The HHV-6 Paradigm

How HHV-6 Develops Resistance to Ganciclovir

http://herpes-online.net/article/nlm-11602788/Zovirax

HHV-6 in Bronchiolitis Obliterans Syndrome

"Bronchiolitis obliterans syndrome (BOS) is the limiting factor to long-term survival after lung transplantation." A new study has found evidence to "warrant further studies to elucidate a possible causal link between HHV-6 and BOS."

Online debate about HHV-6A being the cause of AIDS

An interesting debate has started about the role of HHV-6A in AIDS.

Human Herpes Virus 6 variant A (HHV-6A) directly linked to multiple sclerosis-like illness.

Evidence Presented at American Neurology Association
Annual Meeting

SAN DIEGO, Oct. 5, 2005 (PRIMEZONE) -- Dr. Claude
Genain of the University of California San Francisco
Medical Center presented evidence at the American
Neurology Association Annual Meeting this week that
shows a direct link between human herpes virus 6
variant A (HHV-6A) and a multiple sclerosis-like
illness.

Dr. Genain injected common marmoset monkeys with HHV-6
variants A & B. Most notably, only infection with
HHV-6 variant A resulted in illness. The monkeys
developed lab evidence and signs of chronic autoimmune
demyelination of the central nervous system, the
hallmark of multiple sclerosis. This is the first time
that any animal infected with HHV-6A has developed
clinical pathology of the central nervous system, and
the most direct evidence to date of a possible causal
connection between HHV-6A and multiple sclerosis.

Dr. Genain's marmoset developed weight loss and
paralysis with sensory deficits after exposure to
HHV-6A. Inflammatory lesions of the central nervous
system and evidence of demyelination were seen on MRI
and microscope slides of the brain tissue. However,
the important finding of the study was direct evidence
of the presence of HHV-6 viral antigen within the
nerve cells of the brain stained with an
HHV-6-specific antibody.

HHV-6 variant B (HHV-6B) causes roseola, a
self-limited fever and rash, in over 95% of young
children by age 2. After the initial illness, HHV-6
persists indefinitely in its quiescent, latent form in
the cells of the central nervous system, bone marrow
and immune system. However, HHV-6 can reemerge and
actively replicate later in life, producing new virus
particles that can cause illness. HHV-6 can reactivate
in immunosuppressed patients and cause life
threatening complications, such as opportunistic
infections and encephalitis, in post-transplant
patients.

The quest for a theory of viruses as a causative agent
for multiple sclerosis and other diseases has long
eluded scientists. A direct link between infection
with HHV-6A and multiple sclerosis has been lacking
until now.

According to Dr. Genain, "For the first time,
scientists will be able to look into the biological
process leading to multiple sclerosis at its very
beginning, when no one suspects the disease and people
have not yet experienced its symptoms." In recent
years there has been a considerable degree of interest
in the relationship between HHV-6A and multiple
sclerosis, because HHV-6A DNA has repeatedly been
found in brain tissue and the cerebrospinal fluid of
affected patients, and increased levels of antibodies
to viral antigens in their blood only present during
replication of HHV-6A are frequently detected.

A comprehensive analysis presented by Dr. Dharam
Ablashi, co-discoverer of HHV-6 and Scientific
Director of the HHV-6 Foundation, at the International
Fatigue Conference on Fatigue Science held during
February 2005 in Osaka, Japan, discussed all clinical
studies published in the medical literature on the
association between HHV-6A and multiple sclerosis.

His summary of the existing literature demonstrates
that when lab methods detecting the presence of active
HHV-6A infection are used, an exceptionally strong,
statistically significant association between HHV-6A
and both multiple sclerosis and chronic fatigue
syndrome (CFS) is consistently seen. Lab methods that
detect latent HHV-6A virus are not able to
consistently identify either MS or CFS patients.

Having an experimental animal model linking HHV-6A
infection to central nervous system pathology will
open the door to new types of research investigations.
The common marmoset has a well-known propensity to
develop experimental autoimmune encephalitis, a
chemically-induced animal model of multiple sclerosis
that is commonly used when investigating the efficacy
of new MS drugs. The inflammatory demyelination of
nerve cells in a live primate model after exposure to
the HHV-6A virus has now been demonstrated for the
first time. This marmoset model will add a new
dimension to the drug discovery and development
process for multiple sclerosis.

Dr. Ablashi, who has published numerous medical
studies demonstrating the causative role of human and
primate herpes viruses in various types of lymphomas
and leukemia, commented, "Nonhuman primates are
genetically closest to man. Dr. Genain's pathogenic
model of HHV-6A infection in the common marmoset will
enhance our understanding of the role that the HHV-6A
virus plays in the induction of typical MS lesions.
This model will be very important in the study of the
disease process, and evaluation of new molecules that
can prevent active HHV-6A viral infection and the
development of multiple sclerosis."

Dr. Genain's work was supported by grants from the
HHV-6 Foundation, Multiple Sclerosis Society, Cure MS
Now, DANA Foundation and Lunardi Foundation.

Bush Today on Avian Flu

From President Bush's news conference today:

I am concerned about avian flu. I'm concerned about
what an avian flu outbreak could mean for the United
States and the world. I have thought through the
scenarios of what an avian flu outbreak could mean. I
tried to get a better handle on what the
decision-making process would be by reading Mr.
Barry's book on the influenza outbreak in 1918. I
would recommend it.

The policy decisions for a president in dealing with
an avian flu outbreak are difficult.

One example: If we had an outbreak somewhere in the
United States, do we not then quarantine that part of
the country? And how do you, then, enforce a
quarantine?

It's one thing to shut down airplanes. It's another
thing to prevent people from coming in to get exposed
to the avian flu.

And who best to be able to effect a quarantine?

One option is the use of a military that's able to
plan and move. So that's why I put it on the table. I
think it's an important debate for Congress to have.

I noticed the other day, evidently, some governors
didn't like it. I understand that. I was the commander
in chief of the National Guard and proudly so. And,
frankly, I didn't want the president telling me how to
be the commander in chief of the Texas Guard.

But Congress needs to take a look at circumstances
that may need to vest the capacity of the president to
move beyond that debate. And one such catastrophe or
one such challenge could be an avian flu outbreak.

Secondly, during my meetings at the United Nations,
not only did I speak about it publicly, I spoke about
it privately to as many leaders as I could find, about
the need for there to be awareness, one, of the issue
and two, reporting -- rapid reporting to WHO, so that
we can deal with a potential pandemic.

The reporting needs to be not only on the birds that
have fallen ill, but also on tracing the capacity of
the virus to go from bird to person to person. That's
when it gets dangerous: when it goes bird, person,
person.

And we need to know on a real-time basis as quickly as
possible the facts so that the world scientific
community can analyze the facts and begin to deal with
it.

Obviously, the best way to deal with a pandemic is to
isolate it and keep it isolated in the region in which
it begins.

As you know, there's been a lot of reporting of
different flocks that have fallen ill with the H5N1
virus. And we've also got some cases of the virus
being transmitted to a person, and we're watching very
carefully.

Thirdly, the development of a vaccine. I've spent time
with Tony Fauci on the subject.

Obviously, it would be helpful if we had a
breakthrough in the capacity to develop a vaccine that
would enable us to feel comfortable here at home, that
not only would first responders be able to be
vaccinated, but as many Americans as possible, and
people around the world.

But, unfortunately, we're just not that far down the
manufacturing process. And there's a spray, as you
know, that can maybe help arrest the spread of the
disease, which is in relatively limited supply.

So one of the issues is how do we encourage the
manufacturing capacity of the country, and maybe the
world, to be prepared to deal with the outbreak of a
pandemic? n other words, can we surge enough
production to be able to help deal with the issue?

I take this issue very seriously, and I appreciate you
bringing it to our attention.

The people of the country ought to rest assured that
we're doing everything we can. We're watching it.
We're careful. We're in communications with the world.

I'm not predicting an outbreak. I'm just suggesting to
you that we better be thinking about it. And we are.
And we're more than thinking about it, we're trying to
put plans in place.

Pandemic Flu Awareness Week

http://www.curevents.com/vb/forumdisplay.php?f=40

HHV-6 infects human aortic and heart microvascular endothelial cells

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12115999&dopt=Abstract

J Med Virol. 2002 Aug;67(4):528-33. Related Articles,
Links

HHV-6 infects human aortic and heart microvascular
endothelial cells, increasing their ability to secrete
proinflammatory chemokines.

Caruso A, Rotola A, Comar M, Favilli F, Galvan M,
Tosetti M, Campello C, Caselli E, Alessandri G, Grassi
M, Garrafa E, Cassai E, Di Luca D.

Institute of Microbiology, University of Brescia
Medical School, Italy.

Endothelial cells are important targets for
herpesvirus infection. To evaluate the biological
effects of human herpesvirus-6 (HHV-6) infection,
adult heart microvascular and aortic endothelial cells
were examined for in vitro susceptibility to HHV-6 and
for the alterations induced by viral infection on the
production of monocyte chemoattractant protein-1
(MCP-1) and interleukin-8 (IL-8). Analysis by reverse
transcription-polymerase chain reaction and by in situ
polymerase chain reaction showed that HHV-6 replicates
in endothelium in the absence of cytopathic effects,
and that viral sequences were present in 20% umbilical
vein and in 10% aortic and 1% microvascular
endothelium. HHV-6 infection upregulated the
production of MCP-1 and IL-8, with differences
observed between aortic and microvascular endothelium.
These findings demonstrate that endothelial cells
represent a potential reservoir for HHV-6 infection,
and the altered pattern of chemokine production can
lead to attraction of immunocompetent cells and to the
development of inflammatory processes.

Gallo on HHV-6

Here's what Robert Gallo had to say about HHV-6 in an
NIH interview in 1995:

Have we ever argued for a possible cofactor? Yes, with
the qualification I just told you, that it is obvious
that some things will promote progression and some
things will inhibit progression. One of those things
may be the genetics of me versus you. We can say dose
is a factor that can lead to progression, or lack of
it, and at a greater or lesser rate. But we have
argued for certain herpesviruses as possibly being a
factor in promoting AIDS progression. Several groups
have argued for cytomegalovirus because it does do
things and it does activate more HIV in some subtle
settings.

In the middle of the 1980s, we became aware that the
lymphomas that were associated with HIV infection were
perhaps one-third of the time EBV-positive.
Epstein-Barr virus, as you know, can immortalize some
B cells and, when you have EBV-positive lymphomas,
generally they are the kind of lymphomas that, more or
less... If they do not require EBV, EBV makes the
probability of getting a lymphoma much greater,
because the cell cannot die easily. It is
immortalized. Other genetic events are needed to
develop the lymphoma, but the immortalization of the
cell is perhaps a key factor that makes it probable
that it will be an EBV-containing cell that is the one
that will become a lymphoma.

What about the two-thirds of lymphomas in HIV-infected
persons that were not EBV-positive? We wondered if
there were herpesviruses yet to be discovered. We
looked in the B-cell lymphomas of patients with AIDS
who were negative for EBV and we discovered the first
new herpesvirus in 25 years, and the first herpesvirus
of man that targeted predominantly the T cell.

We had a new herpesvirus, but it was not involved in
the lymphoma, at least not as far as anybody knows,
even today. We even misnamed it. We called it HBLV,
because we found it in a B-cell lymphoma. Then we
studied it more intensively and determined that it
primarily infected T cells, not B cells, which was an
unexpected finding. We learned that it killed T cells
when it replicated. Then we learned that it infected
natural killer cells and, when it did so, it made
those cells attack other natural killer cells. We
learned that it could infect the same cell as HIV and
activate HIV expression. Next we learned that it
infected CD8 cells and activated the gene for CD4, the
only known biological agent I am aware of that
activates the gene for CD4. Now, the CD4+/CD8+ cells
could be targets for HIV.

It was at that stage we proposed that the herpesvirus
might be a cofactor for progression of AIDS. It was
then that I started to be careful of the use of these
words and called it a catalyst for progression, that
is, a nonessential cofactor, but something that makes
disease progression go faster and also makes it more
probable that immune deficiency will develop.

We put that idea out and it got a little bit of a
reception by [Dr. Larry] Corey in Seattle, and by [Dr.
Donald] Don Carrigan at Wisconsin. But then [Dr.
Harold] Jaffe published a paper, the data of which we
already had in hand. I think that paper by Jaffe and
his colleagues at the CDC [Centers for Disease Control
and Prevention] was not a sophisticated look at the
problem. Namely, they said, Look, everybody has
antibody, so how can it be a factor in progression?
That is like saying a cytokine like TNF [tumor
necrosis factor] is not important in disease
pathogenesis because everybody has it. The question
is, if 90 percent of the human population has it, they
also have EBV, but EBV can cause Burkitt's lymphoma
under certain settings. The question is, does it get
activated in an immune-suppressed individual?

We put the problem aside for a while because we did
not have a quantitative assay to measure the amount of
herpesvirus; only this antibody that indicated a
previous exposure to the virus, which everybody
showed. We argued, however, when we presented it, that
we needed to have a quantitative assay for virus in
blood and the amount of human herpesvirus-6 [HHV-6]
DNA in lymphocytes circulating around.

At this time we learned of Carrigan's work. He
reported in a few clinical papers, that sometimes in
immune-suppressed people, following transplantations,
he saw an enormous amount of human herpesvirus-6
replication and that he believed it was responsible
for some of the bone marrow abnormalities in such
people. He showed a lot of virus in bone marrow.
Second, he pointed out and emphasized that
interstitial pneumonia is the cause of death in 10
percent of the deaths of HIV-positive people. No one
knows the cause of that interstitial pneumonia, and he
found the lungs of those who died loaded with human
HHV-6. He presented at our laboratory meeting that he
thought it was very likely that HHV-6 was the cause of
those deaths.

Meanwhile, before this, Japanese workers had shown
that HHV-6 was the cause of roseola infantum, also
known as exanthem subitum, a disease of infants, with
fever and rash, but usually with not much more.

So now what is new? I have discussed with my colleague
[Dr.] Paolo Russo that the only way we are going to
get any proof of this, or get stronger support, is if
we get a specific inhibitor that does not inhibit HIV,
inhibits HHV-6, and as far as we know does not inhibit
anything else, is relatively non-toxic, and then show
that patients do better rather than worse.

Another way of doing it would be to find an animal
model not infected with a parallel virus to HHV-6
which can be infected by SIV [simian immunodeficiency
virus]. SIV can induce some immune deficiency–not the
acute sort–but there are monkeys in which SIV induces
nothing, there are monkeys in which some strains of
SIV induce an acute AIDS, and there are monkeys where
some strains of SIV induce a disease more similar to
the human disease, where it takes time.

We used such a system. This is not published data.
With the SIV alone, there was a little immune
deficiency, and with the HHV-6 alone nothing, but with
the two together they got it. I think we have proven
the point with that rhesus virus and that we can
publish that soon. So, I believe human herpesvirus-6
is a factor in AIDS progression.

http://history.nih.gov/NIHInOwnWords/docs/gallo3_01.html

Diabetes Insipidus may also link AIDS and CFIDS

In a recent Co-Cure posting on CFIDS, Rich Van
Konynenburg writes "we know that many PWCs have mild
diabetes insipidus."

The following appeared on the Aegis site which is
devoted to AIDS research:

Int Conf AIDS 1994 Aug 7-12; 10:196 (abstract no.
PB0797)
Harris P, Curry R; AIDS Clinical Research Center of
Washington, DC 20009.

OBJECTIVE: Ten of 200 patients have complained over
the last year of polyuria, polydipsia and nocturia. We
were interested in whether diabetes insipidus (DI) may
be directly associated with this infection.

METHODS: We measured urine and serum osmolalities,
serum antidiuretic hormone (ADH), serum sodium, BUN,
glucose and potassium levels; calculated serum
osmolalities; evaluated CD4 and CD8 counts, Beta-2
microglobulin and HIV P-24 antigen levels; assessed
recent brain scans; reviewed clinical pictures and
noted current medications.

RESULTS: ADH levels were less than 1 pg/ml, serum
osmolalities 295-312 mos/kg H2O, CD4 levels 3-564/cmm,
CD8 levels 86-1186/cmm, Beta-2 microglobulin levels
3.5-5.6 mg/l. Five had reactive HIV P-24 antigens.
Seven had essentially normal MRI's (3 not done).
Medication and secondary infection did not account for
DI.

DISCUSSION AND CONCLUSIONS: That 5% of our patients
have primary central diabetes insipidus suggests DI
may be an underestimated complication of HIV
infection.

The tonsils are a reservoir for HHV-6

http://www.thedoctorsdoctor.com/bodysites/tonsils.htm

Increased Neutrophil Apoptosis in AIDS and Chronic Fatigue Syndrome

If you're one of those CFS patients or activists who
is desperate to find some little difference--any
difference--between AIDS and CFIDS so you can sleep at
night knowing that they are two separate epidemics
(one for bad people and one for good people) you'd
better not look at the neutrophils. You won't get much
sleep.

That enterprising Merge Group in Britain has financed some
important research that shows yet another similarity
between AIDS and CFS.

Click here to see what happens to the neutrophils in
CFIDS:

http://www.meresearch.org.uk/research/sponsored/neutrophil.html

And Click here to see what happens to the neutrophils
in AIDS.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8981916&dopt=Citation

Looks like Neenyah Ostrom and New York Native had it
right.

H5N1 Watch

Quote of the Day from Marc Santora's article in The
New York Times

"If a pandemic similar to the one of 1918 occurred
today, as many as 2.8 million New York City residents
could be infected within months, sending more than
200,000 to the hospital and clogging the morgues with
400 deaths a day during the peak infection period."

English CFS Activists are Helping to Show that CFS is Related to AIDS

In England, patients with CFS have been under attack
by an aggressive group of psychiatrists who are
determined to prove that CFS is a psychiatric
disorder. It has been a very nasty battle and has
given a great deal of impetus to scientific attempts
to show that CFS is a real physiological illness. As
with most CFS research that has been done in America,
the more serious the research in England gets, the
more it seems to suggest that CFS is part of the AIDS
epidemic. The newest research showing that CFS is a
disease of oxidative stress is no exception.

For a couple of decades a few scientists in Australia
known as "The Perth Group" have insisted that AIDS is
a disease of oxidative stress. They have argued that
HIV has never been properly isolated and has not been
shown to be the cause of AIDS. The Perth Group has
tried to show that gay lifestyle factors have been the
source of the oxidative stress.

A new paper published in Free Radical Biology &
Medicine (2005:39:584-589) By Gwen Kennedy, Vance A
Specne, et al. concludes that "Oxidative
stress levels are raised in chronic fatigue syndrome
and are associated with clinical symptoms." Give that
nobody has yet accused CFS sufferers of secretly
conducting gay lifestyles, the Perth Group may want to
reconsider their theories about the source of
oxidative stress in AIDS. No one has yet proposed a
theory that two kinds of oxidative stress--gay and
straight--are causing a very similar epidemic in both
gay and straight people at the same time.

Dr. Neil Abbot (Director of Operations of the charity
MERGE that funded the research) noted on the MERGE
website (www.meresearch.org.uk), "Circulating in the
bloodstream are highly reactive molecules, known as
free radicals, which can cause damage to the cells of
the body, a process called oxidative stress. In
healthy people, increases in free radicals are
neutralised by antioxidant defences, and it is only
when these defences are overwhelmed that cell injury
results. The source of excessive free radical
generation in ME/CFS patients may be associated
with a variety of altered biological processes".

Dr. Abbot also said that the research "suggested that
many patients currently diagnosed with ME/CFS could
have an inflammatory condition and be in a
'pro-oxidant state'".

What's in a name? Everything and more.

AIDS = Inaccurate construct not reflecting reality

CFIDS/AIDS = Better construct reflecting reality

CIDS (Chronic Immune Dysfunction Syndrome) = Best
construct reflecting reality

HAART for AIDS may cause Oxidative Stress

http://www.aidsportugal.com/article.php?sid=3241

HHV-6 Quote of the Day

In rereading Hillary Johnson's amazing book, Osler's
Web recently, these two sentences about HBLV, which
eventually was called HHV-6, caught our attention:
"Significantly, the Gallo group had found AIDS
patients' T-cells to be co-infected with the new
herpesvirus and HIV. Because HIV itself killed only a
small number of T-4 cells, the herpesvirus might be
responsible for the eventual annihilation of T-4 cells
in AIDS, the team said."

HHV-6 in sarcoidosis and lymphoproliferative disorders

"Serologic studies were done to estimate the antibody
prevalence against human herpesvirus 6 (HHV-6) in
patients with malignant lymphomas, Sjogren's syndrome
and sarcoidosis. Serologic studies showed IgG antibody
titers against HHV-6 in up to 41% of patients with
sarcoidosis, 50-70% with malignant lymphomas and in
36% with Sjogren's syndrome. In situ hybridization on
lymph node biopsies was positive for HHV-6 genome in 1
out of 5 sarcoidosis lymph nodes."
J Virol Methods. 1988 Sep;21(1-4):49-59.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3053745&dopt=Abstract

Biotrin's description of the role of HHV-6 in AIDS

"HHV-6 infects and persists in CD4 T-lymphocytes, a
unique characterstic that it shares with human
immunodeficiency virus and a feature that separates it
from other herpesviruses. There is evidence that it
may interact with HIV and in this way serve as an
important cofactor in the pathogenesis of AIDS."
http://www.biotrin.ie/clinician/hhv/hhv6aids.htm

HHV-6A and HHV-6B are actually different species

http://jvi.asm.org/cgi/content/full/73/10/8040?view=full&pmid=10482553

HHV-6 called "the likely cause of symptoms in a majority of the CFIDS population"

An article by John Addington on the role of HHV-6 in
CFS: http://www.immunesupport.com/message/test.htm

Another New Finding Shows CFS is Real

According to a report by Deborah Haile in the
Manchester Evening News today, "Dr. Raymond Perrin
believes he has proof that chronic fatigue syndrome -
once dubbed yuppie flu - has a physical cause."

Haile writes that "Manchester osteopath Dr. Perrin
believes he has proved that the debilitating syndrome
is the physical result of the way the body deals with
toxins. He believes a picture of varicose lymphatic
vessels taken during a research project at Salford
University shows for the first time the "backflow" of
lymphatic drainage that he believes is the cause of
toxin build-up. And it is this accumulation of toxins
in the central nervous system, which Dr. Perrin
believes is the cause of conditions such as chronic
fatigue syndrome and ME."

Perrin describes the vessels as being "swollen."

An article in the Journal of Nuclear Medicine outlines
the components of the lymphatic system:
"The lymphatic system is a component of both the
circulatory and the immune systems. The lymphatic
system consists of a series of conduits (the lymphatic
vasculature), lymphoid cells, and organized lymphoid
tissues. Lymphoid tissues include the lymph nodes,
spleen, thymus, Peyer's patches in the intestine, and
lymphoid tissue in the liver, lungs, and parts of the
bone marrow (20). Lymphatics are found throughout the
body, with the exception of the central nervous
system, where cerebrospinal fluid fulfills the normal
role of lymph. Lymphatic vasculature and lymphoid
tissue are prevalent in organs that come into direct
contact with the external environment, such as the
skin, gastrointestinal tract, and lungs. This
distribution is probably a reflection of the
protective role of the lymphatics against infectious
agents and alien particles. Absorption of fat from the
intestine occurs through the lymphatic system, which
transports the lipids (chyle) to the liver. The
lymphatic system also transports cellular debris,
metabolic waste products, and fluid excesses (edema
safety factor) from local sites back to the systemic
circulation."
http://jnm.snmjournals.org/cgi/content/full/44/1/43

In the past, Dr. Paul Chency has suggested
hydrotherapy for the damaged lymph system in CFS
patients:
http://www.immunesupport.com/library/showarticle.cfm/ID/3748/e/1/T/CFIDS_FM/

Below is a patient's guide to Lymphedema:
http://www.biocompression.com/library/lymphID.htm

Streptococcus suis in China

If the Chinese Swine Flu story goes anywhere, this is
a great site for the latest news:

http://www.recombinomics.com/whats_new.html

A Summary of HHV-6's Destructivenss

From an article by Abdel-Haq NahedM, Asmar BasimI
in The Indian Journal of Pediatrics (2004,Volume 71,
Issue 1, Page 89-96)

HHV-6 preferentially infects CD4+ T-lymphocytes;[17]
but can also infect other cell lines of epithelial,
fibroblastic and neuronal origins with different
efficiency.[18],[19],[20] The surface marker CD46 acts
as part of a co-receptor for infection by both HHV-6A
and HHV-6B.[21] Although CD46 is expressed by most
nucleated human cells and may explain the wide
cellular tropism of HHV-6, the virus does not infect
all CD46-positive cells. Following infection, HHV-6
persists and establishes latency in different cells
and organs including monocytes/macrophages, salivary
glands, the brain and the kidneys. Because the main
target cells for infection are the CD4-positive
lymphocytes and monocytes, HHV-6 infection has
important effects on the immune system. These include
enhancement of natural killer cells, inhibition of
T-cell proliferation, induction of cytokine release
such as tumor necrosis factor-alpha, and interleukin
1-beta as well as modifying the expression of key cell
receptors such as CD3, CD4 and CXCR4.[17],[22],[23]

http://ijppediatricsindia.org/article.asp?issn=0019-5456;year=2004;volume=71;issue=1;spage=89;epage=96;aulast=Abdel-Haq

Laughter is the Best Medicine

"A spokesman for the Centers for Disease Control today defended

the CDC's inaction on Chronic Fatigue Syndrome by saying

that scientists there did not want to discover anything

about CFS that might upset the patients."

Liam Scheff Deserves a Pulitzer for his Coverage of AIDS Atrocities

In a very short period of time, Liam Scheff has gone
from being a journalistic nobody to being the subject
of a major attack by The New York Times. If the Times
uses precious space to attack a newcomer for
exposing dreadful guinea pig type experiments at a New
York City AIDS treatment center for children, he must
be doing something right.

And he's fighting back. His newest front page piece in
New York Press is devastating:
http://www.nypress.com/18/30/news&columns/liamscheff.cfm

How did The New York Times become such a creepy
enforcer of the establishment? When did it become the
enemy of whistleblowers? Is Judy Miller in jail to
help buttress the reputation of a paper that is
essentially untrustworthy? For a close look at what is
wrong with the Times, we recommend Renata Adler's
brilliant Canaries in the Mineshaft.

New York Press has performed a great service by
standing behind Scheff's journalism and frontpaging
it. Hopefully they won't stop until they've finished the
job on this very important story.

In may ways, the atrocities described by Scheff are
intimately connected to the lies that the public has
been told about HIV, HHV-6 and CFIDS/AIDS. AIDS Fraud
and these atrocities are joined at the hip.

Scientist says there is an urgent need for more research into HHV-6 and HHV-7

In the June, 2005 issue of Current Opinion in
Infection Diseases, an article about HHV-6 and HHV-7
in children concludes that "is an urgent need for more
research on HHV-6 and -7 in children, particularly in
relation to chromosomal integration of HHV-6A and B,
and clinical consequences of HHV-7 infection."

The article by Katherine K. Ward, notes that "both
viruses have been shown to contribute significantly
and equally to the burden of disease in young children
with suspected encephalitis or severe convulsions with
fever."

The Big Medical Story the Media is Ignoring

Any journalist who says that Non-HIV AIDS isn't an
important story worthy of full investigative coverage
is a clown who belongs in the same class as the
clownish journalists who looked the other way when
AIDS first broke out.

On the website for Autoimmune Technologies, the story
is virtually spelled out for any enterprising
journalist:

Idiopathic CD4+ T-lymphocytopenia, or ICL, is an
immunodeficiency syndrome in which human
immunodeficiency virus, or HIV, cannot be detected.
Because HIV is the causative agent of acquired immune
deficiency syndrome (AIDS), ICL can be referred to as
Non-HIV AIDS. As in AIDS patients, Non-HIV AIDS
patients exhibit reduced numbers of CD4+
T-lymphocytes, and many Non-HIV AIDS patients have
developed the opportunistic infections or otherwise
rare cancers associated with AIDS.

Non-HIV AIDS patients may comprise perhaps one percent
of all AIDS patients. While the majority of Non-HIV
AIDS patients do not belong to any of the risk groups
such as blood transfusion recipients, male
homosexuals, and intravenous drug abusers in which
AIDS was first identified, some Non-HIV AIDS patients
do belong to these groups. This suggests that Non-HIV
AIDS may also be transmissible.

Research conducted at Tulane University Medical Center
suggests that Non-HIV AIDS is associated with a
retroviral particle called Human Intracisternal A-Type
Particle-Type II, or HIAP-II. Antibodies to this
particle have been found in a high percentage of
patients with Non-HIV AIDS. Tulane has patented
HIAP-II, and Autoimmune Technologies is licensing
HIAP-II technology in order to develop screening and
diagnostic tests and therapies for Non-HIV AIDS and to
study the possibility of generating vaccines against
Non-HIV AIDS, autoimmune disease, and AIDS.

http://www.autoimmune.com/Non-HIVAIDSGen.html

One percent of all AIDS patients? That means there are
thousands (repeat, thousands) of cases out there.
Maybe something like 400,000 worldwide. And that's
400,000 people with transmissible non-HIV AIDS. And
it's not a page one story? Something is very wrong
with this picture.

It's amazing that Autoimmune Technologies is talking
about developing therapies and vaccines for Non-HIV
AIDS while we've yet to see a single serious story
about this in the media. Where are the Times, the
Washington Post and 60 Minutes? Where is "emerging
diseases" expert Laurie Garrett? Where are the Non-HIV
AIDS activists? Why is The New England Journal of
Medicine looking the other way? Is everyone suffering
epidemic fatigue? Are people afraid of confusing the
public about HIV with this second Non-HIV AIDS
epidemic? Are they afraid to tell the gay community?
Are they afraid that Non-HIV AIDS will give ammunition
to those who for two decades have questioned HIV's
role in AIDS?

Where are all the personal interest stories about
Non-HIV AIDS? It must be very strange for someone to
be told that they have Non-HIV AIDS. What do they tell
their sex partners--"Sorry, I don't have HIV, I have
Non-HIV." How come no obituaries say that people died
of complications of Non-HIV AIDS? Where are the
celebrities with Non-HIV AIDS? Is Non-HIV AIDS being
transmitted by the blood supply?

A few months back the media went nuts over the
possibility that there was a new more lethal strain of
HIV. And that was found in just one person. The fact
that people can contract Non-HIV AIDS strikes us as
being a far more important story with exponentially
far more serious implications for public health. The
media silence is deafening.

We do have to note that one person seems to be telling
her own story of dealing with something that sounds
a lot like Non-HIV AIDS:
http://lemonfoundation.blogspot.com/

If more patients start to speak out about their
struggles with Non-HIV AIDS, the media might be shamed
into giving the story the coverage it deserves.

Finally, Some Dramatic Proof that CFS is an Immune Disorder

Anyone who thinks that Chronic Fatigue Syndrome is part
of the AIDS epidemic received a little support in a
new study that indicates that there is a problem with
the white blood cells in Chronic Fatigue Syndrome.

According to New Scientist, a team led by Jonathan
Kerr "has compared levels of gene expression in the white
blood cells of 25 healthy individuals with those in 25
patients diagnosed as having CFS according to strict
criteria. The researchers found differences in 35 of
the 9522 genes they analysed using DNA chip
technology. The few similar studies done in the past have
produced conflicting results, so the team double-checked their
results using a more accurate method called real-time
PCR. That confirmed that 15 of the genes were up to
four times as active in people with CFS, while one
gene was less active. The results will appear in the
Journal of Clinical Pathology next month."

http://www.newscientist.com/article.ns?id=mg18725093.700

The London Daily Mail summed up the story this way:
"Suspicions that Chronic Fatigue Syndrome (CFS) is
'all in the mind' may finally have been laid to rest
with the discovery that sufferers have biological
abnormalities, it has been reported."

The BBC framed the story this way: "Scientists believe
they have pinpointed biological markers of chronic
fatigue syndrome which could help develop a test and
treatment for the condition."

This could be a very big political and scientific step
for CFS. After two decades of stupidity and
obfuscation on the part of establishment researchers
who always seemed to be pretending to research an
epidemic that they pretended they didn't understand,
CFS now now may have a test showing that it is a
pathological condition. The time consuming battle of
patients fighting psychiatrists and psychologists
over whether CFS is all in the mind can now end. The
test should also be able to show how contagious the
illness is. If members of the same family and
associates of patients are shown to have the condition it will
help support previous informal studies that have
suggested that CFS is contagious. It will also help to
determine the incidence of the disease. In America,
estimates range from 500,000 to over five million. One
study goes dramatically higher.

The question we would like answered along the way is
rather obvious: is this new finding in the white blood
cells of CFS patients also found in AIDS?

New Scientist mentioned a number of pathogens that might be the
cause of this immune defect but, predictably, failed
to mention HHV-6, the virus that was recently linked
to CFS. HHV-6 is the virus that nobody wants to talk
about. Why is that? It couldn't have anyting to do
with the fact that HHV-6 links CFIDS and AIDS, could
it?

HHV-8 and KS in CFIDS

A number of years ago, Neenyah Ostrom reported in the New
York Native on the lesions in CFS patients which seem
to resemble Kaposi's Sarcoma (KS). The current
thinking is that a virus called HHV-8 is the cause of
KS. (Although HHV-6 has recently also been implicated
once again.) If KS is a problem in CFS (and we
suspect it is) then one should be able to find HHV-8 and
HHV-6 in CFS patients. Apparently, in this small
study, one can. Below is a rather explosive abstract:

Prevalence in the cerebrospinal fluid of the following
infectious agents in a cohort of 12 CFS subjects:
human herpes virus-6 and 8; chlamydia species;
mycoplasma species; EBV; CMV; and Coxsackievirus.
Levine, S.
Journal of Chronic Fatigue Syndrome, 2001, 9, 1/2,
41-51.

Abstract:
Over the last decade a wide variety of infectious
agents have been associated with the CFS as potential
etiologies for this disorder. Many of these agents are
neurotrophic and have been linked previously to other
diseases involving the central nervous system (CNS).
Human herpes virus-6 (HHV-6), especially the B
variant, has been found in autopsy specimens of
patients who suffered from MS. Because patients with
CFS manifest a wide range of symptoms involving the
CNS as shown by abnormalities on brain MRIs, SPECT
scans of the brain and results of tilt table testing
we sought to determine the prevalence of HHV-6, HHV-8,
Epstein-Barr Virus (EBV), cytomegalovirus (CMV),
mycoplasma species, chlamydia species, and Coxsackie
virus in the spinal fluid of a group of 12 patients
with CFS (CDC criteria '94).

We found evidence of HHV-6, HHV-8, chlamydia species,
CMV and Coxsackie virus in 6/12 samples. Plasma tests
were negative. It was surprising to obtain such a
relatively high yield of infectious agents in cell
free specimens of spinal fluid that had not been
centrifuged. Future research in spinal fluid analysis,
in addition to testing tissue samples by polymerase
chain reaction (PCR) and other direct viral isolation
techniques will be important in characterizing
subpopulations of CFS patients, especially those with
involvement of the CNS.

The low rate of isolation of HHV-6 may be related to
the lack of gross neurological findings in the
patients at the time of testing.

An overview of KS:
http://www.thebody.com/nmai/ks.html

Except for those who have made a lifelong commitment
to denial, finding the so-called "KS virus" (HHV-8)
and the "supporting KS virus" (HHV-6) in CFIDS patients
should help settle the question of the overlapping
nature of the AIDS and CFIDS epidemics.

Isn't it time to take a closer look at those crimson
crescents in the throats of CFIDS patients?

More info on KS here.

Overview of HHV-6

This overview of HHV-6 is seven years old, but still
very relevant.

http://www-ermm.cbcu.cam.ac.uk/sdr/txt001sdr.htm

HHV-6 Linked to Miscarriages

Neenyah Ostrom reported on the link between HHV-6 and
miscarriages a number of years ago.
http://www.chronicillnet.org/CFS/Ostrom/chp5.html

Glycyrrhizin May Be Useful in Treating HHV-6

A Chinese study suggests that glycyrrhizin may be
helpful in the treatment of HHV-6.

Information about glycyrrhizin itself can be found
here:
http://www.siu.edu/~ebl/leaflets/glycyrrhizin.htm

The study of its effect on HHV-6:
http://www.tcm120.com/tcm/sars/sarsyj/6-27/sarsyj0627_2.htm

The Abstract:
It has been demonstrated that glycyrrhizin inhibits
the growth of different viruses in vitro, among which
are some herpesviruses, of which HHV-6 and HHV-7 are
the most recently discovered. HHV-6 is the etiol.
agent of exanthem subitum, but it may be responsible
for more severe pathologies. HHV-7 has been isolated
from healthy subjects, patients with chronic fatigue
syndrome and children with febrile illness but it has
not been casually assocd. with any pathol. The aim of
our study was therefore to test the activity of
glycyrrhizin and of 18a-and 18b-glycyrrhetinic acids
against HHV-6 and HHV-7. The antiviral activity of
non-toxic concns. of each drug was assayed on
lymphocytes infected with HHV-6 or HHV-7, the growth
of the virus being monitored by immunofluorescence
assay. Results show that glycyrrhizin at 1.2 mM
caused a 2.5-fold redn. of HHV-6 immunofluorescence
pos. cells. A 10-fold redn. was obtained using
glycyrrhizin at 3.6 mM, but at this concn. it also had
a few cytotoxic effects. 18a- And 18b-glycyrrhetinic
acids seem to have a stimulating effect on HHV-6
growth, with a two-fold increase in pos. cells. The
three drugs did not show any activity on HHV-7 growth.

HHV-6 and AIDS

The following quotes provide an overview of the role
of HHV-6 in AIDS:

"Imagine the consternation created during 1990 by
reports that HIV may be neither necessary nor
sufficient to cause the syndrome. The key experiments
have been performed in the laboratory of the
discoverer of HIV himself, Luc Montagnier of the
Institute Pasteur in Paris. If anyone has a stake in
proclaiming that HIV is the primary cause of AIDS and
that he is the primary discoverer of that cause, it is
certainly Montagnier. Yet Montagnier has announced
that HIV is not sufficient to cause AIDS."

--Robert Root Bernstein
Rethinking AIDS
page 25

The response from most other HIV researchers has been
to ignore Montagnier's data. A few, such as Robert
Gallo, have responded by producing counter claims of
their own. Gallo, for example, has published studies
showing that both HTLV I (one of his earlier
discoveries) and herpes simplex type 6, another virus,
greatly increase HIV infectivity, replication, and
cell killing. He, in other words, thinks that
Montagnier has picked the wrong cofactor.
Wrong or right, the necessity for cofactors to
stimulate HIV activity raises the intriguing question
of whether HIV is actually the cause of AIDS.

--Robert Root-Bernstein
Rethinking AIDS
Page 26

Where we have seen HHV-6A in tissue, we see dead
tissue. And where you see HIV-you know, you can have
HIV alone, and you may see some reactive changes, like
the immune system reacting to a viral infection as if
you have flu or something like that. But you don't see
dead tissue. You don't see destroyed organs and scar
formation, and that's what you see when you see
HHV-6A. We find replacement of the normal architecture
of the lymph nodes with scar tissue. HHV-6A kills it.
It kills the lymph node tissue. If I were to place my
bets--I do think the viruses HIV and HHV-6A are
interactive. I think one of the reasons why you almost
always find both of them is that there are viral
products, some of the gene products that they make,
that enhance each other's replication.
I think they're a team. And, when the two of them are
present, they induce the production of more of each
other. It's a mutually enhancing relationship. It's
our feeling that if you could interrupt or limit or
suppress the HHV-6A infection, the levels of HIV would
go down tremendously and HIV would become just a
chronic viral infection. And, potentially, the
antiviral agents that are out there would be able to
manage that. We don't have any evidence, looking in
the tissue, that HIV is responsible for any of the
destruction. And, if you think about it, HIV infects
patients for years-a decade or more-without
progressing to AIDS. When you look in their tissues,
you have to ask how you can have such a long-term
viral infection and have no damage? Then something
seems to happen somewhere in their course of disease.
In some people, it happens earlier; in some people, it
happens later; and there's that small percentage of
people in whom it never seems to happen at all. Our
hypothesis would be that, if we were to look in the
lymph nodes of the long-term non-progressors, we would
not find HHV-6A.

--Konnie Knox
HHV-6 Researcher
An interview with Neenyah Ostrom in "New York Native"
http://www.chronicillnet.org/online/Knox.html

A microbiologist at the University of California,
Duesberg was relentlessly attacking Gallo's view of
HIV as a killer. The point I had raised in particular
was Duesberg's questioning of Gallo's recent interest
in so-called co-factors that helped HIV overwhelm the
immune system. Anyone who bothered searching for a
co-factor, Duesberg reasoned, was obviously unclear of
the actual cause of a disease.

--Nicholas Regush
The Virus Within
page 20

Although Gallo made a strong effort to encourage
researchers to consider the potential of HHV-6 as a
possible co-factor in AIDS, he could not break down
the resistance to the idea that a common virus could
be such a killer.

--Nicholas Regush
The Virus Within
page 54

Knox was fascinated by how HHV-6, like HIV, attacked
T-4 lymphocytes, monocytes and macrophages.

--Nicholas Regush
The Virus Within
Page 69

The 34 autopsy samples harvested from nine people who
had died of AIDS were sent from a Milwaukee hopsital
to the Carrigan lab "fixed" in formalin, a
disinfectant and preservative for biological
specimens, and embedded in paraffin. Soon after the
package arrived in the summer of 1993, Konnie Knox
eagerly yet meticulously analyzed each sample by
drawing on elaborate procedures that determine whether
or not a viral infection is active at the time of
death.
In this first phase of her doctoral project since
being admitted to graduate school, Knox was expecting
to find evidence that HHV-6 played a role in the
development of AIDS. It was turning out that he virus
could be awakened in people with immune-system
defects. It stood to reason the same would apply among
AIDS patients. But she did not anticipate just how
much HHV-6 infection she would find.
The results of her experiments gave her a jolt: all 34
tissue samples of lung, lymph node, liver, kidney and
spleen revealed that at the time of death there was
active HHV-6 infection, as opposed to merely a
biological sign that the virus was "latent" (embedded
in the tissue). Since these tissue types had been
provided for almost all the cases, Knox was also able
to determine that the active infection had become
widespread.

--Nicholas Regush
The Virus Within
Page 83

Knox was particularly struck by the magnitude of HHV-6
lung infected tissue. HHV-6 had attacked the lungs of
all nine of the deceased. In one of the six patients
who had died from respiratory failure, the density of
HHV-6 infection was so great that she suspected the
virus was directly to blame. Previously, the cause of
this patient's lung disease had not been diagnosed.
Here was a likely example of how the virus could cause
lethal organ damage in someone with AIDS.

--Nicholas Regush
The Virus Within
Page 84

In November 1993, Robert Gallo's lab published data
gleaned from autopsies of five people who had died of
AIDS, demonstrating an abundance of HHV-6 infection.
Footprints of the virus were found in areas such as
cerebral cortex, brain stem, cerebellum spinal cord,
tonsil, lymph nodes, spleen, bone marrow, salivary
glands, esophagus, bronchial tree, lung, skeletal
muscle, myocardium, aorta, liver, kidney, adrenal
glands, pancreas and thyroid.

--Nicholas Regush
The Virus Within
Page 85

The culmination of these efforts came in April 1993,
when scientists at NCI demonstrated in the laboratory
that HHV-6 infects and kills natural killer cells.
these are the immune cells that destroy abnormal cells
in the body, particularly those that are infected by
viruses. HHV-6 is the first virus known to be capable
of targeting and seriously damaging such a vital
element of the immune system's antiviral defenses.
In both the Gallo and Carrigan labs, it did not escape
notice that natural killer cell function is, in
varying degrees, disabled in both AIDS and chronic
fatigue syndrome.

--Nicholas Regush
The Virus Within
Page 87

Knox sensed that she could break new ground in showing
how HHV-6 behaves in AIDS patients. She knew that the
virus was extremely active at the time of their
deaths. She also had learned it could cause major
damage to lymph nodes during the early development of
AIDS. Now she wanted to know how early such damage
occurred. Could it be even before AIDS was diagnosed?
That would be an eye opener--an unheralded virus
causing damage considered the sole handiwork of HIV.
But such a finding would not come as a shock to Knox,
considering the nodes were loaded with lymphocytes,
the chief targets of HHV-6.

--Nicholas Regush
The Virus Within
Page 89

Following her instincts, Knox decided to focus on
macrophages, the large scavenger cells that serve as
the lungs' first line of defense against a variety of
infections. Her autopsy-tissue study had already shown
that macrophages were often depleted in the lungs of
HIV-infectd AIDS patiens, and she now wanted to know
how HHV-6 was capable of knocking out those cells. Her
tests showed that, besides destroying macrophages,
HHV-6 interfered with the normal functioning of the
scavenger cells by blocking the release of a type of
oxidant, a substance the cells normally generate to
attack microbes. Knox noted that HIV was not known to
be capable of this specific type of action. She
concluded that, at the very least, HHV-6 could
contribute to the depletion of the macrophages in the
lungs. This in turn woud weaken the immune system,
leaving the body vulnerable to a host of infections
that were normally well controlled.
Did HHV-6 help HIV destroy macrophages in the lungs?
Not necessarily. HHV-6 apparently had the potential to
do a brutally effective job on its own. Perhaps HIV
was giving HHV-6 a boost, not the other way around. Or
more provocative yet, Knox wondered, was HIV doing any
killing in the body, or was HHV-6 the lone assassin?
Clearly, heresy was incubating in the Milwaukee wing
of AIDS science.

--Nicholas Regush
The Virus Within
Page 95

More work in the lab led Knox to further appreciate
the trouble HHV-6 could play in AIDS. She noted that
blood problems are common in AIDS, but the AIDS
scientific community had been far from clear on
whether HIV is actually able to disturb the bone
marrow's normal blood-manufacturing processes. Knox
now wondered whether HIV was really doing anything.
Knox's lab studies demonstrated that HHV-6-infected
marrow cells--not the HIV-infected ones--blocked the
ability of the marrow to produce mature,
differentiated cells.

--Nicholas Regush
The Virus Within
Page 97

Knox obtained lymph-node biopsies from 10 people
positive for HIV and found that all were actively and
predominantly infected with HHV-6A. She also
discovered the colonization had mostly occurred early
on, as suggested by T-4 lymphocytes counts that were
higher than the cut-off point of 200, which qualifies
someone for an AIDS diagnosis. One HIV-positive
individual's biopsy had even produced a count of 711.
HHV-6 was clearly active and reproducing itself before
AIDS had even been diagnosed.

--Nicholas Regush
"The Virus Within"
Page 98

When Knox studied the brains of six people who died of
AIDS and found extensive damage in four to their nerve
fiber sheaths, she also detected active HHV-6
infection. The infected cells were only in areas where
the damage had occurred and never in healthy tissue.
The damage tissue tested negative for signs of HIV,
CMV, and other microbes. Again, there was only HHV-6.

--Nicholas Regush
The Virus Within
Page 101

Joseph Sonnabend, the New York doctor who was one of
the first to care for AIDS patients, placed CMV high
on his list of key suspects for his multiple-factor
theory of how AIDS developed. He had studied many gay
men heavily infected by CMV. Donald Francis, a
researcher at the Center's for Disease Control in
Atlanta also advanced CMV as a possible cause of AIDS,
based on evidence that the virus infected the brains
of AIDS patients. . . . Scientists such as Sonnabend,
Francis, and the many others who proposed CMV early n
as a possible cause of AIDS did not have the benefit
of knowing that a similar, but in many ways a more
immune-destructive, herpes virus would soon be
unearthed by none other than Gallo and his NCI team.
What they thought was caused by CMV might at least
sometimes, if not often, have been caused by HHV-6.

--Nicholas Regush
The Virus Within
Page 102

Science is not a democracy, Knox was learning. Science
sometimes punishes people for pursuing the truth.

--Nicholas Regush
The Virus Within
Page 113

The latest results were straightforward yet
provocative: 16 lymph-node biopsies from HIV-positive
patients all contained cells actively infected with
HHV-6A. Twelve of 16 patients who had been diagnosed
with progressive disease had more dense infection than
the four patients who had been diagnosed as having a
stable condition. Knox and Carrigan also found more
dense infection in areas where the lymph nodes were
losing lymphocytes than in areas free of destructive
change or where normal tissue in the nodes was already
being replaced by the formation of scar tissue. HHV-6
was the apparent cause of the destruction of lymphoid
tissue that occurred in these HIV-positive people.
HHV-6 was not only at the scene of the crime, but it
appeared to have committed the crime as well. While
the evidence was not conclusive, it was closer than
Knox and Carrigan had ever come in their detective
work. In contrast, there were no convincing studies
demonstrating that HIV could cause similar pathology.
Studying the findings, Knox and Carrigan looked at one
another and wondered if they'd found a smoking gun.

--Nicholas Regush
The Virus Within
page 114

In the meantime, they [Knox and Carrigan] learned that
the scientific paper they had written on detecting
active HHV-6 in the lymph nodes of people with AIDS
would not be published by "The Lancet." Since they
believed that the research presented the smoking gun
that HHV-6--not HIV--was what destroyed lymphoid
tissue in AIDS, the rejection by the journal was a
blow.

--Nicholas Regush
The Virus Within
Page 183

When asked why he has neglected HHV-6 research after
promoting the virus for a couple of years as a likely
co-factor in AIDS, Gallo explained that about the time
that he felt he was making some inroads in HHV-6,
aggressive congressional investigations were looking
into reports that he had mismanaged his scientific
work on HIV. There simply was not enough time to
pursue HHV-6 as much as he would have liked, giving
his ongoing HIV research.
Gallo spoke very generously about what Knox and
Carrigan had accomplished, but he emphasized that they
work in too much obscurity to obtain any funding.
"They have clearly shown that HHV-6 is a powerful
pathogen," Gallo said. "If they were headliners at a
major university it would have made a difference."
In other words, if they had the kind of financial
backing and prestige he had, there would be a lot of
interest in HHV-6.

--Nicholas Regush
The Virus Within
page 223

She [Knox] won't divulge her views on AIDS science.
for one thing, she and Carrigan do keep an open mind
on HIV. But their research on HHV-6 has taught them
that the virus often appears to be doing what HIV is
supposed to be doing in different parts of the body
such as lymphoid tissue and brain tissue: it is
killing cells. Their research also suggests that HIV
may not always be necessary as a companion to HHV-6
when the herpes virus is destroying tissue. But even
suggesting this in writing would raise the hackles of
HIV researchers. In fact, some AIDS scientists compare
any questions of the HIV hypothesis, as it currently
stands, to denial of the Holocaust. With such emotions
running strong in AIDS science, why take a chance of
boldly presenting alternative hypotheses?

--Nicholas Regush
The Virus Within
Page 224

Knox and Carrigan, while aware of the issues, want no
active part of this often hostile debate. They can't
see that it holds any immediate consequences, one way
or the other, for their scientific work on HHV-6. They
will continue to document their findings and make an
all-out effort to get the data out. Then their
scientific peers can judge for themselves. If in the
end, they won't make a dent in the current HIV theory,
then it won't be for a lack of solid HHV-6 data. And
furthermore, HHV-6 is much more than a virus that
appears to play a powerful role in AIDS. They have
tracked it step by step through a host of other
trouble that it causes in the bone marrow, lungs and
brain tissue of transplant patients. It's active in
the blood of up to 70 percent of people with chronic
fatigue syndrome that are tested. And Knox and
Carrigan also find it active in the blood and brain
tissue of people with MS.

--Nicholas Regush
The Virus Within
Page 225

Google Report

Number of results for "HIV" today on Google:
47,600,000

Number of results for "HHV-6" today on Google:
64,800

But the future belongs to HHV-6.

A Question for Dr. Joseph Brewer

Dr. Joseph Brewer has offered an interesting paradigm
for Chronic Fatigue Syndrome as a kind of variable HHV-6A
Syndrome. Click here for an explanation of the
paradigm:
http://www.plazamedicine.com/hhv6/hhv6_1.html

Here's our question. Where is the HHV-6A Syndrome
epidemic in the gay community? HHV-6A is transmitted
in a number of ways, including sexually. One would
expect there to be a major epidemic in the gay
community. So where is it?

This rhetorical question was addressed a few years ago
(in a slightly different way) in the Op-ed piece below.

Where is the Massive Gay Chronic
Fatigue Syndrome Epidemic?

By Charles Ortleb

While AIDS has dominated the medical news for the last
two decades, another potentially major epidemic which
the media has generally ignored or minimized, has
grown exponentially. Originally mocked as "Yuppie
Flu," the name "Chronic Fatigue Syndrome (CFS)"
eventually evolved into what is now known as "Chronic
Fatigue and Immune Dysfunction Sydrome (CFIDS)."

The Centers for Disease Control and the National
Institutes of Health (for very mysterious reasons)
have been slow to respond to the potentially
catastrophic epidemic of CFIDS which began to manifest
itself at the same time as AIDS. Given that there have
been many reports of CFIDS breaking out in families,
schools, and communities, there is little doubt among
serious observers that it is contagious. If this is
so, why is it not spreading like wildfire in the gay
community? What biological wall around the gay
community has prevented CFIDS from being a major gay
health problem?

Neenyah Ostrom, who reported on CFIDS for a decade at
"New York Native," has written three books giving a
detailed history of the research on CFIDS. She has
reported on a long list of symptoms and immune
aberrations have been found in Chronic Fatigue
Syndrome; virtually all of them can also be found in
AIDS patients. These include problems with T-cells,
natural killer cells, B-cells, and monocytes. There
are serious neurological, digestive and cardiac
symptoms that AIDS and CFIDS share. Where are all the
gay men with the often serious CFIDS problems? Do they
have some special immunological protection against
CFIDS? Or is it that every gay person who has AIDS
also has CFIDS? How does that work? How do doctors
treat CFIDS in an AIDS patient? How come we never read
anything about that?

The medical literature is full of suggestions that, at
the very least, CFIDS is AIDS-like. Some research
suggests that an even stronger statement about its
relationship to AIDS could be made. Nancy Klimas, one
of the pioneering CFS researchers, led a team of
scientists who concluded in 1990 that Chronic Fatigue
Syndrome could be considered "a form of acquired
immunodeficiency." Paul Cheney, one of the first
medical doctors to look closely at the epidemic of
CFS, has referred to it as "AIDS minor." Others have
somewhat bizarrely called it an epidemic of something
that could be called the "mirror-image of AIDS." Well,
what about the gay community? Where is the epidemic of
the "mirror image of AIDS" in the AIDS-besieged gay
community? What is the difference between a gay person
with AIDS and a gay person with "the mirror-image of
AIDS." I bet that virtually no members of the gay
community are aware that there could be thousands of
members of their community with the contagious "mirror
image of AIDS."

Saying that CFIDS is not a fatal condition and doesn't
deserve any serious attention is not really a
fact-based statement. A number of people with CFIDS do
seem to have died of complications of their
conditions. A Massachusetts-based organization for
CFIDS patients has a page of obituaries in every issue
of their newsletter and many of the deceased people
they report on seem to have died from problems related
to their CFIDS. When was the last time you heard of a
gay person dying of complications of CFIDS? And even
though it may not always be fatal, many CFIDS patients
describe their lives as living hells. Why do we not
read a steady stream of stories in gay publications
about gay people coping with CFIDS?

Some estimates of the number of people suffering from
CFIDS in the United States go as high as 14 million.
If we use the 5% number which is often used to
estimate the number of gay people in America, where
are the 700,000 cases of CFIDS in the gay community?
How about just 100,000? That should still be a
noticeable blip on the medical radar screen.

The gay community has been living under a medical
microscope for two decades. If there is a major
contagious epidemic that is AIDS-like, one would think
that there would be all kinds of studies of this
AIDS-like epidemic in the gay community. Some people
seem to have made careers out of studying the
illnesses of gay people. And yet one never hears of
public health warnings about the transmission of CFIDS
in the gay community. There are no gay CFIDS
commissions, no gay CFIDS ribbons, no gay CFIDS subway
posters, no GAY CFIDS benefits, no CFIDS quilts.

If the worst estimate of CFIDS incidence is accurate, it would
seem reasonable to suggest that for every gay AIDS
patient a gay doctor has in his practice, he should
have one or two--or more--gay CFIDS patients. And given the
similarity of their symptoms, how does the doctor keep
his patients straight? It is theoretically possible
that a new AIDS patient will have more T-cells than an
old CFIDS patient. If a gay person has the symptoms
and immune abnormalities of CFIDS which look just like
the symptoms and immune abnormalities of AIDS, and
tests negative for HIV, is he given a clean bill of
health? And why are gay doctors not warning the gay
community about the possibility of contracting CFIDS
and giving it to others? Gay people are issued every
other imaginable kind of medical and lifestyle
warning. Why none for CFIDS?

Are we supposed to believe that the gay community is
somehow miraculously immune to CFIDS? That would
certainly be a fascinating finding. And perhaps a
bogus one too. There is a far more parsimonious
explanation for why we don't hear about a massive
CFIDS epidemic in the gay community. Let's just say
for now that it is very curious that most CFIDS
patients tend to be neither gay nor Black while most
AIDS patients tend to be gay or Black or both. Nothing
political is going on here, right?

Gay men are told that the key to protecting their
immune system is knowing the HIV antibody status of
their partners. But what if their partners have CFIDS?

Why are gay men and lesbians not warned to ask
about the CFIDS status of their partners, and not
urged to inform their partners if they have any CFIDS
symptoms? For that matter, given that CFIDS has been
presented by research an an essentially heterosexual
AIDS-like illness, why are heterosexuals not warned
about transmitting or contracting CFIDS? Where are
CFIDS warning posters in heterosexual bars?

Needless to say, I think there is a Pandora's Box of a
story here. It is one that could lead to a change in
the way we look at AIDS and CFIDS. It might even lead
to a major medical and scientific paradigm shift.

But for the time being, can someone just answer this
simple question: where is the major epidemic of
Chronic Fatigue Syndrome in the gay community?

HHV-6 Transmission

"Sexual, horizontal, and vertical transmission have
been suggested."

http://www.immunesupport.com/library/showarticle.cfm/ID/1372/

From: "Epidemiology of human herpesvirus 6 (HHV-6)
infection in pregnant and nonpregnant women," J Clin
Virol 2000 May 1; 16(3):149-157. Departments of
Pediatrics, and Obstetrics and Gynecology, The
University of Texas Health Science Center at San
Antonio, 7703 Floyd Curl Drive, San Antonio, TX, USA

Pig to Human Porcine CMV Transmission: What about HHV-6 transmission between people and pigs?

"Given the high frequency of seropositivity of swine
for PCMV and the efficiency of transmission of HCMV
from donor to transplant recipient (6), PCMV may
represent another potential risk to humans."

From "Quantitation of Porcine Cytomegalovirus in Pig
Tissues by PCR" by Jacqueline F. L. Fryer, Paul D.
Griffiths, Jay A. Fishman, Vincent C. Emery, and
Duncan A. Clark published in Journal of Clinical
Microbiology, March 2001, p. 1155-1156, Vol. 39, No. 3

http://jcm.asm.org/cgi/content/full/39/3/1155

It is interesting to see pigs and HHV-6 mentioned in
the same paper which ends this way: "In conclusion,
this report describes the development and application
of a QC-PCR assay for the quantification of PCMV,
similar to assays currently used in our laboratory for
the quantification of human herpesviruses including
HHV-6, HHV-7, and HCMV (2, 7, 9). This assay will be
useful in further studying the pathogenesis of PCMV
and will enable the detection and accurate
quantification of PCMV in porcine organs in pigs being
bred for use in xenotransplantation."

How much does PCMV have in common with HHV-6?
Check this out:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11778702&dopt=Abstract

Joseph Brewer on HHV-6 Transfer Factor for CFS and HHV-6 Viremia

Administration of Transfer Factor for Human
Herpesvirus 6 (HHV-6) in Patients with Chronic Fatigue
Syndrome and HHV-6 Viremia

By Joseph H. Brewer MD, Plaza Internal
Medicine-Infectious Disease and Saint Luke's Hospital
(Infectious Diseases), Kansas City, Missouri and Greg
B. Wilson PhD, BioLogics, Inc., Greenville, South
Carolina

Abstract
Chronic fatigue syndrome (CFS) has been associated
with active HHV-6 infection. CFS has also been
associated with immune dysfunction, especially with
regard to natural killer (NK) cell function. Since the
active infection may be playing a key role in CFS and
the associated immune dysfunction, we wanted to study
the effects of a transfer factor (TF) with activity
for HHV-6 in CFS patients. 28 CFS patients were given
a TF preparation derived from bovine colostrum that
has activity against HHV-6. Patients were analyzed
baseline and monthly for 6 months for symptoms
utilizing a scored symptom profile analysis and
natural killer cell function assays. 10 CFS patients
(controls) received a similar TF preparation derived
from bovine colostrum except that it was devoid of any
specific activity for HHV-6. Following the
administration of the HHV-6 TF preparation,
improvements were noted in symptom scores in 68% and
NK function in 75% of patients studied, as compared to
0% for both symptom score and NK function in the
control group taking the TF preparation without HHV-6
TF activity (p< 0.001). Symptom scores in the HHV-6 TF
group decreased from a baseline average score of 76 to
an average value of 41 after the TF. This represented
an average decrease of 35 points (+/- 15.2, p<
0.0001). NK function in the HHV-6 TF group improved
from a baseline average of 8 LU to an average of 54 LU
after the TF. The average increase from baseline on
treatment was 46 LU (+/- 22.8, p< 0.0001). No change
from baseline was noted in the control TF group for
either parameter. No significant adverse effects were
noted in either patient group. Patients with CFS and
documented HHV-6 viremia improved both symptomatically
and immunologically (NK function) after administration
of a TF preparation with activity for HHV-6. TF may be
important in the treatment of CFS and the associated
active HHV-6 infection.

http://www.immunitytoday.com/hhv6article.html

Human herpesvirus-6 reactivation in a longitudinal study of two HIV-1 infected patients.

An article by Iuliano R., Trovato R., Lico S., Luppi
M., Forastieri G., Barsanti LA., Pizzigallo AM.,
Mecocci L., Barozzi P., Torelli G., Mazzotta F. and
Ceccherini-Nelli L. in the Journal of Medical
Virology:

http://virmap.unipi.it/cgi-bin/virmap/vmibo?doc_pubbl:9519052;main;art

This abstract suggests HHV-6 plays a major role in
AIDS:

"After primary infection, human herpesvirus-6 (HHV-6)
persists in latent form and can be reactivated in
immunocompromised subjects. A longitudinal study of
HHV-6 infection was carried out in two HIV-1
seropositive patients to provide in vivo evidence of
HHV-6 reactivation. Concomitant with a significant
rise of anti-HHV-6 IgG detected by IFA, a transient
increase of HHV-6 viral load was shown in PBLs by PCR.
During HHV-6 reactivation it was also identified
either cell-free HHV-6 by PCR in plasma or IgM
antibody titers. HHV-6 reactivation was followed by a
temporary decrease in CD4+ count and by a progressive
dramatic loss of CD4+ during the following 18 months.
HHV-6 strain characterization by PCR demonstrated that
first patient (MM) initially showed the B variant,
followed by reactivation and persistence of the A
variant, while in the second (SG) only the A variant
was detected. The evidence of HHV-6 reactivation
suggests its involvement in immunologic damage
underlying the disease."

The Strongest Case for the Role of HHV-6A in AIDS

This research conducted by Konnie Knox and Donald
Carrigan still remains one of the strongest
indications that HHV-6 may be the key to AIDS.
http://www.wisconsinlab.com/hiv.htm

The opening of their paper makes an awesome case for
the role of HHV-6 in AIDS:

"The epidemic of the acquired immunodeficiency
syndrome (AIDS) is in its second decade and continues
its worldwide expansion. In some developing countries,
more than 20% of all adults are infected with the
human immunodeficiency virus (HIV).(1) The successful
use of multiple antiviral drug therapies has been
limited by the complex dosing schedules required and
by the emergence of resistant forms of HIV. Work on
vaccines to prevent or treat HIV infections continues,
but it appears that an effective vaccine is still
several years away. Clearly, there exists a need for
new strategies in the treatment of HIV disease,
especially if these strategies can provide new targets
for effective pharmaceutical or immunological
therapies. Human herpesvirus six (HHV-6) may serve as
an important cofactor in the pathogenesis of AIDS and
may provide an alternative target for therapeutic
intervention.

Destruction of lymphoid tissues is the root cause of
the severe immunodeficiency that characterizes AIDS.
The reasons for this tissue destruction remain
unclear. Because high levels of HIV are present in
lymphoid tissues for years before damage begins, HIV
is unlikely to be the direct cause.(2) In addition,
many of the dying cells in the lymphoid tissues of HIV
infected patients are not infected with HIV.(3) Thus,
the event that first triggers the progressive
destruction of HIV infected lymphoid tissues remains
to be defined."

That the Knox and Carrigan work on HHV-6A has not been
recognized as paradigm-challenging by the HIV
establishment is one of the great medical tragedies of
our time.

AIDS ANIMAL HOUSE

From a story by John Solomon (The Associated Press
Sunday, July 3, 2005; 9:27 PM).

"WASHINGTON -- The government's AIDS research agency
'is a troubled organization' and its managers have
engaged in unnecessary feuding, sexually explicit
language and other inappropriate conduct that hampers
its global fight against the disease, an internal
review found."

Grab a toga and go into AIDS research!

Press Release From Hemispherx Biopharma on Ampligen's Impact on Chronic Fatigue Syndrome

The following press release was issued today by
Hemispherx Biopharma, Inc.

New Government Sponsored Research Points to Gene
Malfunction in Chronic Fatigue Syndrome (CFS)

PHILADELPHIA--(BUSINESS WIRE)--July 6, 2005--
Exercise Induced Malfunction in Genes Provides New
Potential Insight into Mechanism of Ampligen(R) Phase
III Clinicals; Exercise Treadmill Improvement as
Primary Efficacy Endpoint

Hemispherx Biopharma, Inc. (Amex:HEB) announces that
newly published independent studies from Center for
Disease Control (CDC) researchers provide molecular
evidence on the central role of exercise intolerance
in the morbidity of patients suffering from CFS.
Although CFS is associated according to CDC criteria
with some 12 other debilitating clinical
manifestations (fever, myalgia, etc.), the overarching
primary symptom is profound exertional fatigue which
undermines the quality of life. Following on its
recent tradition of intense investigation into medical
and economic sequelae of CFS, the CDC now reports
("Exercise responsive genes measured in peripheral
blood of women with CFS and matched control subjects",
BioMedCentral.com/1472-6793/5/5) that a pool of
metabolism (energy) genes, whose function may be
associated with bodily functions such as muscle
contraction and oxygen consumption, are impaired in
women with CFS on exercise challenge. A matched cohort
of sedentary healthy women did not exhibit a similar
pattern of gene malfunction. Other exercise induced
gene abnormalities were also noted, apparently
involving the immune system.

Gene abnormalities, such as those described by the CDC
researchers, might be the result of inherited weakness
in energy transfer/metabolism, or - in the alternative
- the gene weakness might be caused by various
environmental factors such as exogenous viruses and/or
noxious agents such as chemical toxins. Further
clinical and molecular research will be needed to
distinguish between these various etiological
possibilities.

Exercise treadmill impairment is already a recognized
"end point" to quantify disability in various chronic
diseases, particularly including CFS. Thus, the US
Social Security Administration (SSA) has implemented a
policy of recognizing the functional impairment on
treadmill performance as the basis for partial or
complete disability - thereby qualifying CFS sufferers
for long-term governmental subsidies (partial, or
complete financial support). The average age of onset
of CFS is about 35, coinciding with the peak of
professional achievement and income potential.

Accordingly, Hemispherx adopted the exercise treadmill
testing as the primary therapeutic (efficacy) endpoint
in its recently completed Phase III Study (active drug
vs. placebo in a one-to-one randomization) of 234
patients evaluated for 64 weeks. By predetermined
regulatory/scientific criteria, the drug arm evidenced
certain medically and statistically significant
changes over the placebo arm. These clinical effects
were recently summarized at the peer reviewed XVIII
International Congress in Barcelona, Spain. Separate
investigations have indicated that double-stranded RNA
drug molecules (of which Ampligen(R) is an example)
may activate a battery of human genes. Thus it appears
that the physical performance changes observed on
treadmill testing might be due in part to changes at
the gene level. While gene modulation studies were
conducted apart from the recently completed Phase III
studies (which relied on clinical endpoints) parallel
in vitro studies on interferon inducers (such as
double-stranded RNAs) have suggested a possible role
in modulating gene activity associated with energy
transport and metabolism.

About Hemispherx

Hemispherx Biopharma, based in Philadelphia, is a
biopharmaceutical company engaged in the manufacture
and clinical development of new drug entities.
Hemispherx's flagship products include Alferon N(R)
and the experimental antiviral products, Ampligen(R)
and Oragens(TM). These novel Alferon-N proteins,
commercially available for a category of STD
infection, and experimental nucleic acids are being
developed for globally important chronic diseases and
disorders of the immune system including HPV, HIV, CFS
and hepatitis and avian flu. Its four major technology
platforms include large-and small-agent components for
potential treatment of various chronic viral
infections, and are being developed with various
corporate, governmental and academic collaborators
worldwide. Hemispherx has in excess of 150 patents
comprising its core intellectual property estate, a
fully commercialized product (Alferon N(R)) and GMP
certified manufacturing facilities for its novel
pharma products. Presently it is expanding its
facilities to accommodate GMP production of
Ampligen(R). For more information please visit
www.hemispherx.net

Information contained in this news release other than
historical information, should be considered
forward-looking and is subject to various risk factors
and uncertainties. For instance, the strategies and
operations of Hemispherx involve risk of competition,
changing market conditions, change in laws and
regulations affecting these industries and numerous
other factors discussed in this release and in the
Company's filings with the Securities and Exchange
Commission. Any specifically referenced
investigational drugs and associated technologies of
the company (including Ampligen(R) and Oragens) are
experimental in nature and as such are not designated
safe and effective by a regulatory authority for
general use and are legally available only through
clinical trials with the referenced disorders. The
forward-looking statements represent the Company's
judgment as of the date of this release. The Company
disclaims, however, any intent or obligation to update
these forward-looking statements. Only Clinical
Studies under well-controlled conditions can establish
efficacy and safety of any product. Clinical trials
for other potential indications of the approved
biologic Alferon N do not imply that the product will
ever be specifically approved commercially for these
other potential treatment indications.