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Sweet7

Reduction of Viral Lood ???

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Sweet7

I had the theory that T cells could clear the virus from our neurons based on this study: http://jvi.asm.org/cgi/content/full/82/19/9678

However, I now think that this study only proves that T cells gather in the spinal cord and sensory ganglia to zap the virus as it tries to leave the neurons. After reading about the HerpV vaccine, I also now realize that T cells also gather at nerve endings. I am assuming that occurs in case some viral particles make it past the T cells in the spine and sensory ganglia. The HerpV vaccine would be a great candidate because it will train the T cells to be better able to detect the proteins secreted by the virus as Accelerate the Response pointed out in another link. With that said, my theory of T cells clearing the virus from our neurons could be wrong.

So, what causes a reduction of viral load? This virus not only has a protein coat, but is even enveloped. I see that as like double protection from our immune system. Much like wearing two latex gloves for extra protection. Our bodies make antibodies that are so specific that blood test can distinguish between the two strains. I have to admit that is fascinating in itself that the human population makes the same antibodies for each pathogen the same way.

Anyhow, I am now wondering if the reduction of viral load has something to do with antibodies. For quite some time I had thought that HSV antibodies were useless because of what I read in this study:

http://www.guardian.co.uk/science/2010/nov/01/viruses-immune-system-antibody

This study reveals that for viruses that shed their protein coats, the Trim21 gene does not get tripped so to speak. So, the virus is able to replicate in the cell it has attacked without the natural immune response inside the cell taking place. If I’m not mistaken, HSV works this way. If HSV only inserts it’s dna into cells (including neurons), our antibodies are not going to go into the cell with it. This may explain how the virus can just sit in our neurons without being noticed by our immune system.

Now, with that said, would if AIC-316 or CMX001 is mistaken for an antibody? These drugs stop replication at different points in the process of replication. They are completely different in the chemical makeup of current antivirals and CMX001 is able to be taken up by most if not all cells. Acurius claim AIC-316 reduces the viral load and animal studies conclude that CMX001 reduces viral load. When these antivirals enter the cells, it could be flipping the Trim21 Gene on. They could very well be mimicking our antibody by helping the Trim21 Gene target the HSV dna. The protein secreted from the Trim21 Gene can then dismantle the virus and dispose of it.

I have emailed the researchers in the Trim21 link with no response. Is there someone in the UK that can send them this theory in an email and follow up with a phone call?

If anyone knows what actually causes a reduction in viral load while taking antivirals, please explain it or send me a link. I would greatly appreciate it. Thanks.

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BucFan1

I'd be curious to hear Struggles take on this...very interesting read Sweet7...thanks.

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Sweet7

I know, I hope he doesn't get mad at me. I had him going on the T cells but he actually made me think a little deeper about it.

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struggle83

LOL. I can never get mad at Sweet! And I hope I don't come across as angry. That said...

I just don't know how the researchers are determining viral load. This virus sits as re-programmed DNA inside an otherwise healthy cell. How can this be detected? But then I am not a virologist. But I did order a med-school text on virology so give me a few weeks!

The reduction in viral load is another problem. The virus is able to turn off cellular apoptosis, similar to cancer cells. So an inhibiting antiviral can't kill the cell, say, over the course of many years of inhibition. Something would have to either assasinate the infected cell or would have to turn apoptosis back on. I don't know any antivirals or human processes that can detect then kill the cells. But then I am not an immunologist. But I might order a book on human immunology after I finish the book on virology.

You know the old saying...I know enough to be dangerous!

Sorry for the additional questions. I wish I had the answers.

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camomile

Someone posted this link, not sure who had posted this anymore.

http://discovermagazine.com/2009/sep/02-second-coming-of-gene-therapy/article_view?b_start:int=2&-C

"At the Center for Cell and Gene Therapy at Baylor College of Medicine in Houston, director Malcolm Brenner, a geneticist, says he has turned “AdV from poacher into gamekeeper.” He is using the virus to cure a rare form of blood cancer called EBV lymphoma, caused when B lymphocyte immune cells get infected with the Epstein-Barr virus (EBV). Best known as the cause of mononucleosis, EBV is so widespread that most of us have been exposed and still carry small quantities of the virus in our B cells—generally in a form so benign it fails to stimulate the T cells, immune cells crucial to pathogen search-and-destroy. In EBV lymphoma patients, however, things take a sinister turn. The virus causes B cells to proliferate and expand, and they do so unimpeded because the immune system fails to recognize or destroy the weak but dangerous virus that is driving the disease."

This sounds so similar to the way HSVs operate.

According to National Cancer Institute, human B Cell lymphotropic virus (HBLV) is "believed to be a member of herpes family". A publication I was reading has said (hopefully falsely) that ppl with HSV have increased risk of cervical cancer. I thought cervical cancer is associated with HPV.

Going back to OT, "If anyone knows what actually causes a reduction in viral load while taking antivirals, please explain it or send me a link. I would greatly appreciate it. Thanks."

I only wonder, are you referring to Valtrex or Acyclovir?

xx

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Sweet7

Cammomile, I was speaking of AIC-316 and CMX001. I also think that maybe the antiviral is not technically mimicking an antibody, but maybe the Trim21 gene sees it as an invader and attacks it. Since it is clinging to viral dna, the protein expressed from the Trim21 gene dismantles it along with the antiviral. I had read the article you posted before and thought that the Trim21 gene had something to do with why replacing the faulty gene with an AAV virus failed for hematologist Kathy High to cure hemophilia. It worked for a few weeks, enough time for the body to create antibodies that tripped the Trim21 gene. I will be surprised if study to cure Cystic Fibrosis works for the same reason. One really good thing about the studies you pointed out in that article is the training of T cells to go after weak EBV cells in 8 out of 12 patients. That shows just how promising therapeutic vaccines such as HerpV should be since that’s pretty much the same process. Yet, people may wonder why I’m so concerned with reducing the viral load. It is because of some study I have read about the Thymus organ. Our T cells are born in our bone marrow, but matured by the Thymus. The thing is, the Thymus shrinks over time and is the major cause of decline in our golden years. By age 70, it is difficult to distinguish the Thymus from fat. It still works, but not like it used to. My concern is even if we do have a therapeutic vaccine but it does not clear the virus from our bodies, what kind of trouble are we going to have after 70? I would say that would be one big reason to welcome such a vaccine asap. However, if Acurius has stated that AIC-316 can reduce the viral load, and animal studies prove that CMX001 reduces the viral load, then one would think the virus would clear the body after a period of time on either antiviral. Both antivirals stop replication, but they don’t kill the virus. Something has to clear the viral template from cells to reduce viral load. I want to know for sure what that is.

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Sweet7

AIC-316 formerly known as Bay 57-1293 states that replication does not take place in neuronal tissue unlike Valtrex:

http://aac.asm.org/cgi/content/full/46/6/1766

Our data show that HSV infection is very susceptible to treatment with BAY 57-1293. Early treatment of primary herpetic disease with current antivirals in humans does not appear to reduce the level of latent DNA and thereby influence the frequency and severity of subsequent recurrent infections. In this regard, it is especially interesting that in contrast to treatment with valacyclovir, no detectable HSV replication took place in the neuronal tissue of BAY 57-1293-treated animals (Fig. 2). Pharmacokinetic measurements confirmed that the thiazolylsulfonamides are able to pass the blood-brain barrier. BAY 57-1293 is efficacious even when treatment is initiated after the onset of symptoms in the murine zosteriform spread model of cutaneous infection (Fig. 6). This is of utmost importance for episodic treatment in recurrent herpetic disease when the patient initiates treatment only after first symptoms are apparent. The ability of BAY 57-1293 to be efficacious when treatment is delayed or the viral load is increased is also essential for successful treatment of life-threatening herpes infections like herpes encephalitis and disseminated herpes. In that regard, combination therapy with current nucleosidic DNA polymerase inhibitors and the nonnucleosidic primase-helicase inhibitor BAY 57-1293 is also an option.

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camomile
I will be surprised if study to cure Cystic Fibrosis works for the same reason

You know that there is already a cure for CF (I saw once on tv) but it is only happening in the research level at medical establishment either Kings College or Imperial College (London)? To be honest, I don't remember precisely which. Clinicians already knew the treatment works and a couple of ppl who appeared on tv received this treatment.

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camomile

The ability of BAY 57-1293 to be efficacious when treatment is delayed or the viral load is increased is also essential for successful treatment of life-threatening herpes infections like herpes encephalitis and disseminated herpes. In that regard, combination therapy with current nucleosidic DNA polymerase inhibitors and the nonnucleosidic primase-helicase inhibitor BAY 57-1293 is also an option.

Thank you for the clarification xx

I seem to have seen someone (I think, it was you xx) posted an article written by a researcher either at Kings or Cambridge. It was a British research team anyway. Unfortunately, I haven't got the link anymore.

Are you fairly new to this H infection? I have been living with H over two decades+ so it was interesting to find out what you meant by reducing the "viral load"?

what do pharma researchers mean by "viral load"? The extent or amount of infected cells involved with H?

xx

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struggle83
Thank you for the clarification xx

I seem to have seen someone (I think, it was you xx) posted an article written by a researcher either at Kings or Cambridge. It was a British research team anyway. Unfortunately, I haven't got the link anymore.

Are you fairly new to this H infection? I have been living with H over two decades+ so it was interesting to find out what you meant by reducing the "viral load"?

what do pharma researchers mean by "viral load"? The extent or amount of infected cells involved with H?

xx

The term viral load is typically used for HIV patients, although it applies to any virus. It's a measure of the amount of virus in the body and therefore a measurement of the effectiveness of any given treatment (AZT etc.). I believe this is based off of blood tests. Since HSV doesn't get into bloodstream (so they say) there is no good way to measure viral load. In animal models they measure the infected cells after sacrifice. For a living human being this is much more difficult. I think there are researchers trying to develop novel ways of measuring viral load in living people. Maybe someone can verify that if they know.

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camomile
The term viral load is typically used for HIV patients, although it applies to any virus. It's a measure of the amount of virus in the body and therefore a measurement of the effectiveness of any given treatment (AZT etc.). I believe this is based off of blood tests. Since HSV doesn't get into bloodstream (so they say) there is no good way to measure viral load. In animal models they measure the infected cells after sacrifice. For a living human being this is much more difficult. I think there are researchers trying to develop novel ways of measuring viral load in living people. Maybe someone can verify that if they know.

Thank you so much for that easy-to-understand explanation. :D It was soooooo much appreciated, Struggle. :p

An excellent point you made about HSV. In UK, recently there's a ban for any blood donation by patients with Chronic Fatigue. I think, this is directly in response to the research (whether that was true or not in the end) that CFS was implicated with XMRV.

http://blogs.wsj.com/health/2011/01/20/xmrv-testing-the-blood-supply/

I think, what we really need is a government-led task force. Not sure if there are such entities behind the scene. Yes, it would be extremely useful if there are lab tests which can actually measure the viral load and where in the body etc as that can be used as a diagnostic tool.

It seems there is this anecdotal belief (?) on this site, that sooner you begin Valtrex/anti-viral, the better the outcome/prognosis would be. I'm not sure if this is merely a wishful thinking or mere hypothesis of some researchers or is this a likely truth based on proven scientific research?

xx

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Sweet7

Yes, Camomile, I'm still pretty much a newby and am learning a lot. As far as taking Vatrex within 72 hours of the onset of symptoms or predome, I read that strait from the prescription information packet from the pharmacy. Struggle explained viral load well and there are MRI diagnostic tools being developed. It may be quite a few years before it is available though. I’ve been reading more about T cells and their role in immune response, how the Trim21 gene works, and which cells have the highest levels. Come to find out, CD4 T cells have a high level of the Trim21 protein. The very cells that I believe HIV attacks.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803686/

I know that natural cell death occurs and can be the reason for a large reduction of viral load, but Isentress (a HIV drug) is supposed to reduce the viral load to where it is undetectable. Also, patients taking Isentess showed a significant increase in T cell levels. Now, I know that most T cells die but a few are kept around for memory of the pathogen dna. So, I would think those cells would continue to have an HIV template. But if not, how is that possible? Or maybe those cells weren’t infected in the first place. Yet, would if Isentress stops replication at a point and alerts the Trim21 gene that then dismantles it along with the viral dna it is bound to? If that is possible, then maybe CMX001 or AIC-316 would do the same thing for HSV. However, I haven’t been able to figure out if the Trim21 gene expresses proteins within the neuron, if it does, both of these drugs have molecule that cross the blood brain barrier and could very well get into our neurons. Even if some of our own dna got wiped out, our cells have the ability to repair dna damage. I really hope that I’m onto something here. It would be nice if we could get a researcher to do an in-vitro study to see if this is possible.

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hfighter

Sweet7 what does this mean ?:

In this article a team of scientist found a way to observe the movement of herpes inside a nerve cell (the article is from 2000, pretty old), they describe the process of whow it comes into the nerve cell.

http://www.brown.edu/Administration/News_Bureau/2000-01/00-001.html

The scientists stripped herpes simplex virus Type I of its envelope and injected the human virus into the squid axon. The study showed that the viral particles travel at an “enormously” fast and consistent speed of 2.2 microns per second, which indicates a single mechanism for movement, Bearer said

.....The study showed that the viral envelope is not required for transport of the virus...........

I'm looking if herpes comes into the cell with its envelope or if it leave it away, but I haven't found a good article about it

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camomile

It seems there are quite a lot to consider, there, Sweet. :)

You are so well read and it's really awesome you are taking this very seriously.

I do hear immunology is a fairly new area?

You are so so right to consider aging process and H infection. (you mention about Thymus action at the age of 70s)

Please keep up with the great work :D

x x x x x x x

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camomile

:flowers:

“For a long time, it was believed that herpes traveled back to the central nervous system by infecting other cells in the nerve sheath,” Bearer said. The virus does infect these cells, but this research showed that the virus moves much faster inside the axon."

This goes to show scientists hadn't known much about H and how it affects people who have H.

Thank you for the link, hfighter

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struggle83
Sweet7 it seems that the virus losses it evelop when infecting the first time, you can see it in this video:

http://darwin.bio.uci.edu/~faculty/wagner/hsvbinding.html

:(

There's also a good video on YouTube showing how the envelope is removed once the hsv enters the cell. For this reason I think Trim21 won't be effective with hsv. Also I posted a thread about how the infected cell puts up a marker outside the cell and other viral particles bounce off of those markers. This allows the virus to move faster than scientists had realized. It is ridiculous at how little is known about this potentially dangerous virus. After all it is a disease of the nervous system. That is significant.

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Sweet7

First of all, let me get caught up. One lnk does prove that Trim21 does not get triggered when HSV infects a cell which is what I thought. So, even though we make antibodies, they may be useless. What I have been trying to say is if antiviral medication such as AIC-316 or CMX001 is still seen as an invader of the infected cell, the Trim21 gene may be alerted, and then the proteins it secretes to start garbage collection could begin on the antiviral and maybe even dismantle the viral dna along with it. We make all sorts of antibodies. Does each cell in our body know what each antibody is for? Well, I don’t know, maybe, maybe not. I am just curious if the base antiviral in these drugs could sort of mimic an antibody. If not, this is still a good therapy option to look at. CMX001 has such a small molecule that mimics something that is metabolized by all cells which is how it delivers the cidifovir. If these drugs don’t mimic an antibody, a drug could be developed and deliver an antibody the same way. The only thing I don’t know is how quickly the Trim21 gene works. Normally for viruses that still have the antibody attached; the Trim21 gene can destroy it before it does any damage. If such a drug is created, the antibody would have to have enough time to find the viral dna and bind to it. I do believe it is possible due to the fact that antiviral medications have enough time to find the viral particles and stop replication. I have to say the speed of HSV is pretty remarkable. I think that study was mainly to look at how quickly the virus travels and find out if the envelope is needed for travel. Many experiments focus on small steps like that. It takes small steps to ensure accuracy, but each step is vital in figuring things out.

Struggle, I couldn’t get your link in your Bouncing Viral Particles to work so I looked it up. http://www.nature.com/news/2010/100121/full/news.2010.26.html

This is very interesting and yes, targeting those proteins could lead to a viable treatment, as long as only HSV secretes those proteins. Now I’m beginning to wonder if that’s how HerpV will work. Maybe people who are immune have T cells that detect those protein markers. I would think the same marker would be available on our neurons. Oh, did you notice in the video of how HSV infects that the viral dna is circular?

Thanks for posting those articles guy’s.

I’ve been thinking about how AIC-316 showed a reduction of antibodies in animal studies. That could only mean that it caused enough suppression to where the virus is not being detected by the immune system. This may be a way to prove a cure until diagnostic tools become available. We may always test positive, but if the antibodies drop over time after being vaccinated, that may be considered a similar tool for stating that a person is in remission. After so many years, a person could be declared cured. Much like cancer patients. I know that is off topic, but I just wanted to get that out there. Maybe our antibodies will become useful after all. But then again, I thought it might be possible for them to detect viral load from a spinal tap.

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Sweet7
http://www.ncbi.nlm.nih.gov/pubmed/12116026

"HSV DNA copy numbers in serum and cerebrospinal fluid (CSF) were quantified using a real-time PCR assay."

Info re. viral load sounds like a key to access a prognosis..

This study was done on new borns with active infection, not latent infection. Latent infection of HSV-2 doesn't take place in the central nervous system, but in the I guess I should have made my post about viral load of latent infection. That's what I meant. Latent infection for GH takes place in the Dorsal Root Ganglia which is not part of the central nervous system but the pheripheral nervous system.

http://www.answers.com/topic/dorsal-root-ganglion

The

axons of dorsal root ganglion neurons are known as afferents. In the peripheral nervous system, afferents refer to the axons that relay sensory information into the central nervous system (i.e. the brain and the spinal cord). These neurons are of the pseudo-unipolar type, meaning they have an axon with two branches that act as a single axon, often referred to as a distal process and a proximal process.

I'm not sure about Orall Herpes since it has been found to be latent in brain cells which is why there is a link between HSV-1 and Alzheimers.

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camomile

The axons of dorsal root ganglion neurons are known as afferents. In the peripheral nervous system, afferents refer to the axons that relay sensory information into the central nervous system. These neurons are of the pseudo-unipolar type, meaning they have an axon with two branches that act as a single axon, often referred to as a distal process and a proximal process.

I'm not sure about Oral Herpes since it has been found to be latent in brain cells which is why there is a link between HSV-1 and Alzheimers.

Thank you for the link. :) xx

I guess, we all have our own thinking process when we post which may not be obvious from what we write. :)

" I thought it might be possible for them to detect viral load from a spinal tap."

This has always been a point of contention somewhat. There ought to be a test to measure the viral load in certain patients or measure the same during cerebral functional imagining.

From what I read, sometimes it's HSV 1 & sometimes it's HSV 2 (almost as if they are almost interchangeable when it comes to CNS infection?) when researchers order autopsy. There were some papers by researchers at Queen's Square, London who are working in and around London. They might be useful ppl to talk to, Sweet.

Imho, when you say, "latent" or "latency", it does not mean H will always stay quiet sitting around in one defined spot to be polite for the host. At least, that's what some doctors seem to genuinely believe anyway.

Have a nice Sunday :D x x x x x x x

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