this is interesting, so you're saying producing something like a "super STD" much like how antibiotic resistant strains of bacteria, ie superbugs, are bred in hospitals for example. So in this petridish of unprotected sex we create the conditions for the formation super STDs?
I don't think it works that way. Why would unprotected sex lead to super-std's? People getting a cold on a regular basis dont generally lead to super-colds.
You of course may get drug resistence in std's just like other non-sexual infections, but im not sure why the emphasis on unprotected sex.
it's a good question, I always thought STDs were more infectious just because their direct route of transmission into the body with the large mucous bodies that are involved. Thinking about that recent term that's come up in COVID with viral load, it seems like with an STD you're opening the doors to a direct viral/bacterial load punch unlike the diffuse air transmission routes that drop like a mold spore and have to reproduce. I'm curious now when it comes to STDs is there any way to quantify just how much concentration/load shows up in body fluids and how potent the infectiousness would be for those fluids given that concentration.
But now that I think about it, I'm curious which cavities in the body present the widest mucosal surface areas if you cut and open them up and measure them. The pharynx, the throat, the anus and colons, the urethra, the vagina cervix and uterus, how do each of those measure out. I've heard the colon is susceptible to infection because of the large network of lymphatic tissue just on the otherside and because it's designed to absorb stuff being the last mile of the digestive tract where traces of anything left behind at that final stage and still useful can be absorbed by the body. The application of suppositories come to mind in this space.
Another angle might connect with the point brought up by the other individual about bacteria being a frequent origin of STDs, and bacteria generally share genetic material from what I understand. Maybe that bacteria to bacteria mingling is where the risk comes in?
> I'm curious now when it comes to STDs is there any way to quantify just how much concentration/load shows up in body fluids and how potent the infectiousness would be for those fluids given that concentration.
Yes, this data exists and can be measured. Viral Load, detectable load, etc are common terms when discussing HIV.
Not a doctor, but from what I've heard the colon is the mucus membrane that presents the greatest risk for STD transmission.
> Maybe that bacteria to bacteria mingling is where the risk comes in?
I think its "simpler" in that we've seen bacteria become resistant to antibiotics. So bacterial infections could become resistant. I'm not sure its a valid concern since most people will kill the infection before spreading it (which increases rate of mutation), which is easier to do for an STD than something airborne by a hospital patient who can't leave.
> People getting a cold on a regular basis dont generally lead to super-colds.
This is actually a good point applicable to the broader context, that I hadn't really thought about. Billions of people get cold/influenza infections every year. Why don't we see more mutations of strains that are highly virulent/tending to more severe outcomes?
To be fair, influenza is a bit of a different beast than colds, it mutates a lot relative to other diseases. We do get bad strains of influenza from time to time. Most famously in 1918, but we had a flu pandemic as recently as 2009.
Influenza can cross species boundaries and that's what tends to make it generally more dangerous than the natural mutations in seasonal flu. The "swine flu" pandemic of 2009 involved bird and pig influenza viruses mixing genetic materials with human influenza.
Because there is no evolutionary pressure on viruses towards more severe outcomes - if anything, the opposite is true. Higher virulence is occasionally seen though, as was the case with the swine flu some years ago.
> Because there is no evolutionary pressure on viruses towards more severe outcomes - if anything, the opposite is true.
I get this, but it doesn't intuitively follow to me that the incidence of severe strains would be as low as they are. The evolutionary pressure against severe strains shouldn't be enough to stop them from emerging in the short term. And yet, for example, all the severe coronavirus strains seem to be zoonotic, rather than mutations of strains already circulating in humans.
> Higher virulence is occasionally seen though, as was the case with the swine flu some years ago.
I guess higher virulence is also hard to measure. If there's a rhinovirus strain one year that infects twice as many people as normal, who's going to notice that?
I imagine that with normal virus evolution, many people already have at least partial immunity to the new strain as its a minor change, where if it crosses the species barrier that's a bigger "jump" so probably nobody has partial immunity so its more unchecked.
COVID-19 is unique in the sense that it sits in a neat "uncanny valley" of virulence and lethality where it's able to attack our healthcare infrastructure (aided by modern travel), but is sufficiently non-lethal that it can keep spreading. The notable issue with SARS (which was incredibly lethal) was that the incubation time was too short - one or two days before you weren't going anywhere, way too high visibility.
