Aa
HPV
I had a similar incident where I went to a relatively high end massage place, and I was not expecting sex at all. I was basically really bored and had excess time in a city. Anyways it suddenly evolved into protected sex, and.....
idk **** happens I guess.
I walked down the blocks and immediately bought a bottle Valtrex maybe 10 minutes after and took 500mg followed by 500mg more 12 hours later, and will probably continue for 14 days. I know Herpes tends to infect Epithelial cells first, then Mac's and T-cells and B-cells and various lymph cells before it eventually makes its way to a sensory nerve cell to enter a lysogenic lifecycle, in which case there's no getting rid of it. I have no idea if it enters a lysogenic cycle in the other cells as well or not. Neurons do not have MHC class 1 molecules on their surface so that it is very difficult for the body to fight back against viruses in neurons. This fact would make you wonder why HSV one that infects the Trigeminal Nerve normally doesn't just keep on going back and infect all of the brain and finish you off, but I think it's something to do with the virus's evolution so it doesn't kill people but I don't know details. Anyway..
So the immediate Valtrex (Valaciclovir) consumption was my lame attempt to fix a dumb error, but while on my walk home I started thinking about what I could have picked up and I figured that I'd hate myself later even more if I walked passed the pharmacy and didn't start a regimen of Valtrex just in case it actually did something. Hell if I have the virus, at least I won't get huge lesions this week or the next. Or if I'm lucky the Valtrex will knock it out before it manages to get into the Sacral plexus sensory neurons where it will live. Like I said...idk if it enters a lysogenic phase in every cell type it affects (probably) or if it stays in lytic until it gets to the sensory neurons. whatever.
I was already taking Amoxicillin and Clavulanic acid for some strep a few days earlier so I started taking that too since the other danger is Syphilis and who knows whatever else.
This discussion is related to protected sex with high risk partners - chances of std?.
idk **** happens I guess.
I walked down the blocks and immediately bought a bottle Valtrex maybe 10 minutes after and took 500mg followed by 500mg more 12 hours later, and will probably continue for 14 days. I know Herpes tends to infect Epithelial cells first, then Mac's and T-cells and B-cells and various lymph cells before it eventually makes its way to a sensory nerve cell to enter a lysogenic lifecycle, in which case there's no getting rid of it. I have no idea if it enters a lysogenic cycle in the other cells as well or not. Neurons do not have MHC class 1 molecules on their surface so that it is very difficult for the body to fight back against viruses in neurons. This fact would make you wonder why HSV one that infects the Trigeminal Nerve normally doesn't just keep on going back and infect all of the brain and finish you off, but I think it's something to do with the virus's evolution so it doesn't kill people but I don't know details. Anyway..
So the immediate Valtrex (Valaciclovir) consumption was my lame attempt to fix a dumb error, but while on my walk home I started thinking about what I could have picked up and I figured that I'd hate myself later even more if I walked passed the pharmacy and didn't start a regimen of Valtrex just in case it actually did something. Hell if I have the virus, at least I won't get huge lesions this week or the next. Or if I'm lucky the Valtrex will knock it out before it manages to get into the Sacral plexus sensory neurons where it will live. Like I said...idk if it enters a lysogenic phase in every cell type it affects (probably) or if it stays in lytic until it gets to the sensory neurons. whatever.
I was already taking Amoxicillin and Clavulanic acid for some strep a few days earlier so I started taking that too since the other danger is Syphilis and who knows whatever else.
This discussion is related to protected sex with high risk partners - chances of std?.
That's the dose people take for Herpes prevention (twice daily Valtrex). As for the HIV- I'm not concerned with it obviously since I didn't mention it.
"You are still panicking over a very low risk exposure."
Not really. I just knew that if I took Valtrex immediately after exposure that the virus would be unable to function well with that in my body. It takes about 2 days before the virus makes its way to the Sacral Sensory Ganglion. It gets into epithelial cells first and then on to T-Cells, Mac's, B-cells in the lymph nodes etc and finally at about day two it starts a latent infection where ithides.
The treatment for herpes is purely palliative, and makes no sense to me. I only had about three days worth of meds (one day left) and my doctor told me to discontinue the medicine so that he could get a positive test on me.
I told him that was in my opinion refusing care. I know she had it. I know I have a generic itch although it could by hypochondria heh. I know I was exposed to it.
Why in the world would you want to get a giant lesion and stop treatment. It strikes me as idiotic.
Read this part again....it's pretty damn convincing. Docs use drugs all the time for stuff the FDA didn't approve the drug for,
"Famciclovir and valaciclovir have high oral bioavailability, minimal toxicity and proven efficacy in treating HSV. Available data suggest that treatment with these drugs after documented exposure to HSV reduces the severity of acute disease, limits the number of neurones infected and may reduce the frequency of subsequent recurrences. If started early enough, postexposure prophylaxis may prevent latent infection altogether. "
"You are still panicking over a very low risk exposure."
Not really. I just knew that if I took Valtrex immediately after exposure that the virus would be unable to function well with that in my body. It takes about 2 days before the virus makes its way to the Sacral Sensory Ganglion. It gets into epithelial cells first and then on to T-Cells, Mac's, B-cells in the lymph nodes etc and finally at about day two it starts a latent infection where ithides.
The treatment for herpes is purely palliative, and makes no sense to me. I only had about three days worth of meds (one day left) and my doctor told me to discontinue the medicine so that he could get a positive test on me.
I told him that was in my opinion refusing care. I know she had it. I know I have a generic itch although it could by hypochondria heh. I know I was exposed to it.
Why in the world would you want to get a giant lesion and stop treatment. It strikes me as idiotic.
Read this part again....it's pretty damn convincing. Docs use drugs all the time for stuff the FDA didn't approve the drug for,
"Famciclovir and valaciclovir have high oral bioavailability, minimal toxicity and proven efficacy in treating HSV. Available data suggest that treatment with these drugs after documented exposure to HSV reduces the severity of acute disease, limits the number of neurones infected and may reduce the frequency of subsequent recurrences. If started early enough, postexposure prophylaxis may prevent latent infection altogether. "
actually the study you mentioned was a health care provider who was lancing an active hsv1 lesion and accidently injected herself with active hsv1. She started famvir in high doses very early on. It's just a case report and there isn't anything else out there like it to confirm that it wasn't a fluke or even what doses to use or anything else.
I do understand your theory's as to why you are thinking the way you are however their practical application is not something we have good studies on ( nor will we probably ever have them in humans ) to know if it's even a worthwhile way of thinking for when it comes to herpes. You are still panicking over a very low risk exposure. Even folks with hiv are not contagious 24/7/365. A higher quality massage parlor wouldn't have anyone with hiv working for them anyways.
Also for all the reading you've done - you didn't even manage to figure out what the dose of valtrex should be for a presumed newly acquired infection. I have no idea how you chose 500mg 2x/day for 14 days.
grace
I do understand your theory's as to why you are thinking the way you are however their practical application is not something we have good studies on ( nor will we probably ever have them in humans ) to know if it's even a worthwhile way of thinking for when it comes to herpes. You are still panicking over a very low risk exposure. Even folks with hiv are not contagious 24/7/365. A higher quality massage parlor wouldn't have anyone with hiv working for them anyways.
Also for all the reading you've done - you didn't even manage to figure out what the dose of valtrex should be for a presumed newly acquired infection. I have no idea how you chose 500mg 2x/day for 14 days.
grace
Look at this way...
When you get HSV-1 in the mouth, which isn't a big deal, you develop a full blown T-cell mediated immunity. The problem is the virus goes into lysogenic phase (becomes a lysogen) and integrates into the DNA of sensory ganglia of trigeminal nerve. You'll never get rid of. Furthermore, nerve cells don't have MHC class 1 molecules so even if the cell is corrupted by virus particles, it can't fight back like a normal cell.
However, the T-cell mediated response you've developed prevents you from getting HSV-1 "down there" in the sacral sensory ganglia.
The PEP (post-prevention prophylaxis) could theoretically do the something of the same thing to a new infection. Keep all the circulating viruses low while your body responds and builds a response. There is no way Valtrex is as good as a full blown T-cell response, but it's better than nothing I'd hope.
Well it made sense to me at the time when I was thinking this over.
When you get HSV-1 in the mouth, which isn't a big deal, you develop a full blown T-cell mediated immunity. The problem is the virus goes into lysogenic phase (becomes a lysogen) and integrates into the DNA of sensory ganglia of trigeminal nerve. You'll never get rid of. Furthermore, nerve cells don't have MHC class 1 molecules so even if the cell is corrupted by virus particles, it can't fight back like a normal cell.
However, the T-cell mediated response you've developed prevents you from getting HSV-1 "down there" in the sacral sensory ganglia.
The PEP (post-prevention prophylaxis) could theoretically do the something of the same thing to a new infection. Keep all the circulating viruses low while your body responds and builds a response. There is no way Valtrex is as good as a full blown T-cell response, but it's better than nothing I'd hope.
Well it made sense to me at the time when I was thinking this over.
Well, One you develop a full blown T-cell mediated immunity, the virus will have difficulty spreading from sensory neuron to sensory neuron. All it can do is go into Lytic cycle and go down the neuron to the end and cause a small lesion. As soon as it does, you bodies immune system is all over it and forces it back into lysogenic cycle to go dormant again.
The theory behind that study I posted (i tried to post html link but it removed it) was that the anti-virals limit the # of sensory ganglion the virus can get into hopefully while your body is building up its immune response.
If you could keep the virus shut up to small area, then even when it goes into a lytic cycle at least it would be very tiny. Or if I was lucky stop it all together.
I think you're wrong about the low-risk thing though. If a person has say AIDS, they will be immuno-compressed and would be spreading HSV like crazy almost nonstop.
In retrospect I think I had a high risk of exposure. Anything I can do to limit the damage (which is reasonably likely) is a good thing in my mind.
The study I read also mentioned one case of a person who was needle poked with HSV-4, and took Valtrex, and never developed it at all due to the PEP action.
Who knows...better than nothing...
The theory behind that study I posted (i tried to post html link but it removed it) was that the anti-virals limit the # of sensory ganglion the virus can get into hopefully while your body is building up its immune response.
If you could keep the virus shut up to small area, then even when it goes into a lytic cycle at least it would be very tiny. Or if I was lucky stop it all together.
I think you're wrong about the low-risk thing though. If a person has say AIDS, they will be immuno-compressed and would be spreading HSV like crazy almost nonstop.
In retrospect I think I had a high risk of exposure. Anything I can do to limit the damage (which is reasonably likely) is a good thing in my mind.
The study I read also mentioned one case of a person who was needle poked with HSV-4, and took Valtrex, and never developed it at all due to the PEP action.
Who knows...better than nothing...
It was a one time protected encounter. Your risk of acquiring hsv2 was rather low in the first place. Sounds like you are just panicking for the most part that you had sex with a sex worker?
We have no real studies that confirm that starting antivirals early on makes much of a difference. personally I wouldn't have even bothered taking anything after this protected encounter.
grace
We have no real studies that confirm that starting antivirals early on makes much of a difference. personally I wouldn't have even bothered taking anything after this protected encounter.
grace
Heh the way to avoid it would have been to not be a *******, but a weak attempt at salvaging the situation is better than nothing I guess..
Study on post-exposure postexposure prophylaxis for HSV 1 (obviously I’m worried about 2) Along with 90% of the population or whatever it is, I already have type 1
There are few guidelines available for postexposure prophylaxis for HSV-1, and no controlled clinical trials in humans. The short incubation period and early establishment of latency in HSV infection remain obstacles for effective delivery of postexposure prophylaxis. HSV can establish latent infection of neurones in the absence of peripheral replication.2 In an animal model, postexposure treatment with famciclovir or valaciclovir inhibited peripheral replication of HSV, reducing latent infection but not preventing it altogether.2 In one case report, a patient who started taking famciclovir within one hour of a needlestick injury did not develop whitlow and remained seronegative for HSV.4
Famciclovir and valaciclovir have high oral bioavailability, minimal toxicity and proven efficacy in treating HSV. Available data suggest that treatment with these drugs after documented exposure to HSV reduces the severity of acute disease, limits the number of neurones infected and may reduce the frequency of subsequent recurrences. If started early enough, postexposure prophylaxis may prevent latent infection altogether.
Study on post-exposure postexposure prophylaxis for HSV 1 (obviously I’m worried about 2) Along with 90% of the population or whatever it is, I already have type 1
There are few guidelines available for postexposure prophylaxis for HSV-1, and no controlled clinical trials in humans. The short incubation period and early establishment of latency in HSV infection remain obstacles for effective delivery of postexposure prophylaxis. HSV can establish latent infection of neurones in the absence of peripheral replication.2 In an animal model, postexposure treatment with famciclovir or valaciclovir inhibited peripheral replication of HSV, reducing latent infection but not preventing it altogether.2 In one case report, a patient who started taking famciclovir within one hour of a needlestick injury did not develop whitlow and remained seronegative for HSV.4
Famciclovir and valaciclovir have high oral bioavailability, minimal toxicity and proven efficacy in treating HSV. Available data suggest that treatment with these drugs after documented exposure to HSV reduces the severity of acute disease, limits the number of neurones infected and may reduce the frequency of subsequent recurrences. If started early enough, postexposure prophylaxis may prevent latent infection altogether.
Have an Answer?
You are reading content posted in the STDs / STIs Community
Herpes spreads by oral, vaginal and anal sex.
Herpes sores blister, then burst, scab and heal.
STIs are the most common cause of genital sores.
Millions of people are diagnosed with STDs in the U.S. each year.
STDs can't be transmitted by casual contact, like hugging or touching.
Syphilis is an STD that is transmitted by oral, genital and anal sex.
