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?