Re: Why doesn't bum-f%&king act like a vaccine against AIDS

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Date: 7 Oct 2004 19:36:11 -0700

The following post expresses my opinions, unless otherwise noted:

I want to see the data from the experiment that demonstrated HIV
activity in asymptomatic patients, causing the CD4T+ cell depletion
directly, and leading to “AIDS.” That experiment was
never done, and guess what? Now the “mainstream” agrees
(at least those who don’t have their heads all the way up their
you-know-whats, like Ho). For example:

“Researchers affiliated with the Gladstone Institute and the
University of California at Berkeley suggest that the previous theory,
 with its presumed flurry of T-cell output, was an illusion of faulty
assumptions and poor measurement techniques. The Bay Area scientists
used a newly developed molecular tag to track the ebb and flow of
helper T cells. They spent more than a year studying immune systems in
healthy people and in 21 AIDS patients being treated at San Francisco
General Hospital. This produced what the authors described as the
first direct clinical measurements of immune-system activity both in
AIDS patients and an uninfected control group.
Results found no T-cell speed-up-and-collapse pattern in the infected
people. What researchers found instead was that, along with reduced
cell longevity, the virus caused slower cell production -- the
opposite of what had been assumed to occur during this critical stage
of the disease. Just how the AIDS virus might damage T-cell production
has yet to be unraveled. [so you are assuming that because the people
are HIV-antibody positive, any problems they have are the result of
having neutralized HIV – this is in contradiction to all
knowledge of viruses, and retroviruses in particular] And there are
as yet no proven therapies to address the new view of the disease,
which would call for treatments that defend the immune system,
insulating it from HIV or making it robust enough to withstand the
virus. By comparison, today's therapies take direct aim at stopping
the virus from reproducing.
An editorial in Nature Medicine portrayed the UCSF-Berkeley study as
definitive evidence, but Ho indicated through a spokeswoman at the
Aaron Diamond AIDS research center in New York that he is not yet
convinced. Greene, by contrast, called the new study a "paradigm
shift." "This completely alters the way we think about the
pathogenesis of AIDS," he said. By all accounts, the AIDS virus
infects and kills T cells. The argument is whether that's the main
cause of fatal illness or if something else is at play.
"This study tells us HIV does two things," said UCSF researcher Joseph
McCune. "It does destroy cells, but its main affect appears to be on
the systems of cell production. What that tells us is that we have to
get rid of the virus, no question about that, but we really need to
focus our attention on the systems of cell production."
.Old view: 1. Multiplying HIV particles infect T cells. 2. Immune
system responds by cranking up production of new T cells in an effort
to keep pace with the virus. 3. In the end stage of disease, the
immune system collapses from exhaustion.
New view: 1. HIV infects mature T cells, but not in sufficient
numbers to explain how the disease progresses.
2. Researchers suspect that the virus may attack the immune system's
cell-making capacity. 3. Final stage of disease caused primarily by
collapse of immune system and reduced lifespan of T cells. HIV virus
attacks T cell production system, probably in bone marrow and
thymus.”

Source: http://www.bonusround.com/dickie/research1.html

Note that they say: “Just how the AIDS [meaning HIV, of course,
though they do like to be confusing whenever possible, it seems] virus
might damage T-cell production has yet to be unraveled.” My
point is that there is no known mechanism that could exist in this
universe that could do such damage! So we’re either dealing
something that will render the know “laws” of biochemistry
and virology worthless, or we are dealing with a simple, human rush to
judgment by people who had everything to gain by doing so, and
everything to lose by not doing so. Also notice that we hear things
like “suspect” and “no question about it”
(then there’s “devious,” “paradoxical,”
“puzzling,” etc. – you’ve heard these words
used to describe HIV if you’ve kept up with the literature, and
they are words used by scientists who are wrong about their
“theory”). A scientist quotes an experiment, he/she
doesn’t say there’s no question about it, because science
is simply where the evidence points at a given time. The problem
occurs when the “experts” who decide for those who
aren’t scientists where the evidence seems to point are
conflicted, corrupt, fearful, or not particularly competent. There
are countless examples of assumptions with no solid evidence to
support them in the biological sciences today, such as the
“lipid bilayer,” which is supposed to withstand tremendous
shearing forces, but without any chemical bonds (see Gilbert
Ling’s works for definitive refutation). Then there’s the
notion of “essential fatty acids,” which turn out to be
the most dangerous “food” people are consuming in large
amounts in the “advanced” nations. Cholesterol, salt,
fat, etc. Back to the main point here, which is that they (Gladstone)
are saying that they know the immune system is declining in many
“AIDS” patients, but they can’t make the direct
connection with HIV. If a scientist wants to make an extraordinary
claim, such as this, he/she had better have extraordinary evidence.
All Duesberg is saying is that if you’ve got a claim that
violates everything that’s know about biochemistry, virology,
etc., then you better have more than anecdotal evidence and flawed
clinical trials before you abandon other possibilities and subject
people to dangerous prescription drugs. For that he’s been
called a madman (or worse). The reason is that those whose
reputations rest on such shaky foundations try and get the masses to
allow emotion to cloud their judgment. Asking me if I’d be
willing to become HIV infected is just such an example. If I’m
alive 30 years from now, what would you say? What would the
establishment people say? “Oh, he must have strong
genes.” I may have strong jeans, but the strong genes argument
can always be used when a scientist errs badly. It’s like a
general saying that things could have been worse, even though his men
got slaughtered due to his mistakes. Here’s my proposal.
I’ll be glad to become HIV antibody positive (but without any
other substances – just the virus itself), but you’ve got
to take all the retroviral medication that is being given to those
with full insurance coverage in the USA – until you die, which
will likely not take very long. I get the retail cost of these drugs
at today’s prices to “treat” myself, for as long as
I live. So if the drugs cost $35,000 a year retail price, I get that
every year from now on, for the remainder of my life, guaranteed.
Also, asking about friends is not scientific. It’s none of your
business who my friends are. You just don’t have the goods, and
this is the best you’ve got, that is, an emotional appeal with
no scientific grounding. I’ll take your money if you’d
like, but it’s sad. However, you won’t get me to bite on
name calling, because I’m only interested in it scientifically
(and economically, if I can get someone to pay me that $35,000 a year
or so).

Another proposal: you get Gallo, Montagnier, the head of the NIH or
CDC, Ho, etc. (any one will be fine) to agree to a debate with
Duesberg in public, with full press coverage, moderated by a
journalist or scientist who has never professed personal views on
HIV/AIDS (at least in public), using typical high school debate team
rules. If you can do that, I’ll get Duesberg for you
(he’ll be licking his chops over the opportunity). A debate was
already arranged by a journal to have Duesberg debate Montagnier via
fax machine. After Montagnier read what Duesberg wrote (Duesberg was
first to make a statement), Montagnier made some ridiculous excuse not
to continue, and then not long after unveiled his mycoplasma co-factor
claim, which may be more pathetic than the original HIV/AIDS claims.

What is the treatment I will give myself if you accept my proposal?
Fresh coconut products, dark chocolate, organic butter, raw goat milk
cheese, organic eggs, organic fresh and dried fruit, some organic
broccoli florets, organic white tea, and absolutely no polyunsaturated
fatty acids, except for the small amounts found in the foods listed
above. Also, digestive aids, including stomach acid (betaine HCl),
and pepsin, and at least 9 hours of sleep a night.

As for the arachidonic acid/HIV connection, see below:

“Free Radic Biol Med. 1997;22(1-2):195-9.

Activation of human immunodeficiency virus long terminal repeat by
arachidonic acid.

Carini R, Leonarduzzi G, Camandola S, Musso T, Varesio L, Baeuerle PA,
Poli G.

Department of Experimental Medicine and Oncology, University of
Torino, Italy.

Arachidonic acid is the precursor of highly reactive mediators,
including prostaglandins and leukotrienes, and the most abundant n-6
polyunsaturated fatty acid in mammalian cell membranes. It is released
from phospholipids upon many inflammatory stimuli. In this study, a
chloramphenicol acyltransferase reporter gene, under control of the
human immunodeficiency virus-1 long terminal repeat, was strongly
induced upon treating human promonocytes with arachidonic acid. The
n-3 fatty acid eicosapentenoic, found in abundance in fish oil, had no
effect. HIV-1 long terminal repeat activation by arachidonic acid was
suppressed by inhibitors of both lipoxygenase and cyclooxygenase
pathways, suggesting that metabolites, rather than arachidonic acid
itself, mediated the stimulatory effect. This is the first report
linking HIV-1 expression to the metabolism of arachidonic acid.”

”J Neurochem. 2000 Jul;75(1):196-203.
  
HIV-1 coat glycoprotein gp120 induces apoptosis in rat brain neocortex
by deranging the arachidonate cascade in favor of prostanoids.

Maccarrone M, Bari M, Corasaniti MT, Nistico R, Bagetta G,
Finazzi-Agro A.

Department of Experimental Medicine and Biochemical Sciences.
"Mondino-Tor Vergata" Center for Experimental Neurobiology, University
of Rome "Tor Vergata," Rome, Italy.

Human immunodeficiency virus type-1 coat glycoprotein gp 120 causes
delayed programmed cell death (apoptosis) in rat brain neocortex.
Here, we investigated the possible role of the arachidonate cascade
and membrane peroxidation in this process. It is shown that gp 120
causes a rapid increase in the activity and expression of the
arachidonate-metabolizing enzyme prostaglandin H synthase, paralleled
by increased prostaglandin E(2) levels. The selective inhibitor of
prostaglandin H synthase indomethacin inhibited enzyme activity,
reduced prostaglandin E(2) content, and partially protected neocortex
against gp 120-induced apoptosis. Conversely, the activity and
expression of the arachidonate-metabolizing enzyme 5-lipoxygenase
decreased upon gp 120 treatment, as well as the level of its product,
leukotriene B(4). Treatment with gp 120 also reduced membrane lipid
peroxidation, and this may be implicated in the execution of
programmed cell death. These results suggest that early derangement of
the arachidonate cascade in favor of prostanoids may be instrumental
in the execution of delayed apoptosis in the brain neocortex of
rats.”
“Ann N Y Acad Sci. 1994 Dec 15;747:205-24.

AIDS-related dementia and calcium homeostasis.

Lipton SA.

Department of Neurology, Children's Hospital, Boston,
Massachusetts.

Approximately a third of adults and half of children
with acquired immunodeficiency syndrome (AIDS)
eventually suffer from neurological manifestations,
including dysfunction of cognition, movement, and
sensation. Among the various pathologies reported in
the brain of patients with AIDS is neuronal injury and
loss. A paradox arises, however, because neurons
themselves are for all intents and purposes not
infected by human immunodeficiency virus type 1
(HIV-1). This paper reviews evidence suggesting that
at least part of the neuronal injury observed in the
brain of AIDS patients is related to excessive influx
of Ca2+. There is growing support for the existence of
HIV- or immune-related toxins that lead indirectly to
the injury or death of neurons via a potentially
complex web of interactions between macrophages (or
microglia), astrocytes, and neurons. Human
immunodeficiency virus-infected monocytoid cells
(macrophages, microglia, or monocytes), especially
after interacting with astrocytes, secrete substances
that potentially contribute to neurotoxicity. Not all
of these substances are yet known, but they may
include eicosanoids, that is, arachidonic acid and its
metabolites, as well as platelet-activating factor.
Macrophages activated by HIV-1 envelope protein gp120
also appear to release arachidonic acid and its
metabolites. These factors can lead to increased
glutamate release or decreased glutamate reuptake. In
addition, gamma interferon (IFN-gamma) stimulation of
macrophages induce release of the glutamate-like
agonist quinolinate. Human immunodeficiency
virus-infected or gp120-stimulated macrophages also
produce cytokines, including tumor necrosis
factor-alpha and interleukin-1 beta, which contribute
to astrogliosis. A final common pathway for neuronal
susceptibility appears to be operative, similar to
that observed in stroke, trauma, epilepsy, neuropathic
pain, and several neurodegenerative diseases, possibly
including Huntington's disease, Parkinson's disease,
and amyotrophic lateral sclerosis. This mechanism
involves the activation of voltage-dependent Ca2+
channels and N-methyl-D-aspartate (NMDA)
receptor-operated channels, and therefore offers hope
for future pharmacological intervention. This review
focuses on clinically tolerated calcium channel
antagonists and NMDA antagonists with the potential
for trials in humans with AIDS dementia in the near
future.”

I can’t say that HIV is totally harmless, only because if your
body is severely immunocompromised you’ll have all kinds of
viral reactivations, and who knows what the interactions will be.
People don’t realize how rudimentary science is when it comes to
biology, and that’s the reason to stick to the simple realities,
one of which is if there’s no discernable biochemical activity,
then don’t worry about it. However, when you’re full of
polyunsaturates, you’re in trouble, HIV antibody positive or
not. The key is not to allow viral reactivation. Sadly, some people
may have done things to their bodies that are beyond repair.
There’s an interesting experiment that could be done. Let some
HIV antibody positives who refuse retroviral drugs live in the
proverbial plastic bubble (not literally) and avoid all
immunosuppressive substances. Why can’t this be tried? Because
all the money is being pumped into drug trials and high tech nonsense
(if you want to start a camp fire, you use matches, not a flame
thrower).

 Corticosteriods and many other drugs are immunosuppressive, as are
polyunsaturates. Once that happens, you get viral reactivation. And
that takes out your stomach acid. You then go into protein
malabsorption, and “AIDS wasting syndrome occurs.” You
might also get “osteoporosis,” B12 deficiency, etc.
Won’t take too long to finish you off from there – but HIV
is the most minor of players, probably having no adverse effect at
all, unlike CMV, EBV, HHV6A, candida, p. carinii, etc.

Here’s a proposal for all the scientists of the
“mainstream” view. How many would sign the following?

I, ***************, will take the next 3 years to completely solve the
AIDS epidemic, and if I don’t I will give back all the money I
have used up in grants, etc., up to the point of personal bankruptcy.
I will then only work in poor, urban neighborhoods as a science
teacher in public schools, and never again make any claims about
curing diseases unless I can establish a direct connection between the
agent and the symptoms/progression.

First, we were told that a vaccine would be available in 6 months,
then a couple of years, then 5 years (twice), and now it’s
“pandemic” time. If they are correct, then within a few
years the world will have substantially less people. The opposite
will be the case. Let’s get these guys out of the key positions
and give some scientists with fresh ideas a chance. You can’t
kill the dead (HIV isn’t Dracula, though I wouldn’t be
surprised to hear one of these geniuses use this analogy), and a
latent virus is for all intents and purposes, dead, and more
importantly, harmless.

The retroviral “therapy” is a cause of “AIDS,”
though the definition of AIDS these days seem to include anything an
HIV antibody positive person dies from. Let’s get an
independent scientific panel to investigate. HIV would have to be
doing some discernable harm to the relevant cells (in sufficient
numbers) when the patient’s body took a nosedive. Otherwise,
the panel would have to conclude that the AIDS was caused by the
therapy (unless some other direct cause could be found). This is the
way to do science. You don’t say, “gee wiz, look at that,
there are all kinds of horrible side effect to the therapy, but
we’ve got to keep doing it, because otherwise, the dead virus is
going to do something – we don’t know what – but
we’ve got to attack it, even though it’s dormant and
harmless.”

And I’d like someone to define AIDS in a way that makes sense.
Blaming HIV for Kaposi’s Sarcoma, CMV, candidiasis, etc., is
ridiculous. If you can show me the direct sequence of events,
biochemically, fine. But you can’t and you never will, because
if you could, they would have done it already. It would be easy to do
if HIV was actually doing anything, but it isn’t doing enough,
literally, to hurt a fly. It was a nice guess, I’ll give them
that, but they never did the hard work to determine exactly what was
going on, and they were predisposed to see viruses or bacteria as the
cause of any “epidemic,” though there are plenty of
historical examples to the contrary.

There’s lots more to be discovered about the immune system, but
it’s clear that when you stress your body in particular ways,
the immune system starts to fail in many (but not all people).
It’s like what Dr. Rosedale said about type II diabetes, that
is, some people can withstand the insulin hanging around for much
longer than others, but at some point, the insulin desensitization
occurs, and the diagnosis of type II diabetes can be made (though it
might be easily dealt with through diet – eat a little
nutritional yeast with meals, avoid polyunsaturated fatty acids as
much as possible, eat fruit rather than processed sugar food, cut down
on calories, and remember that lard is mostly unsaturated, and
chicken/turkey is largely unsaturated, so don’t eat them at all.
 Eggs, shellfish, raw cheese, non-denatured whey powder, eggs, etc. is
the way to go for good quality protein).

Now here’s something you should know, and please at least tell
your HIV antibody positive friends:

Your body either makes polyunsaturated fatty acids (called Mead acid)
or else it uses those from the diet if you eat too much of them, and
you get arachidonic acid incorporated into your cells as the dominant
stressor-induced fatty acid (if you eat like a traditional Eskimo,
you’d incorporate DHA, which is dangerous in a different way
– your blood vessels essentially disintegrate by your fifth
decade, if you’re lucky to get that far).
All this is well-known and not subject to scientific debate (though
obviously some are suggesting that balancing arachidonic acid and DHA
is the way to go, sort of like holding a cobra in one hand and a
mongoose in the other, with your head in between). However, most
scientists have assumed, based on a terribly flawed experiment done on
rats in 1930, that dietary polyunsaturates are “essential”
for humans. Now if you look at the evidence, you see that arachidonic
is a stone cold killer, just do a pubmed.com search and see for
yourself. Mead acid, on the other hand, is very stable biochemically,
and doesn’t get released for metabolization easily. It also
doesn’t metabolize into dangerous substances, such as PGE2 or
LTB4. You must know of the importance of COX 2 inhibitors. Guess
what? No need for them when your body is packed with the Mead acid.
Mead acid doesn’t go that route. It will take about 2 years to
get the arachidonic acid out of your body on the diet I mentioned
above. At that point, assuming you haven’t damaged your immune
system through drugs/toxins/foreign protein exposure to an extreme
degree, you’ll be fine, HIV antibody positive or not.
That’s what the evidence suggests, biochemically and
physiologically (though stomach acid is necessary, and you may have to
supplement for life, which is not expensive). For the most part,
epidemiology has become a tool of those who want to make a point that
is not supported by biochemistry or physiology. And of course most
people don’t even know the difference. Now I’d like to
see some establishment big-wig do an experiment and say,
“we’re going to do everything known in biochemistry to try
and find HIV doing some incredible harm while people are asymptomatic,
leading directly to immune system collapse, but if we can’t,
then we’ll conclude it’s harmless until someone can make
such a showing.” Latent infection means nothing, because
that’s what retroviruses do. Mice have hundreds of them
normally. There could be a “freak of nature” virus, like
Rous sarcoma, but then you would see exactly what it was doing when
you looked. That’s the difference – HIV is doing nothing,
until the body has so fallen apart, in one way or another (viral
reactivation, immune system collapse, wasting) that there is enough
stress for it to become active, though I’d still have to see
evidence of it actually doing something damaging before it would make
sense, scientifically, to make any claims against it.

Here’s some more to chew on, which fits my idea that one should
avoid polyunsaturated fatty acids (due to the oxidative stress they
cause if consumed in large amounts, as is the case in the USA today):

http://www.altheal.org/treatments/oxidative.htm

"It has been found that AIDS is characterised by a persistent
oxidative imbalance. An increasing deficiency of the non-toxic
anti-oxidant glutathione plays a crucial role in the transition from
pre-AIDS to full blown disease (1,2) To quote from Montagnier (the
discoverer of HIV) et al (3):

Page 655:

"A large body of data on in vitro human immunodeficiency virus (HIV)
infection and biochemical clinical studies suggests that oxidative
stress plays a role in AIDS pathogenesis*. Recent reports have
implicated intracellular excess of reactive oxygen species (ROS) in
the induction of HIV expression (4-7) and in the initiation of
apoptotic cell death ** (8). Studies showing a decrease in glutathione
in peripheral blood mononuclear cells from symptom-free persons offer
further evidence of a metabolic alteration leading to the decreased
ability to counteract oxidative stress (9). These findings, together
with other alterations of biochemical indicators of systemic oxidative
damage that have been observed (10-12) suggest that antioxidants can
be useful in inhibiting viral replication and cell death in patients
with HIV infection and AIDS"

"Lymphocytes from subjects infected with the human immunodeficiency
virus type 1 (HIV-1) undergo an inappropriate programmed cell death
(apoptosis), a major mechanism for the decline of CD4 and CD8 cells
that is crucial to the progression towards the overt acquired
immunodeficiency syndrome (AIDS).1-8 Indeed, lymphocyte apoptosis
correlates with disease progression and lower CD4 counts: a high
degree of apoptosis has been detected in patients with AIDS in
comparison with long-term nonprogressors.1-8."(57). "Patients with
AIDS have significantly higher lymphocyte-associated ceramide levels
than healthy individuals and HIV-1-infected long-term nonprogressors
have less elevated lymphocyte-associated ceramide levels than subjects
with evolving disease.8,20,21 Remarkably, this is paralleled by a
lower frequency of apoptotic CD4 and CD8 cells in long-term
nonprogressors than in patients with AIDS.8,21".(57) "

"Last year however, Carbonari et al showed that apoptotic (apoptosis =
programmed cell death) lymphocytes in AIDS patients consist for the
most part of CD8 T-cells and CD19 B-cells.(1) They concluded from this
that the phenomenon of in-vitro apoptosis might not be related to the
depletion of CD4 T-cells in AIDS. Finkel et al recently showed that
apoptosis occurs predominantly in bystander cells and not in
productively infected cells of HIV- and SIV-infected lymph nodes.(2)
In their commentary, Pantaleo and Fauci did not wish to give any
conclusive answer to this.(3) (44)"

Here again, the scientists saying “remarkably” turn out to
be wrong. What a surprise.

And here are a couple more of those studies about the
“catastrophic success” of retroviral therapy you found
interesting:

AIDS. 2004 Aug 20;18(12):1615-27.
  
Immune restoration disease after antiretroviral therapy.

French MA, Price P, Stone SF.

Department of Clinical Immunology and Biochemical Genetics, Royal
Perth Hospital and School of Surgery and Pathology, University of
Western Australia, Perth, Australia. martyn.french@health.wa.gov.au

Suppression of HIV replication by highly active antiretroviral therapy
(HAART) often restores protective pathogen-specific immune responses,
but in some patients the restored immune response is
immunopathological and causes disease [immune restoration disease
(IRD)]. Infections by mycobacteria, cryptococci, herpesviruses,
hepatitis B and C virus, and JC virus are the most common pathogens
associated with infectious IRD. Sarcoid IRD and autoimmune IRD occur
less commonly. Infectious IRD presenting during the first 3 months of
therapy appears to reflect an immune response against an active (often
quiescent) infection by opportunistic pathogens whereas late IRD may
result from an immune response against the antigens of non-viable
pathogens. Data on the immunopathogenesis of IRD is limited but it
suggests that immunopathogenic mechanisms are determined by the
pathogen. For example, mycobacterial IRD is associated with
delayed-type hypersensitivity responses to mycobacterial antigens
whereas there is evidence of a CD8 T-cell response in herpesvirus IRD.
Furthermore, the association of different cytokine gene polymorphisms
with mycobacterial or herpesvirus IRD provides evidence of different
pathogenic mechanisms as well as indicating a genetic susceptibility
to IRD. Differentiation of IRD from an opportunistic infection is
important because IRD indicates a successful, albeit undesirable,
effect of HAART. It is also important to differentiate IRD from drug
toxicity to avoid unnecessary cessation of HAART. The management of
IRD often requires the use of anti-microbial and/or anti-inflammatory
therapy. Investigation of strategies to prevent IRD is a priority,
particularly in developing countries, and requires the development of
risk assessment methods and diagnostic criteria.

Curr HIV Res. 2004 Jul;2(3):235-42.

Immune restoration disease: a consequence of dysregulated immune
responses after HAART.

Stone SF, Price P, French MA.

Department of Clinical Immunology and Biochemical Genetics, Royal
Perth Hospital and School of Surgery and Pathology, University of
Western Australia, Perth, Australia. sfstone@cyllene.uwa.edu.au

Immune Restoration Diseases (IRD) are a collection of atypical
'opportunistic infections' and inflammatory diseases seen in human
immunodeficiency virus (HIV) patients after HIV viraemia is suppressed
by highly active antiretroviral therapy (HAART). IRD probably reflect
dysregulated immune responses against pre-existing infections by
opportunistic pathogens, with different immunopathological mechanisms
for different pathogens. For example, mycobacterial IRD are associated
with delayed type hypersensitivity (DTH) responses to mycobacterial
antigens, whereas patients who experience cytomegalovirus (CMV) IRD
have elevated plasma levels of soluble CD30, a marker of a T2 cytokine
environment expressed by activated CD8 T-cells. As IRD are often
compartmentalised to organs, monitoring serological markers such as
pathogen-specific IgG antibody, may be informative, as demonstrated
for CMV and hepatitis C virus (HCV)-associated IRD. Genetic studies
have provided evidence of distinct immunopathological mechanisms and
inherited susceptibility to IRD associated with mycobacterial and
herpesviridae infections. The expansion of HAART in the developing
world where many HIV patients have low CD4+ T-cell counts and high
rates of concomitant infections will place a large number of patients
at-risk of developing IRD. It is therefore important to understand the
immunopathology so that prevention, diagnosis and treatment can be
improved. Copyright 2004 Bentham Science Publishers Ltd.

You either have an overall understanding of biochemistry and
physiology or you don’t, and those who do realize that being HIV
antibody positive is not going to do harm by itself. However, it is a
marker. In other words, the same people doing the same things (to
destroy their immune systems, reactivate viruses, waste away, etc.),
do those things with each other, passing this HIV around, so a lot of
people with HIV in specific communities go on to develop
“AIDS.” There was a recent Nip/Tuck episode, in which a
promiscuous woman was infected with HIV, and without retroviral
therapy, went on to develop AIDS. It was fiction, but if the HIV/AIDS
direct connection claim is accurate, then there should be thousands of
such women dying annually, if not monthly, in the USA alone, or they
should at least be on retroviral therapy (because if they
weren’t, they’d have the symptoms the fictional character
had). That is the “pandemic” prediction of the HIV/AIDS
claim. It isn’t happening, and it never will, and it is likely
that in 100 years or so, most people will have HIV antibodies, and
they’ll have a good laugh at how stupid their grandparents or
great-grandparents were. They’ll compare us to those who feared
witches in the medieval period.

You want a biochemical mechanism? Interestingly, it was given in
1979, before the AIDS “outbreak.” In Sultan Karim
(editor), “Practical Applications of Prostaglandins”
(1979), page 173: “Tumors can produce material which depresses
the immune system, and a substantial amount of evidence suggests that
prostaglandins are involved… mice bearing tumors induced by
chemicals… became decreasingly responsive immunologically…
PGE2 also caused immunosuppression.” Notice that these guys
talk about “substantial evidence” (and they review much of
it), not “devious, paradoxical, puzzling” non-mechanisms.
The probable cause of the wasting syndrome is covered above, but this
is a mechanism for Kaposi’s Sarcoma, that is, you do a lot of
poppers (and probably plenty of other drugs, legal and illegal), which
induces a tumor(s), then the tumor metabolizes arachidonate to PGE2,
breaking down the immune system, causing all kinds of free radical
damage to cells and organs, viral reactivation, etc. Since drugs in
combination with high polyunsaturate consumption can be very
immunosuppressive, that explains the AIDS cases that are just viral
reactivations getting out of control, though foreign protein exposure
also is immunosuppressive. Interestingly, common cancers (breast,
colon, prostate) take the LTB4 route, whereas PGE2 is the
“AIDS” route, though retroviral therapy seems to shunt the
arachidonate metabolism over to LTB4, which is nothing to be proud,
obviously. Arachidonic acid is something of a slow poison, that is,
if it’s the dominant stressor-induced fatty acid in your body.
Plenty of women get breast cancer at ages similar to HIV antibody
positives (and negatives) going into “full-blown AIDS,”
and many are younger. The only mystery here is that our great
“experts” are so incredibly out of touch with biochemical
reality. Somewhere along the line, “group think”
occurred, and suggestions to consume more “essential fatty
acids” when one is ill are now common, though crazy. Those with
what one might call “classic AIDS,” that is, a failing
immune system coupled with opportunistic infections becoming
uncontrollable, should close down the PGE2 pathway ASAP. But if you
don’t get the arachidonic acid out of your body, you’ll
just be subject to LTB4 maladies. Now whether former
immunosuppressive behavior (if beyond a certain threshold) is
something of a ticking time bomb is not known due to the current state
of that biological field, but the only sensible thing to do at this
point in history is clear. Dr. Paul Cheney, who pioneered attempts to
understand what one might call “classic chronic fatigue
syndrome,” suggested that extreme RNase-L activity causes the
fatigue. I would not be at all surprised if this was caused by the
arachidonic acid in these people, which has a hypersensitization
effect on everything (at least in the human body). In any case,
it’s interesting that HIV infected people are not chronically
fatigued, in general. Mono viruses seem to be the ones most likely to
do this, and it just shows you how ridiculous the Ho claims were,
namely, that there is this massive biochemical activity with the
immune system fighting HIV. Anyone who had such massive biochemical
activity would likely be in a coma, if not dead. But common sense has
left the building, apparently. If HIV was as nasty as is claimed, it
would either kill quickly or it would do what “chronic fatigue
syndrome” does, in terms of ratcheting up RNase-L activity. If
HIV reactivated and began to damage CD4T+ (or any other) cells, it
would be discernable, and there would be a cause of the reactivation
that could be prevented, at least in patients willing to do what was
necessary. The fact that our great “experts” cannot
detect either after more than 2 decades and billions of dollars is due
to the fact that neither is happening, or they are incredibly
incompetent/corrupt. So why listen to them? Do your own homework
people. This is not that complicated. Either they have clear and
convincing evidence (which they undeniably don’t’), or you
should just avoid anything immunosuppressive and do as much as you can
to limit biochemical activity (stay away from polyunsatures –
and that includes meat fats, and instead eat coconut products, white
tea, antioxidant rich foods like blueberries and dark chocolate,
etc.). Clearly, our “experts” are only interested in
looking for bacteria or viruses as “causes,” then passing
the ball to Big Pharma, so they and their friends can make big bucks
(on drugs and tests) and/or receive prestige/career perks. Even if
they can’t find anything real, they blame a bacterium or a virus
(can you say “SMON” – how insane was that
little-known episode?). Biochemistry is about thresholds. Even the
worst epidemic doesn’t kill everyone. When arachidonic acid
dominates your body, your ability to withstand various physiological
stresses is lowered dramatically – hardly any room for
“error,” that is, extreme immunosuppressive behavior
(compared to being on the Mead acid). And once you open up a highly
active pathway, such as PGE2, you’re in deep stuff. And then
our “experts” get their hands on you, and you’re
done.

Here’s some more Cheney material you can find on the web.
Notice the similarity to “AIDS.” The difference, in the
many cases in which there appears to be one, is likely due to the
immunosuppressive behavior of IV drug users, users of drugs like
poppers, those who take too much antibiotic or corticosteriod
medications, and those who have had multiple transfusions. HIV is
nothing, or near nothing, in this model, which has a biochemical
mechanism, unlike the establishment HIV/AIDS nonsense:
“Viruses, especially herpes viruses (such as Epstein-Barr virus,
cytomegalovirus, and human herpes virus 6), make proteins that mimic
IL-10, which activates the immune system and remains untouched by the
body's natural defenses.
Addressing the two different types of T-helper cells has been the
focus of work by Paul Cheney, M.D. His protocols are designed to
stimulate Th1 and inhibit Th2.
According to Dr. Cheney, chronic fatigue patients have activation of
T-helper 2 cells (Th2). Th2 activation suppresses T-helper 1 (Th1)
activity, particularly cytotoxic T-cells and natural killer (NK)
cells, which are the main defense against viruses. In this way the
viruses are able to "fool" the immune system.

An article in the Journal of Clinical Infectious Disease measured NK
cell activity in 50 healthy individuals and 20 patients with
clinically defined chronic fatigue immune dysfunction syndrome
(CFIDS). The patients were divided into three groups based on severity
of clinical status. NK cell activity decreased with the increasing
severity of the clinical condition (Ojo-Amaize et al. 1994).”

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