I'm about as fucking sick and tired of HIV as the rest of you guys, believe me. I wish the fucker would just go away so we could stop talking about it and start enjoying sex again, too.
But that's not about to happen any time soon. So I guess my nearly twenty years of discussing HIV isn't about to end any time soon, either.
While it is true that viruses can and do replicate in bacteria, and are often created this way in laboratories as well as in nature, and while it is true that Microbiology 101 addresses this method of replication and infection...
It is ALSO true that HIV does NOT replicate inside any other cell except those which contain the CD4 receptor protein on the surface, to which HIV binds.
So if you want to detail the semantics of the term "piggyback," we can do that -- but I'd just as soon NOT.
What I was inferring from the term "piggyback" was the notion that HIV binds itself to gonnococci or another bacterial STD cell and "hitches a ride" into the new host body via this method. THAT is incorrect -- and that is why I took exception to it.
However, if someone wants to use the term "piggyback" to imply that larger doses of HIV are present and thusly make infection "easier" for the new host -- well... then it's JUST semantics of of little concern. I have no problem relinquishing the debate over a word, as long as the correct information is given.
Now, I'll make this brief (because it's dull) and wrap it up (because I'm sick of it). I'll also put it into simplistic terms because quite frankly, sub-cellular chemical reactions really don't grab the attention of too many readers these days!
We often refer to T-cells as CD4 cells (or the other way around, actually). They are also called "helper cells," and are a component of the human immune system. They are not the ONLY immune cells in the body, of course. But a SYSTEM is called a SYSTEM because all the pieces work TOGETHER to handle any given task. In this case, protect the human body from invaders. So the CD4 cells are very important as a part of the SYSTEM. Without them, the system fails, AIDS develops -- and that is that.
CD4 is the protein sequence that "coats" the T-cell. Now, OTHER immune cells DO have this same protein. Consequently, HIV CAN and DOES infect those cells, too.
However, for our purposes -- we can pretty much just focus on the T-cells.
Very little information about HIV infection goes into much detail about the OTHER cells which contain the CD4 receptor protein. This is because... frankly... it really doesn't matter much.
HIV MOSTLY targets the T-cells, so that's all you really need to know, unless perhaps you are ready to start working on a cure in a lab.
So, for HIV to bind to a cell and infect it, the CD4 protein must be present.
Human immune cells have this protein. As far as I know, no other cells, bacterial or otherwise, have the CD4 receptor protein and therefore cannot bind with HIV.
(If I am wrong about this, by all means -- SHOW ME. I'd love to learn something new, but I seriously can't imagine it. Exhaustive research tells me otherwise, and I'd be happy to admit being wrong about this because if there are CD4 protein receptors elsewhere in nature, this would allow a new route toward a cure or vaccine prevention since it would give us many new ways to study HIV infection without worrying about human test subjects.)
Now, the above parenthetical alludes to the fact that the "H" in HIV stands for HUMAN. No other species can catch HIV.
Cats can get FIV (the "F" is for FELINE). Monkeys can get SIV (the "S" is for SIMIAN). But interspecies transmission of these viruses is NOT possible. And... damn lucky cats... there's a preventative vaccine for them!
So... HUMAN cells can become infected with HIV. OTHER cells from other species CANNOT. Furthermore, the CD4 receptor protein must be present in order for HIV to bind to and infect the cell.
To me, the term "piggyback" just doesn't cut it here, but that's OK.
Now, everything else discussed here is certainly correct: if you have another STD, you are far more likely to catch HIV if you have sex with an infected individual.
Since CD4 cells are abundant in areas of existing infection, if that infection is present in a person who has HIV... not only do you have CD4 cells en masse in the localized area of infection, but you also have HIV-infected CD4 cells en masse in the localized area of infection.
It's easy to see WHY MORE infected cells increases the risk of further infection to another host.
And mode of entry is another factor: open sores, etc. allow for greater chance for a non-infected person to get HIV into their body.
Also, if you have syphilis, for example, and have an open sore, YOU have more CD4 cells near that lesion -- making for an even greater risk.
So... HIV+ folks are more likely to pass it along if they have an STD. HIV neg folks are more likely to GET IT if they have an STD.
It is POSSIBLE that the genetic mutation as mentioned in another thread with regard to those Nairobi prostitutes may have something to do with the CD4 receptor protein. For some reason, HIV cannot bind to this protein in individuals who have the mutation.
Survival of the fittest comes to mind. In a few thousand years, perhaps the human genome will mutate so that EVERYONE has an innate immunity to HIV. Wouldn't that be nice? Too bad we can't hurry that along... at least not yet.
Here's a shitload of links you can browse if you ever have a seriously dull weekend like I just did... Warning: the last one will certainly put you to sleep.
http://www.thebody.com/oralsex.html
http://www.gayhealthchannel.com/hivaids/
http://www.thebody.com/cria/forums/stds.html
http://www.cdc.gov/hiv/pubs/facts/transmission.htm
http://www.cdc.gov/hiv/pubs/facts/oralsexqa.htm
http://www.cdc.gov/mmwr/preview/mmwrhtml/00054174.htm
http://www.bio.davidson.edu/Courses/...20Protein.html
I may have posted one or two of these before -- I don't feel like checking.
Some repeat what we all agree upon and some repeat facts in a very basic way, but that's good for the youngins out there.