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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