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HHV-6 testing: PCR vs IgG?

Sasha

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UK
This is on Mindy Kitei's blog today (writing about the FDA workshop):

Peterson talked in his meeting across the hall about his success with Vistide when used on patients with active infections by PCR with HHV-6, Epstein Barr or CMV—meaning the virus is actively replicating—as opposed to just the high antibody numbers to these herpes viruses that many with ME sport. Probenecid, Peterson explained, potentiates Vistide’s effects. He found that VO2 max—one’s aerobic threshold—improves on Vistide/Probenecid, and natural killer cells increase. Peterson asked: Why should getting rid of the virus result in VO2 max shooting up? His theory: The virus is messing with mitochondria. One of Peterson’s patients on Vistide checked out of a nursing home and went back to work. Of the 27 patients on Vistide, 18 didn’t relapse off the drug.

Other ME doctors such as Montoya have used IgG tests, which check for antibody levels, and if you have high titres and ME symptoms including cognitive ones (the immune ones go without saying, presumably), reckon that shows that you have an active HHV-6 infection.

It says on the HHV-6 Foundation website about whether PCR DNA tests for HHV-6 can differentiate between active and latent infection:

Yes. HHV-6 is never found in plasma or serum unless there is an active infection. However, the absence of HHV-6 DNA in the plasma/serum does not mean that there is no active infection. HHV-6 does not circulate in the plasma/serum except during the initial infection and transiently during an acute infection.

I'm wondering how this ties in with Dr Peterson's approach - why he's rejected IgG testing for PCR testing (apparently)? Won't he be leaving a lot of false-negative patients untreated? Or has thinking changed on this?
 

Sasha

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Found this also on the HHV-6 Foundation website that sums up both the overlap and the dichotomy:

Elevated IgG antibody levels. Elevated IgG antibody levels can suggest, but not prove active, chronic infection. In a 1996 study of HHV-6 in CFS patients, 89% of the patients with IgG titers of 1:320 and above were found to have active infections by culture. (Wagner, Journal of Chronic Fatigue Syndrome)Stanford infectious disease specialist Jose Montoya believes that the best evidence of smoldering central nervous system (CNS) infection is the IgG antibody to the virus, and not the virus itself. In a pilot study, he found that when patients with high titers of HHV-6 IgG (1:320, 1:640 or higher) and EBV are treated with a potent antiviral; their titers fall substantially along with a significant improvement in symptoms.​
 

Sushi

Moderation Resource Albuquerque
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Sasha

There is also the question of whether the immune system is able to produce antibodies in its compromised state. I was neg by IgG and have just been tested by PCR. Waiting for results.

Sushi
 

Sasha

Fine, thank you
Messages
17,863
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UK
Interesting. I've tested high on IgG but my new NHS consultant has just sent some blood off for a PCR test and I'm wondering what I should do if that's negative. Montoya's approach suggests I should be treated, Peterson's suggests I shouldn't be.

I'm hoping I'm among the 89% of PWME with high IgG who also test positive by PCR.

But still, I wonder why the different docs have different approaches. I wonder if Dr Peterson is more cautious because he's treating with (more dangerous?) Vistide whereas Dr Montoya uses Valcyte.
 

SOC

Senior Member
Messages
7,849
But still, I wonder why the different docs have different approaches. I wonder if Dr Peterson is more cautious because he's treating with (more dangerous?) Vistide whereas Dr Montoya uses Valcyte.

I would guess that Dr Peterson is researching the use of Vistide at this point so he is probably selecting clearly active-HHV-6 patients for the study.
 

globalpilot

Senior Member
Messages
626
Location
Ontario
This is on Mindy Kitei's blog today (writing about the FDA workshop):

Peterson talked in his meeting across the hall about his success with Vistide when used on patients with active infections by PCR with HHV-6, Epstein Barr or CMV—meaning the virus is actively replicating—as opposed to just the high antibody numbers to these herpes viruses that many with ME sport. Probenecid, Peterson explained, potentiates Vistide’s effects. He found that VO2 max—one’s aerobic threshold—improves on Vistide/Probenecid, and natural killer cells increase. Peterson asked: Why should getting rid of the virus result in VO2 max shooting up? His theory: The virus is messing with mitochondria. One of Peterson’s patients on Vistide checked out of a nursing home and went back to work. Of the 27 patients on Vistide, 18 didn’t relapse off the drug.

Other ME doctors such as Montoya have used IgG tests, which check for antibody levels, and if you have high titres and ME symptoms including cognitive ones (the immune ones go without saying, presumably), reckon that shows that you have an active HHV-6 infection.

It says on the HHV-6 Foundation website about whether PCR DNA tests for HHV-6 can differentiate between active and latent infection:

Yes. HHV-6 is never found in plasma or serum unless there is an active infection. However, the absence of HHV-6 DNA in the plasma/serum does not mean that there is no active infection. HHV-6 does not circulate in the plasma/serum except during the initial infection and transiently during an acute infection.

I'm wondering how this ties in with Dr Peterson's approach - why he's rejected IgG testing for PCR testing (apparently)? Won't he be leaving a lot of false-negative patients untreated? Or has thinking changed on this?

The reversing of the VO2 max ties in nicely with the March2013 Cheney video posted. He finds very poor aerobic metabolism resulting in low VO2max. It looks like viral can be a cause and lead to all sorts of downstream effects, including diastolic dysfunction and CCSVI

I wonder though about the comment regarding the virus not being found in the blood/plasma. Why, then would antibodies be produced and how does the virus spread ?
 

snowathlete

Senior Member
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5,374
Location
UK
I would guess that Dr Peterson is researching the use of Vistide at this point so he is probably selecting clearly active-HHV-6 patients for the study.
this is probably it. It may well be that vestide would work on patients with negative PCR but with high IgG as well, but perhaps less dramatically.
 

heapsreal

iherb 10% discount code OPA989,
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i would think that if u tested positive to any of the herpes viruses pcr or igg and had low nk function, then there is a very good chance viruses are reactivating. This is because the nk cells control these viruses???
 

JT1024

Senior Member
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582
Location
Massachusetts
Interesting thread.

I've been tested for HHV-6 IgG Ab (titer of 1:320). I also has positive results for EBV -VCA IgG Ab (3.28), EBV-EBNA IgG Ab (1.72), M. Pneumonia IgG (1.98), and C pneumonia IgG (1:128). The doctor that ordered these tests had also tested for Lyme and co-infections which came back positive for Lyme, Babesia duncani and Anaplasmosis phago...something.

He wants me to see a Lyme specialist (LLMD). I just wish there were more comprehensive pratices that could handle all the different issues we deal with. There are just so few great doctors for so many of us. My PCP has me on doxycycline only at the moment. I went to him only because I couldn't decide what doctor to see... most LLMD's don't take insurance.