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    • WilsoInAus
      I am not sure that is the correct interpretation. Your antigen levels are quite high indicating that the lymphocytes did not stop the replication of the antigen. One of your dilutions is also negative. Hence overall this would appear to be a negative result. Note that IgG does not measure activity of the virus, it measures whether there are a specific antibody to the virus in your blood.
    • WilsoInAus
      Great news @Stolo868 hopefully you are now able to put this behind you.  I am not quite sure what the barb is about though, there are no doctors here, self appointed or otherwise, only people trying to help you reach rational decisions on the basis of your experience and testing. If you think you received inappropriate comments from anyone then let us know and they will be addressed. Hey @Just a human being My understanding of how the test works is that antigen cells (the virus) are placed in an growth-rich environment and allowed to replicate. If your blood has the lymphocytes then they will be detected and the growth of the antigen will be restrained. Hence for a positive, you need to see high values of lymphocytes and low values of antigen.
    • Southwestrancher
      https://link.springer.com/article/10.1007/s12325-019-00995-6
    • Stolo868
      Above 2 is positive. Compare to IGG it measures activity of virus. It’s recommended in Europe for seronegative people with ongoing symptoms and those with immune deficiency.  Basically mine is positive for type 1and negative for type 2 which means my t-lymphocytes had contact with hsv1 in the past. 
    • Just a human being
      I do not wish to engage with the difficult politics on this forum regarding rare difficulty in some subsets with diagnosis or debates there in, but could you please explain the LTT test your numbers and your professional opinions in regards to this test, pros and cons of this test and how and why it may be recommended in some cases. I realise the care that needs to be taken as sometimes one will encounter some with irrational fear of HSV. In no way am I suggesting your case as such. 
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Sanguine108

Herpes Cure in 2020

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hk81

@Cas9 I think that those are very old beliefs that I have read occasionally in some articles of 1 decade ago. I also do not trust them too much. They assumed that the reason why the immune system is not reacting to the infection in the neurons is because the activity of these infected cells is too short to be detected. There are immune cells inside of the nervous system; but the activity of the immune system in the nervous system is not well known, so no one knows if the immune system would attack the infected neurons and what would happen in that case (as disrupting certain pathways inside of the nervous system can lead to severe impairments).

I reported that as an example of what is known about latency and detectability of infected cells in a latent stage. These concepts are common to other viruses. I remember to have read similar things about HPV. It creates latently infected cells in the basal epidermal layer; these cells produce a minimal activity and are not attacked by the immune system. They are much more accessible to the immune system than the HSV infected neurons, but still the immune system is not attacking them and it is not recognizing them as an external pathogen; even if it is able to recognize and attack HPV infected cells on the external epidermal layers (which are in a replication stage and more active).

The success of CRISPR lays in the possibility of discovering how the gRNA interacts with the DNA of the copies of HSV in the neurons and how this DNA is accessible for editing. I think that researchers of the above article have tried to gain more understanding of these processes, instead of using a "trial and error" approach (as in the development of vaccines). I'm trying to learn how to read this scientific literature with a critic eye to be able to understand what I can expect from these researches.

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veagle

the latest article i got is december from harvard Med. ended with Dr Knipe said: “We still have a long way to go in ensuring hyperprecision and safety of new gene-editing tools so local editing could offer a safer, more limited first step,” Knipe said. 

https://hms.harvard.edu/news/herpes-achilles-heel

 

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hk81

Local = they will not transport the gRNA in the ganglia, but they will keep it locally in the area of the infection. This is probably the same approach that excisionBio wants to use. I do wonder how effective it can be, since the genital area has a large extension (will the gRNA reach all those cells?)

What is confusing is the fact that the scientific article that I have posted indicates some researches in the direction of editing the latent HSV copies. Can the local copies go into a latent stage? I don't know..

2 extracts from your article:

"Now, using human fibroblast cells infected with herpes simplex virus (HSV), researchers at Harvard Medical School have successfully used CRISPR-Cas9 gene editing to disrupt not only actively replicating virus but also the far-harder to reach dormant pools of the virus, demonstrating a possible strategy for achieving permanent viral control."

"However, Knipe cautions, the arch-challenge of delivering gene-editing therapy to neurons—where the virus hides and enters a state of dormancy—remains to be solved, Knipe added."

The interpretation can be misleading. I read it in this way:

- it is possible to edit the latent virus; it is indeed easier to edit the virus in a replicating stage
- they still have not studied how to bring the gRNA to the neurons; but if they can bring it there, it can edit those copies

My comments:

- if they studied the possibility of editing latent copies, I assume that their long-term target are the neurons. In short-term they can apply the therapy locally, to HSV in replication stage.
- why did they force HSV to go latent into fibroblast cells (by using a non-replicating engineered HSV)? Is it because it's possible to find latent HSV in fibroblasts (and they actually wanted to study this situation)? or because they want to mimic what happens in neurons? I assume that it's nearly impossible to have a cell culture of human neurons, while it is possible to have a cell culture of human fibroblasts.
- is it right to define the virus in the ganglia as "dormant pools of the virus"? wouldn't it reactivate from time to time to generate new viral particles and therefore going in a replicating stage in which the DNA is more exposed?
- Fred Hutch is working on the possibility of reaching the neurons and it seems that they have been successful in that. I do wonder why it is not mentioned in articles and there is no collaboration between research groups.

I always read this kind of scientific journalism with a critic eye; you never know who is writing the article.

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Cas9

@hk81

In my comment, I stated:
" I don't believe the immune system would not attack the neuron."
That was mistake; i.e. I had modified the beginning of the sentence and forgot to modify the end, thus ending up with a double negative. So what I meant to say was:
" I don't believe the immune system would attack the neuron."
Just wanted to make that clear. I updated the comment accordingly.

OK, so I said that the immune system does not attack the actual neuron. The neuron may have some defensive properties against the virus, but that's not the same as the immune cells that float around in different areas of the body to fight infections.  Are you disagreeing with that?

Edited by Cas9

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hk81

@Cas9
I have no idea, but I assume the same.. If that happened, there would be many more disabled people

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Cas9
13 minutes ago, hk81 said:

@Cas9
I have no idea, but I assume the same.. If that happened, there would be many more disabled people

So what did you mean when you said: " I think that those are very old beliefs that I have read occasionally in some articles of 1 decade ago. "  ?

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hk81

It was not the main point of the discussion. Did I write that I believe in such an approach? I only referred to it because I wanted to point out that researchers have always been looking at the condition called latency, trying to demystify it.

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Cas9
6 hours ago, hk81 said:

It was not the main point of the discussion. Did I write that I believe in such an approach? I only referred to it because I wanted to point out that researchers have always been looking at the condition called latency, trying to demystify it.

No, you did not write that you believed in such an approach, nor did I say you did. So I'm not sure what you are talking about.

You asked for input regarding your original comment and I responded (providing an explanation regarding the immune system attacking the neuron) where I thought you got it wrong. You then responded to my explanation (i.e. directly to me) by stating: "those are very old beliefs", which I took as meaning that my explanation was out of date.

Anyway, I think we should leave it as is since there seems to be some confusion.

Edited by Cas9

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hk81

with "those are very old beliefs" I was not referring to your explanation, but to the approach of forcing the copies of HSV out of latency so that the immune system attacks/causes apoptosis of the neuron.

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