it.
Edit: Of course, you wouldn't have to sequence it, you could probably design a pretty efficient probe and find what you were looking for that way.
[ March 04, 2004, 03:10 PM: Message edited by: Bob the Lawyer ]
Posts: 3243 | Registered: Apr 2002
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Yeah, it sounds like they think it's competing with HIV. The article said they were going to do a test-tube experiment to see which one was able to infect the cells better. I guess it might be something like the "good" bacteria that live in our intestines. One advantage, as far as I know, is that the bacteria outcompete the pathogenic bacteria, keeping us all healthy. It might be that this virus is doing the same thing with HIV.
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It's odd, though. For this virus to be doing the same thing it'd have to be in the lysogenic cycle (benign) while in the cell. But that doesn't make sense because then no new virii get made and it wouldn't be blocking the cell sites any more. The head and tail don't really stick around on the outside of the cell after injecting their DNA, and if they were to dissociate/get digested HIV could happily move in. If they were in the lytic cycle they'd be killing the cells just like HIV does, so where's the benefit?
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