Ablashi's Latest Work Shows HHV-6A Culprit
By Robert Huntington

In an article in the Journal of Clinical Virology (in press), Dr. Dharam Ablashi, one of the world's leading experts on HHV6, concludes that CFS (ME/CFIDS) patients are acquiring HHV-6A as a primary infection as adults and not reactivating it from childhood as many have hypothesized. He also found that the infection has been shown to downregulate the central nervous system, the cardiac system, and the cerebral systems. While variant B was found to be the culprit in multiple sclerosis, variant A was doing the damage in CFS and is found in similar numbers as affects those with AIDS (70%). Reporting on his newest discoveries at the New Jersey CFSA Conference, he said, despite prior reports to the contrary, there were no (0%) controls found with the infection of the A strain, although some healthy controls were found to have the B strain. Dr. Ablashi did the work by short-term culturing, PCR or RNA for the PCR, and IGM in antibody serum and plasma and found HHV7 was not found, but there was no doubt about HHV-6A being the culprit in the majority of patients tested. Many hypothesis have been proposed. While he cannot rule out Epstein-Barr Virus (EBV), he has done work looking for an enterovirus along with Dr. Robert Gallo and found none. This hypothesis was mainly promoted by Dr. Peter Behan. In 1991, Dr. Elaine DeFreitas found evidence of this but the CDC couldn't replicate her work. He mentioned that they had used a different probe which made their evidence useless. Dr. John Martin claimed to have discovered a spuma virus as causative, but Dr. Jay Levy "failed to be able to support his work. Then, later on, when CFS patients and healthy controls were tested, Martin could not tell the difference." Martin's novel "stealth" virus, he reported, belongs to the same HHV6 and 7 category. The same strain found in AIDS is found in ME/CFIDS. Others have come up with the same scenario such as Zorzeinon from Italy who found 65% had active HHV6. Buchwald, et al found that 70% of the Lake Tahoe patients had an active HHV6A strain. (Ann Intern Med 1992; 116) He has tested Ampligen patients before they took Ampligen and afterward and found the HHV6 had disappeared which "suggests Ampligen can block HHV6." He is now seeing if the same can be found with ganciclovir. Blocking it may not be permanently killing the virus. It may also be activating B cells that only make the condition worsen once you go off the drug.

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