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motorcyclemaintainance

CJ9-gD

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motorcyclemaintainance

This is a modified HSV-1 virus developed by a scientist at Harvard Medical School.

It's been found to be effective in preventing HSV skin lesions in most mice and guinea pigs tested who were infected with "regular, wild-type" HSV-1. The research was (and hopefully still is) funded by NIH/NIAID.

This is the upgraded version of a previous virus design CJ83193

No information on when / if CJ9-gD is going to be tested on humans.

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curecomingverysoon

Sounds interesting. Again with the replication defective though... the only effective chickenpox vaccine was made from replication competent live strain virus. Bill Halford believes that the replication negative stuff will be flushed out of the system in a matter of weeks, which would mean constant boosters. I believe that the worry is that using live replication competent virus will actually cause someone to catch the virus but come on, what about those of us who already have it?

*end of rant*

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motorcyclemaintainance

The delivery system is certainly a big question with replication defective viruses. Anything more regular than an annual IV booster isn't very practical...

In my opinion, Bill Halford is right, and a replication competent live strain is our best hope for a vaccine. It's intensely frustrating that one was made for chickenpox, but there is none for HSV. In theory, the HSV live vaccine would be a strain of HSV you'd actually *want* to catch, because it would not manifest symptoms, and would defend against the wild strain. You could actually save money on vaccination by partnering up with someone who already had the live vaccine type virus, and then "catch" it from them.

Hilarious possibilities. Imagine how popular you'd be if you were first in successful clinical trials for a live attenuated HSV vaccine.

A while ago this thread discussed a posting on craigslist where an individual was looking to fund a research project. Maybe (s)he should fund Bill Halford.

In the meantime, bring on the helicase-primase inhibitors, or something a bit more post-1970s than the usual.

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curecomingverysoon

Well, I suppose it could be worse than monthly shots (could become sort of like diabetes?).

Correct me if I'm wrong but I don't think that the vaccination would be contagious, particularly when administered therapeutically? That's just not how they work, I don't think. The way the successful vaccine would work is that the virus would lie utterly dormant in your system, not producing anything "new", just fighting what's already there into submission (in the case of therapeutic) or defending against new invaders (in the case of preventive). No outbreaks, no shedding - it would be inert.

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motorcyclemaintainance
Correct me if I'm wrong but I don't think that the vaccination would be contagious

Since it doesn't manifest symptoms, then you may be right to assume it doesn't shed virus either. An actively shedding virus, even if inert, might be a hard sell to the FDA or similar.

It is an interesting concept, anyway, the idea of a cure for a condition that is itself a benign contagious infection. You could do away with vaccines for lots of stuff in the future by engineering contagious cures. Probably 500 years in the future though!

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Herpes Awareness

Let's not get confused here. This piece of research has effectively created a de-activated vaccine to protect against future exposure to a live wild virus. It works like any vaccine, to stimulate the body to produce antibodies against a future attack. The presence of these antibodies will then work against a future skin infection, hopefully preventing the virus from creeping down the nerves and into the spine by disabling it at or near the site of infection.

In the same way, people who have HSV-1, even an oral infection, are somewhat protected against catching HSV-2, as the antibodies for 1 can act against 2, or else mutate very quickly on the first sign of invasion by 2.

Don't confuse this vaccine idea with the GM HSV virus approach of U Fl which drops a 'live' virus which does not cause outbreaks into your system, which then invades your actual nerve cells and produces hammerhead ribozymes to continually neutralise other wild strains of HSV you may have.

This is the low-tech version, which may have some positive results, and works by stimulating the immune system. Although, like Gardasil, probably ineffective if you already have say HSV-1. The high-tech version is the U Fl idea which is also potentially more dangerous to the subject and would need much more testing and development on a range of fronts before human trials could commence. Other solutions like helicase-primase inhibitors represent an interim solution that is more effective than current antivirals and would still be very useful in preventing transmission once a proper screening effort was put in place in the community.

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motorcyclemaintainance

Thanks for clarifying, Herpes Awareness.

Also, something you wrote got me thinking:

people who have HSV-1, even an oral infection, are somewhat protected against catching HSV-2, as the antibodies for 1 can act against 2, or else mutate very quickly on the first sign of invasion by 2.

I also assumed that HSV-1 protects against HSV-2 to some degree. But this study says all it does is reduce / eliminate symtoms. It doesn't reduce the likelyhood of catching it:

"Previous HSV-1 infection did not reduce the rate of HSV-2 infection, but it did increase the likelihood of asymptomatic seroconversion, as compared with symptomatic seroconversion."

And this extensive study found no evidence to support any relationship, suggesting that:

"Hypothetically, previous infection with one type could lead to cross protection against the other. Less likely, but also possible would be a facilitation of infection with one type by the other. Also likely is there being no direct mechanism for one infection influencing the other. HSV-2 is likely to have evolved so that it is not influenced by previous HSV-1 infection."

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