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Betsy Herold Delta GD2 Vaccine Being Pursued by X-Vax

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T9000

So did you find out about this back in 2015, or was it only recently?

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StayingUpbeat

I've been keeping an eye on them since I spotted the filing for incorporation with Betsy Herold in the paperwork.  I don't recall exactly when that showed up.

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Cas9
On 2/8/2019 at 6:36 PM, T9000 said:

So did you find out about this back in 2015, or was it only recently?

The delta gd2 vaccine was developed a few years back. At that point they needed funding and animal trials. And now they're being pursued by the biotech noted above. Progress is being made. I've always liked this vaccine and it's good news that it's moving along.

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Cas9
1 hour ago, Crispr1900 said:

Do they have a therapeutic vaccine?

A separate therapeutic vaccine? No. But they will be trying this prophylactic vaccine as a therapeutic also. It will not cure those who have the virus, but may help. If this vaccine is successful at both ends, you wont need to worry about infecting anyone (that's huge)AND you will get some relief from OBs.

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Miss Horne

I really hope this works as a therapeutic vaccine as well :thumbsup:

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Voyager2

What I like about this vaccine is that it was the unexpected result of a counter-intuitive approach. They happened upon something that works! So glad they are moving it forward. If it's only a prophylactic vaccine, that's okay. Either type will be a game changer. The other vaccine to watch is the equally promising trivalent vaccine. 

Edited by Voyager2

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Pokemon
35 minutes ago, Cas9 said:

A separate therapeutic vaccine? No

A layman's question - if an immune response is triggered against the latent virus, does that create a risk of the immune system targeting and destroying neurons??

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Cas9
13 minutes ago, Pokemon said:

A layman's question - if an immune response is triggered against the latent virus, does that create a risk of the immune system targeting and destroying neurons??

A layman's (that's me) response:
No. The latent virus replicates somewhere in the neuron I believe. The emergent viral particles are then attacked by the immune system. The latent virus remains in the neuron. The immune system does not attack that virus in the neuron. It essentially has no access.

Your immune system does not attack and destroy neurons.

Edited by Cas9

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Pokemon
2 minutes ago, Cas9 said:

The immune system does not attack that virus. Your immune system does not attack and destroy neurons.

Understood...but if the vaccine now allows the immune system to target copies of the virus that were otherwise evasive, since these copies reside in the neurons, would the virus in the neurons now be targeted, resulting in destruction of those cells?

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Cas9
2 minutes ago, Pokemon said:

Understood...but if the vaccine now allows the immune system to target copies of the virus that were otherwise evasive, since these copies reside in the neurons, would the virus in the neurons now be targeted, resulting in destruction of those cells?

The immune system has no access to the virus that resides in the neurons; only the virus outside the neurons.

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Pokemon
2 minutes ago, Cas9 said:

The immune system has no access to the virus that resides in the neurons; only the virus outside the neurons.

I see......so one would still need an agent such as that being pursued by Jerome labs to effect a cure.

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Pokemon
1 hour ago, Cas9 said:

The immune system has no access to the virus that resides in the neurons;

Is this relevant:

"In mice infected with herpes, they observed a previously under-recognized role of CD4 T cells, a type of white blood cell that guards against infection by sending signals to activate the immune system. In response to herpes infection, CD4 T cells entered the nerve tissue, secreted signaling proteins, and allowed antibody access to infected sites. Combined, CD4 T cells and antibodies limited viral spread."

https://news.yale.edu/2016/05/18/yale-study-how-antibodies-access-neurons-fight-infection

 

 

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StayingUpbeat
37 minutes ago, Pokemon said:

I see......so one would still need an agent such as that being pursued by Jerome labs to effect a cure.

Unfortunately yes.  The key when considering the "virus" in an infected neuron is that there really isn't such a thing after infection occurs.  Shortly after a viron enters a cell it sheds it outer coat and is simply a strand of DNA floating around in the neuron of the cell.  Periodically that DNA strand gets read by cellular machinery and new viral copies are made.  The original strand of HSV DNA never moves from the neuron once it's there.

Exactly why natural antibodies against HSV aren't as effective as the ones generated against VZV (chickenpox) or the other herpes viruses (EBV, CMV, etc...) is not totally understood.  The prevailing theory however is that most antibodies catch virus when either:

  1. The new viral copy exits the cell into the extracellular space
  2. The infected cell expresses proteins on it's surface from the foreign strand of DNA

In both cases HSV has evolved a series of evasion techniques.  In the case of 1. HSV is able to spread directly from cell-to-cell.  When a new viral copy is created in an infected neuron it travels down the nerve axon directly to a skin cell.  As the skin cells start vigorously replicating HSV and exploding (i.e. an outbreak) the immune system finally becomes engaged and kills infected skin cells faster than new ones can become infected. 

In the case of 2 it's been noticed that very soon after HSV infection cells will express a protein anti-HSV antibodies target but that not long after a section of HSV DNA tells the cell to retract that protein off the cell surface.  Its believed that this window, in which the surface protein anti-HSV antibodies can target is expressed, is why we can't reinfect ourselves in other sites once a we have established anti-HSV antibodies. 

Now there are types of antibodies that can limit cell-to-cell spread and, in theory, cells that know they are infected (even neurons) will commit suicide via process called apoptosis.  But instructions in the HSV DNA sequence also block those. 

The whole thing is a complicated dance evolved over millions of years.  The thing I really like about the Betsy Herold delta-GD2 vaccine is that a postmortem on why exclusively GD2 vaccines failed (i.e. GSK Herpevac) showed that GD2 ends up covering HSV surface protein targets that appear much better suited to effective antibodies (including antibodies that limit cell-to-cell spread).

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Pokemon
4 minutes ago, StayingUpbeat said:

Its believed that this window, in which the surface protein anti-HSV antibodies can target is expressed, is why we can't reinfect ourselves in other sites once a we have established anti-HSV antibodies. 

Thanks for your detailed and informative response. Correct me if I am wrong, but I thought that I read on this site where persons have reinfected themselves on different sites

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MikeHerp
56 minutes ago, Pokemon said:

Is this relevant:

"In mice infected with herpes, they observed a previously under-recognized role of CD4 T cells, a type of white blood cell that guards against infection by sending signals to activate the immune system. In response to herpes infection, CD4 T cells entered the nerve tissue, secreted signaling proteins, and allowed antibody access to infected sites. Combined, CD4 T cells and antibodies limited viral spread."

https://news.yale.edu/2016/05/18/yale-study-how-antibodies-access-neurons-fight-infection

 

 

That's the work being pursued by Doctor Akiko Iwazaki.  It suggests the immune system does have some limited access to neurons and the nervous system.  But it's unclear exactly how it works.  

What @Cas9 said above is the general rule and reflects current understanding, but the recent research is suggesting that it's not cut and dried, black and white.  Akiko has been trying to figure out how that works, and she's been working on the therapeutic side of the trivalent vaccine, using a "prime and pull" approach.

Edited by MikeHerp

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MikeHerp
10 minutes ago, StayingUpbeat said:

The thing I really like about the Betsy Herold delta-GD2 vaccine is that a postmortem on why exclusively GD2 vaccines failed (i.e. GSK Herpevac) showed that GD2 ends up covering HSV surface protein targets that appear much better suited to effective antibodies (including antibodies that limit cell-to-cell spread).

That's the thing.  And that's why I just shake my head and laugh when people claim that there's been no progress in vaccines.  We needed the GD2 "failures" to get to the the delta-GD2 vaccine and the trivalent vaccine.  

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MikeHerp
1 minute ago, Lost-hope said:

@MikeHerp can you explain the “ prime and pull” process if possible 

I should qualify what I said.  I'm not sure whether the prime and pull approach is based on her research about the immune system's access to neurons.

The prime and pull approach is explained here.

https://www.ncbi.nlm.nih.gov/pubmed/23075848

and it's also mentioned here:

https://www.acsh.org/news/2017/10/11/herpes-vaccine-update-interview-penns-dr-harvey-friedman-11940

 

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Cas9
14 minutes ago, Pokemon said:

Thanks for your detailed and informative response. Correct me if I am wrong, but I thought that I read on this site where persons have reinfected themselves on different sites

It does happen, but it's rare. The culprit would be that you are immunocompromised. Not everyone that comes to this forum and believes they were reinfected, is correct. Note that reinfection means that you've developed antibodies, but still infected yourself elsewhere.

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Cas9
24 minutes ago, MikeHerp said:

That's the work being pursued by Doctor Akiko Iwazaki.  It suggests the immune system does have some limited access to neurons and the nervous system.  But it's unclear exactly how it works.  

What @Cas9 said above is the general rule and reflects current understanding, but the recent research is suggesting that it's not cut and dried, black and white.  Akiko has been trying to figure out how that works, and she's been working on the therapeutic side of the trivalent vaccine, using a "prime and pull" approach based on that research.

Yes, I heard about that but left it out of the conversation because it's too preliminary; i.e. we don't know to what extent the antibodies have access to the neuron and whether they can make a difference.

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MikeHerp

yep, I agree.  Currently, it is understood the immune system doesn't really access the nervous system.  Akiko has been studying whether there might be exceptions to that, but it's still unclear.  

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Voyager2

I know this is supposed to be about the Einstein vaccine, but in re-reading the Josh Bloom article about the Trivalent subunit prophylactic vaccine that Mike referenced above, I see they hoped for human testing in 18 months. Since the article was dated October 2017, they could be very, very close to clinical trials. Let's keep our fingers crossed. We need to have BOTH vaccines in the clinic.  

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vzhe
8 hours ago, Voyager2 said:

I know this is supposed to be about the Einstein vaccine, but in re-reading the Josh Bloom article about the Trivalent subunit prophylactic vaccine that Mike referenced above, I see they hoped for human testing in 18 months. Since the article was dated October 2017, they could be very, very close to clinical trials. Let's keep our fingers crossed. We need to have BOTH vaccines in the clinic.  

So to my knowledge there are now three companies seriously pursuing a vaccine, two of which are live attenuated (Rational, Einstein) and one trivalent subunit (Friedman). Realistically we should have either a prophylactic or therapeutic vaccine on the market in 5-10 years.

We have to thank Dr. Halford a lot more than some people here give credit. His offshore trial brought attention to a space that was previously unfundable. I don't think the Einstein vaccine would have ever gotten off the ground without his actions. For sufferers it doesn't matter which of the three vaccines wins, but both funding and FDA approval wise things should be a lot easier now with all the attention he got for the space.

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