Please correct me if I am wrong.
1) Virus enters the body
2) Looks for T4 cells
3) Doesn’t find them (in healthy bodies) die off quickly
4) finds them (in unhealthy bodies) and replicates.
4a) Is t4 the immune response to HIV?
5) Virus is at low levels
6) starts replicating again slowly-body seemingly has no response to it
this time.
6a) replication is at the expense of t4 cells which the body calls up
in response?
My question in all of this is simple. Is T4 cells the auto response for
HIV?
If it isn’t how does T4 get decimated by HIV?
On 21 Aug 2006 05:32:06 -0700, kqurty…@gmail.com wrote:
>Please correct me if I am wrong.
>1) Virus enters the body
>2) Looks for T4 cells
>3) Doesn’t find them (in healthy bodies) die off quickly
Wrong. A body would not be defined as healthy if it did not have T
cells. They usually call that "AIDS."
HIV readily infects people of quite robust health.
>4) finds them (in unhealthy bodies) and replicates.
When someone is infected with HIV, the virus replicates quite readily
in a number of sites, mostly the gut.
>4a) Is t4 the immune response to HIV?
t4 is a shorthand for CD4 which is a co-receptor on a subset of immune
system cells known as lymphocytes. Here, you need to read a bit of
basic immunology.
>5) Virus is at low levels
Wrong. After initial infection, virus spikes up quite dramatically,
for example. So this statement is meaningless.
>6) starts replicating again slowly-body seemingly has no response to it
>this time.
Absolutely wrong. The body’s response to HIV is sometimes excessive;
part of the reason lymph nodes deteriorate and gut function is
compromised.
>6a) replication is at the expense of t4 cells which the body calls up
>in response?
The major cell type that is depleted during HIV disease is the CD4+ T
lymphocyte or T cell. "T4" is a rather arcane term at this point.
>My question in all of this is simple. Is T4 cells the auto response for
>HIV?
What the hell is auto response? Do you mean autoimmune?
Simple answer: no. HIV is an external agent.
Nuanced answer: some people with HIV may also have some autoimmune
reactions develop as a result of HIV infection.
>If it isn’t how does T4 get decimated by HIV?
An excellent question–a number of mechanisms. See below.
George M. Carter
At 06:43 PM 8/19/2006, you wrote:
What mitochondrial damage do you know of which is caused by HIV?
To the best of my knowledge, all mitochonrial damage in people with
HIV is caused by nucleosides and NNRTIs.
An excellent question!
There are myriad ways HIV can cause mitochondrial damage. Broadly
speaking, one could say through direct and indirect mechanims.
For example, involvement of HIV in the peripheral nervous system
manifests as neuropathy while in the central nervous system as minor
cognitive motor disorder and dementia. Here, as with many of the CD4+
T lymphocytes that die, the neurons are NOT infected by HIV, but
rather by expression of inflammatory cytokines and/or by various HIV
proteins like gp120 (e.g., second abstract below). How does this
happen?
Indeed–why is that the majority of CD4 cells lost in the progression
of HIV disease are not infected?
Within infected cells, there are a variety of ways that HIV proteins
can affect mitochondria. One candidate mechanism to explain induction
of apoptosis (cell suicide) for example is the vpr protein (see first
abstract below). Others have noted that vpr may induce apoptosis by
directly depolarizing the mitochondria membrane potential (see Biochem
Biophys Res Commun. 2003 May 9;304(3):583-92).
The apoptosis of UNinfected cells may be brought about by expression
of fas or TNF, which are part of the aberrant and overactive immune
response to HIV infection that are part of the underlying CAUSE of the
clinical development of AIDS. (By contrast, sooty mangabeys, for
example, have an infection that has actively replicating virus but
their lymph nodes remain intact, gut function normal and CD4 counts
generally don’t decline too much–they don’t develop AIDS).
This is a critical point: HIV disease leads to hyperactivation of
immune functions which result in the eventual deterioration of lymph
node architecture, damage to the CNS, depleted gut function and so
forth that are the ultimate cause of AIDS. Indeed, as the forth
abstract below notes, "Finally, HIV-infected cells from naive patients
behaved identically to activated T cells, displaying hyperpolarized
mitochondria, while lymphocytes from patients under highly active
antiretroviral therapy (which included HIV protease inhibitors) seemed
to react as resting cells."
The third abstract below gives a nice little precis of these
"intrinsic" and "extrinsic" pathways to cell death. The mitochondria
play a key role in sending a cell into that abject state of cell
suicide. Part of that acitvity may be regulated by the intracellular
redox status, as underscored in the 5th abstract below. The
therapeutic implications are delineated in the last
abstract–underscoring the need for further clinical evaluation of
these types of approaches, both in people with higher CD4 counts not
on ARV and those on ARV.
Of course, the last one was written 12 years ago. Have we had the
studies? Will we get them? Probably not. NIH is in the pocket of
pharma which can’t patent these so they can’t rob every dime from
every pocket so they can maintain the high lifestyle and power
politics to which they have become accustomed and, apparently,
entitled.
George M. Carter
**
Zhao LJ, Zhu H. Structure and function of HIV-1 auxiliary regulatory
protein Vpr: novel clues to drug design. Curr Drug Targets Immune
Endocr Metabol Disord. 2004 Dec;4(4):265-75.
Institute for Molecular Virology, St. Louis University School of
Medicine, 3681 Park Avenue, St. Louis, MO 63110, USA. zh…@slu.edu
Vpr is a 96-amino acid auxiliary regulatory protein that is packaged
in the HIV-1 virion. It enhances the nuclear transport of the
pre-integration complex, and regulates cell cycle, transcription and
apoptosis. These biological activities suggest strongly that Vpr
interacts with cellular biochemical pathways to regulate HIV-1
replication and pathogenesis. The karyophilic property of Vpr appears
to be due to direct interaction of Vpr with nuclear transport factors
and residents of the nuclear pore complex, whereas transcriptional
effects of Vpr may be exerted through direct and indirect mechanisms.
Cell cycle arrest at the G2/M checkpoint by Vpr is correlated with the
hyperphosphorylation of Cdc2. The pro-apoptotic activity of Vpr is
dependent on the subtype of the HIV-1 isolate, and may be dramatically
enhanced by a single L64P mutation. Mitochondria- and
caspase-dependent mechanisms appear to mediate Vpr-induced apoptosis.
Recent evidence suggests that Vpr interacts with a cellular
ubiquitination machinery and promotes degradation of Vpr mutants
carrying the L64P mutation. Vpr interaction with the ubiquitination
machinery may contribute to the regulation of the HIV-1 life cycle at
various stages. NMR studies of Vpr have shown a Vpr monomer with three
helical domains arranged in a twisted-U shape. However, Vpr most
likely exists as a trimer in vivo. Structural/functional domains have
been tentatively mapped for Vpr induction of apoptosis and for Vpr
interaction with the ubiquitination machinery. Structural refinement
of Vpr, specially by crystallography of the potential Vpr trimer,
should help design therapeutic approaches to specifically target Vpr.
**
Ahr B, Robert-Hebmann V, Devaux C, Biard-Piechaczyk M. Apoptosis of
uninfected cells induced by HIV envelope glycoproteins. Retrovirology.
2004 Jun 23;1(1):12.
Laboratoire Infections Retrovirales et Signalisation Cellulaire, CNRS
UMR 5121-UM1, Institut de Biologie, 4, Bd Henri IV, CS 89508, 34960
Montpellier Cedex 2, France. barbara….@univ-montp1.fr
Apoptosis, or programmed cell death, is a key event in biologic
homeostasis but is also involved in the pathogenesis of many human
diseases including human immunodeficiency virus (HIV) infection.
Although multiple mechanisms contribute to the gradual T cell decline
that occurs in HIV-infected patients, programmed cell death of
uninfected bystander T lymphocytes, including CD4+ and CD8+ T cells,
is an important event leading to immunodeficiency. The HIV envelope
glycoproteins (Env) play a crucial role in transducing this apoptotic
signal after binding to its receptors, the CD4 molecule and a
coreceptor, essentially CCR5 and CXCR4. Depending on Env presentation,
the receptor involved and the complexity of target cell contact,
apoptosis induction is related to death receptor and/or
mitochondria-dependent pathways. This review summarizes current
knowledge of Env-mediated cell death leading to T cell depletion and
clinical complications and covers the sometimes conflicting studies
that address the possible mechanisms of T cell death.
**
Lum JJ, Badley AD. Resistance to apoptosis: mechanism for the
development of HIV reservoirs. Curr HIV Res. 2003 Jul;1(3):261-74.
Ottawa Health Research Institute, University of Ottawa, Ottawa,
Ontario, Canada.
New insights into the physiological cell death program in mammalian
cells have further confounded the central issue of T lymphocyte
destruction during HIV infection. Although infected and uninfected
cells die following infection, recent evidence indicates that infected
and uninfected cells may have unique pathways controlling death. Two
widely accepted models for apoptosis have been described, namely the
intrinsic and extrinsic apoptotic pathway. In the extrinsic pathway,
ligation of TNF death ligands to their receptors causes
oligomerization of the death receptors and recruitment of adaptor
proteins typically involving caspase 8 activation. In the intrinsic
pathway, apoptotic signals converge on mitochondria to cause
activation and subsequent release of cytochrome c, which leads to
formation of a multiprotein complex containing Apaf-1, cytochrome c,
dATP and procaspase 9. Expression of HIV proteins alters these
pathways resulting in enhanced levels of apoptosis. Although HIV
infection results in T cell apoptosis, under some circumstances a
small fraction of CD4+ T cells and macrophages do not die following
infection, indicating that this may be a critical step in the
development of viral reservoirs. In addition, monocyte differentiation
into macrophages leads to an apoptosis resistant phenotype
characterized by upregulation of antiapoptotic molecules and lower
levels of proapoptotic molecules. The
…
read more »
The "virus" spikes, Mr. Carter, and yet no scientist can find particles
that are both the correct shape and size for any retrovirus (let alone
a specifiic one) in any part of the body of such a person so
"infected?" You are saying that there is what is called viremia, and
yet it is undetectable. If you have a citation from the scientific
literature that demonstrates something more than markers, associations,
correlations, etc., please post it here. In reality, what the
"experts" are doing is modifying assumptions that have been
demonstrated to be wrong. They use various "markers," some of which
are common in those whose cells are undergoing exceptional stress, such
as oxidative or nitrosative, but they never find the "virus" – just
parts of destroyed cells that they decided had to belong to "HIV." Why
does it have to belong to "HIV?:" Because if it does not, promotions,
profits, funding, etc. will be at risk and there will be plenty of
"negative publicity."
In fact, poor nutrition can do everything that "AIDS" is said to do,
though excessive antigenic exposure (such as in those who engage in
receptive anal intercourse and IV drug abusers, for example) greatly
exacerbate the situation. In "Modern Nutrition in Health and Disease"
(by Shils and Young, 7th edition), for example, the following passages
make this point:
…there are two prominent T-lymphocyte subsets: one
comprised of T helper/inducer cells (T4) and a second
subset of T suppressor/cytotoxic cells (T8). The
intravenous injection of antigen tends to favor the
development of T suppressor cells that are abundant in
the spleen. Page 597.
…secondary immune deficiencies are the consequence of
some other systemic disorder that indirectly causes a
defect in the response of the immune system. Page
598.
The major defects seen in severe PEM seem to involve
T-lymphocytes and the complement system. A marked
depletion of lymphocytes from the thymus and atrophy
of the gland occur. In addition, cells from the
T-lymphocyte regions of the spleen and lymph nodes are
depleted… These deficiencies may explain the high
susceptibility of severely malnourished patients to
gram negative bacterial sepsis… The B-lymphocytes
areas of he spleen and lymph nodes and the circulating
levels of B cells and immunoglobulins are relatively
normal… The overall consequences of all these
alterations in severe PEM are a greater predisposition
to infections and to severe complications in otherwise
less important infectious diseases. Pages 752-753.
If you want to learn more about how "diseases" usually occur, go to my
website, at:
http://groups.msn.com/TheScientificDebateForum-
monty1…@lycos.com wrote:
> The "virus" spikes, Mr. Carter, and yet no scientist can find particles
> that are both the correct shape and size for any retrovirus (let alone
> a specifiic one) in any part of the body of such a person so
> "infected?"
Yawn.
This paper is from 1987!
http://tinyurl.com/ogoh2
Nice spikes.
Chris Noble
On 22 Aug 2006 10:12:53 -0700, monty1…@lycos.com wrote:
>The "virus" spikes, Mr. Carter, and yet no scientist can find particles
>that are both the correct shape and size for any retrovirus (let alone
>a specifiic one) in any part of the body of such a person so
>"infected?"
Ah–yes they can. And have.
Shows how much you keep up with the data.
<plonk>
‘
Mr Carter, I am looking at the bigger picture-an overview if you like.
The question is simple. Does the HIV virus infect, destroy and spawn
new virii via the t4 cells?
If it doesn’t what is the mechanism for inactivating the T4 cells?
Here is the study Noble cited:
Virology. 1987 Jan;156(1):171-6. Links
Fine structure of human immunodeficiency virus (HIV) and
immunolocalization of structural proteins.Gelderblom HR, Hausmann EH,
Ozel M, Pauli G, Koch MA.
Ultrathin section and surface replica electron microscopy were applied
in combination with immunoelectron microscopy to elucidate the fine
structure of HIV. The shell of the tubular core shows p24 antigenicity,
while p17 is located at the inner leaflet of the lipid membrane. The
virus particle is studded with 70-80 protrusions. These knobs have a
diameter of 15 nm, a height of 9 nm, and are probably arranged in a T =
7 I symmetry. The major envelope protein gp120 is spontaneously shed
from the viral surface. A possible role of released gp120 in
pathogenesis is discussed.
Sounds wonderful, but the problem is that they are just finding pieces
of things that they they belong to "HIV."
As of 1997:
QUOTE:
Two historic papers in the leading science journal Virology in March
this year provide astonishing new data on the purification and
isolation of HIV. For the first time in the history of AIDS, elusive
electron microscope images of ‘HIV’ collected or ‘banded’ at the
official density required for retroviruses, 1.16 gm/ml, have been
published, by a research group in Germany. The electronmicrographs
disclose "major contaminants" in "pure HIV".
HIV expert Hans Gelderblom of Berlin’s Robert Koch Institute, whose
photos of non-banded ‘HIV’ material have been the industrial benchmark
since 1987, co-authored the first paper which describes the
contamination as "an excess of vesicles" – particles of cellular
proteins, that may contain DNA or RNA. In a consecutive paper, a US
research team from the AIDS Vaccine Programme in Maryland reveal
carefully, "It is unknown how these cellular proteins associate with
the virus" and warn, "The presence of microvesicles in purified
retroviruses has practical implications": both teams discuss the
resulting nonspecifity of HIV tests, all of which are based on early
unchecked "purified HIV".
In an historic admission that it has never been established which
proteins constitute ‘HIV’, the US scientists conclude, "The development
of various purification strategies to separate microvesicles from
HIV-particles … will greatly enhance our ability to identify
virion-associated cellular proteins." The imaging step in attempts at
retroviral isolation was deemed essential when isolation procedure was
discussed and decided at the Pasteur Institute, Paris in 1972, but it
has never been published before in the 13-year history of ‘HIV’.
(Continuum autumn 1997). UNQUOTE.
Since then, the "HIV experts" just assume that the textbook claims are
correct, but my point that now that the "experts" are saying that "HIV"
does not destroy the T cells in question, but just "turns them off," so
to speak, why can’t large amounts of intact "HIV" be found in those
said to be infected? Why is there just this abundance of what appears
to be nothing more than cellular debris?
Source of the above quotation: http://www.polder.net/aids/award.htm
For those interested in this subject, also see:
http://www.polder.net/aids/data/ehremarks.htm
In above post, "they they" should be "they think."
Here is the key passage from the latter link, above:
QUOTE:
In the case of RNA tumor viruses, now called retroviruses, the
demonstration of viremia in the blood plasma of experimental leukemic
animals (chickens and mice) was published more than 35 years ago. A
most efficient purification method including ultrafiltration and
ultracentrifugation of a 1/1 dilution of plasma in heparinized Ringer’s
solution, allowed me to demonstrate packed retroviruses by transmission
electron microscopy (7) in thin sections of pellets obtained by high
speed centrifugation of the purified virus, quite clearly establishing
that the amount of contaminating cell debris was remarkably small, a
conclusion which could never have been reached by using the negative
staining EM method. Using this simple ultrafiltration procedure,
virions were never exposed to hypertonic shock. However, sedimentation
in sucrose density gradients, at the density of 1.16 gm/ml, soon became
the most popular method for retrovirus purification.(8) Interestingly,
it was very well known by electron microscopists in the 1960s, that
sharp bands sedimenting at the density of 1.16 frequently contained
large amounts of microvesicles and cell debris of non-viral nature.
These debris just happened to sediment in sucrose gradients at a
density very similar to that of retroviruses clearly indicating that
finding a "sharp band" at the density of 1.16 gm/ml was of little
significance and was certainly far from any demonstration of
retroviruses isolation. UNQUOTE.
All I ask for is a demonstration of this kind of retroviral viremia in
those said to be "AIDS patients" or "HIV infected using the method
described as "most efficient," and for perhaps 1000 "non HIV infected"
control subjects who are very ill with a variety of other "diseases" to
also be tested in the same way. If the "HIV/AIDS patients" are the
only ones to have abundant retroviral viremia, then at that point we
can say that a retrovirus is present and may be the cause of some
symptoms. At this point, there is nothing but wishful thinking on the
part of those who have staked their reputations on the "HIV/AIDS"
notion and those who profit from the industry that is devoted to
"treating" so-called HIV/AIDS.
- Hide quoted text — Show quoted text -
monty1…@lycos.com wrote:
> Here is the study Noble cited:
> Virology. 1987 Jan;156(1):171-6. Links
> Fine structure of human immunodeficiency virus (HIV) and
> immunolocalization of structural proteins.Gelderblom HR, Hausmann EH,
> Ozel M, Pauli G, Koch MA.
> Ultrathin section and surface replica electron microscopy were applied
> in combination with immunoelectron microscopy to elucidate the fine
> structure of HIV. The shell of the tubular core shows p24 antigenicity,
> while p17 is located at the inner leaflet of the lipid membrane. The
> virus particle is studded with 70-80 protrusions. These knobs have a
> diameter of 15 nm, a height of 9 nm, and are probably arranged in a T =
> 7 I symmetry. The major envelope protein gp120 is spontaneously shed
> from the viral surface. A possible role of released gp120 in
> pathogenesis is discussed.
> Sounds wonderful, but the problem is that they are just finding pieces
> of things that they they belong to "HIV."
Who would have guessed it? Rather than read the article and look at the
excellent EMs of HIV Monty regurgitates virusmyth nonsense.
Look at the EMs in the paper and tell me they are microvesicles. Why do
antibodies to HIV p24 bind to the tubular core of these viral
particles? Why do antibodies to HIV p17 bind to the lipid membrane of
these particles?
All these wild coincidences!
Read the article before you dismiss it.
Chris Noble
On 23 Aug 2006 07:41:44 -0700, kqurty…@gmail.com wrote:
>Mr Carter, I am looking at the bigger picture-an overview if you like.
>The question is simple. Does the HIV virus infect, destroy and spawn
>new virii via the t4 cells?
A better framed question than your latter list.
HIV infects CD4+ cells. Mostly lymphocytes. Some macrophages and
dendritic cells.
>If it doesn’t what is the mechanism for inactivating the T4 cells?
Some of the cells so infected die. Much of the loss of uninfected CD4+
cells is related to effects of either HIV proteins or
activation-induced cell death that occurs as a result of HIV
infection.
George M. Carter
On 23 Aug 2006 20:01:49 -0700, "Chris Noble" <ChrisJNo…@hotmail.com>
wrote:
snip…
>Read the article before you dismiss it.
Twill be a cold day in hell, my friend, before monty manages to read
ANYTHING that conflicts with his psychotic views of the world.
That’s why we call it DENIALISM.
George M. Carter
>From the very paper you cite, the researchers say that there was "an
excess of vesicles." Are you disagreeing with the interpretation of
the researchers who wrote up the study you cited?
As for the other questions; they all depend upon assumptions which were
never demonstrated. It is like the proverbial house of cards, except
that with a house or cards, there are actually some cards there, though
it’s not much of a "house," structurally.
Here is the crux of the issue:
QUOTE:
This March [1997], two papers [18,19] were published with electron
micrographs of sucrose density gradient banded material. In one of
these papers the authors confirmed that:
"Virus to be used for biochemical and serological [using "viral"
proteins to test for antibodies in patients] analyses or as an
immunogen [to produce antibodies in animals and test patients for
"viral" proteins] is frequently prepared by centrifugation through
sucrose density gradients. The fractions containing viral antigen
[proteins] and/or infectivity are considered to contain a population of
relatively pure viral particles" [19] (italics ours).
However, to the contrary, the data in these papers support our claim
that the existence of HIV is unproven:
1. The authors of both papers concede that the particles which are
present in the banded material and which are said to be HIV represent
only a very small fraction of the total material. Gelderblom et al.
state that the material contains "an excess of [cellular] vesicles with
a size range 50-500nm, as opposed to a minor population of virus
particles…cellular vesicles appear…to be a major contaminant of HIV
preparations enriched by sucrose gradient centrifugation".
2. For the small number of particles deemed to be "HIV" no evidence is
given that they are even a retrovirus-like particle. Indeed, to the
contrary:
(a) the particles do not appear to have surface spikes (knobs),
although the possibility that such projections may be present cannot be
excluded. (However, in other papers published by many researchers
including Gelderblom and his associates such projections are noted to
be absent [14,20];
(b) the particles referred to as "HIV" are not spherical and have
diameters exceeding 100-120 nM. In the EM in Gluschankof et al. [19]
there are arrows pointing to five "HIV" particles devoid of surface
projections whose dimensions are 121 X 145; 121 X 169; 121 X 145, 121 X
145 and 133 X 145 nM respectively. In Bess et al. [18] there are a
total of six "HIV particles" also devoid of surface projections whose
dimensions are 160 X 240; 200 X 240; 280 X 280; 208 X 250; 167 X 250
and 250 X 292 and nM respectively.
Thus, by definition, the particles cannot be retroviral-like particles
and even less, a unique retrovirus, HIV. Furthermore, the particles
noted by Gluschankof et al. and Bess et al. cannot be the same
particle. Indeed, the method adopted by all HIV researchers for proving
the existence of HIV, that is, excluding proof based on purification of
particles with retroviral morphology shown capable of faithful
replication but rather by detection of antibody/protein reactions, does
not satisfy any scientific principle and defies common sense.
UNQUTOE.
Thus, it is clear that there is difference of opinion how to interpret
the data obtained. This is quite common in academia, and it is rare to
call a colleague a "kook," "crank," etc., though it is common for
industry shills to employ these tactics. The Perth Group’s
interpretation appears to be totally consistent with the data. Just
because a group of researchers obtained the data does not mean that
their interpretation of it is accurate. This is something that Carter
and Noble seem incapable of comprehending.
monty1…@lycos.com wrote:
> >From the very paper you cite, the researchers say that there was "an
> excess of vesicles." Are you disagreeing with the interpretation of
> the researchers who wrote up the study you cited?
Those words are not found in the 1987 paper that I cited. You have not
read the paper. You have not looked at the evidence. You are a pathetic
troll.
The paper from 1987 has excellent electron micrographs of HIV. You can
clearly see the conical core and the spikes. They also used
immunoferritin labelling to demonstrate that the HIV proteins p24 and
p17 were localised in the core and lipid membrane respectively. They
are quite clearly not vesicles.
Chris Noble
If you believe there is an error in any citations, go ahead and provide
the link so that anyone can decide for himself/herself. Otherwise, you
apper to be the "troll." I cite professional sources. You have
mentioned a study, and I already responded; interpretations and results
generated are not the same thing. The point the Perth Group makes is
clear: if they are not of both the right size and shape, then a
retrovirus is not involved and the basic "HIV/AIDS" claim is
contradicted. Thus, at this point, I suggest to explain exactly what
your position is. However, viruses either overwhelm the organism
quickly or else "reactivate" under particular circumstances, and so I
have no problem with the notion that a virus could be present; I just
don’t see evidence that there is anything here except cellular debris.
And because cellular debris comes in all manner of shapes and sizes,
you will always be able to "fish out" pieces of this debris that appear
to be consistent with "HIV." However, if the shape is more or less
correct, but the size is not and there are very few of these particles
of the correct shape and size, then what you have demonstrated is that
"HIV" is not present, not that it is. If it was established that
abundant particles of the correct shape and size were present, the next
step would be to see if it was present in all "AIDS patients" and not
present in people dying of other diseases. This would be consistent
with the scientific method. If those like yourself were so interested
in silencing "dissidents" the intelligent thing to do would be to
create a website that contained the evidence that is in contention, not
just what you want people to see, along with your interpretation of the
evidence. This is all an academic can do: you make your case, citing
the relevant evidence and explaining why you consider your
interpretation superior to all others. Again, I ask you to explain
your position precisely, and then provide the evidence. I have seen
EMs that are supposed to be "good pictures of HIV," and they are
pathetic, at best. If you have seen something better, go ahead and
post a link to the EMs you consider very convincing.
On 26 Aug 2006 09:59:02 -0700, monty1…@lycos.com wrote:
> I have seen
>EMs that are supposed to be "good pictures of HIV," and they are
>pathetic, at best.
So you say. Why should we believe anything you have to say?
In short, back up this claim with a specific rationale of why the EMs
are no good? Compared to what?
And given that most viral infections and many bacterial ones are
identified by PCR, why does that not add significant weight and
evidence to the fact HIV exists?
You certainly have not demonstrated any bona fides to merely accept
your statements at face value as far as intellectual rigor goes.
George M. Carter
monty1…@lycos.com wrote:
> I have seen
> EMs that are supposed to be "good pictures of HIV," and they are
> pathetic, at best. If you have seen something better, go ahead and
> post a link to the EMs you consider very convincing.
You pathetic troll.
I provided you with a citation. You have not bothered to look at the
paper.
Chris Noble
I love it when the denialists raise the issue of Gelderblom seeing
vesicles. His papers demonstrate clearly that he can distinguish
between virus particles and vesicles. He talks about the problems of
vesicle contamination and precisely how to distinguish between this and
viral particles.
Denialists never read beyond the word "vesicle", and merely parrot the
word repeatedly to themselves in the forlorn hope that someone might
conclude that Gelderblom has become confused.
I don’t want anyone to "believe" anything; I want the scientific
method to be followed. I am not telling people to take highly toxic
"medicines" in order to try and killoff a deadly virus. I am
asking for evidence for that claim. The Hippocratic Oath is clear: a
doctor should do no harm first and foremost, and it is undeniable that
taking highly toxic medicines for years will do harm, so there must be
very strong evidence in order to justify this situation, and I am
asking for that evidence. For years, I did not think twice about the
"HIV/AIDS" claims; I just assumed they were correct. The
difference between you and I, it appears, is that when I investigate
something of interest, I leave my preconceptions behind, and examine
the evidence closely. In science, one proposes a hypothesis, along
with the evidence that seems to support it, as well as suggestions for
future experiments that will verify the claim. If this is not done,
what is presented is not science, and I will leave it to you to call it
what you will, because I am not interested in it. Often,
interpretations of the data generated in such experiments will differ,
and this is considered academically acceptable. This is why so much of
"modern medicine" is something of a sham – the scientific method
is not followed, often because those with political authority deem a
"public health threat," which is ludicrous considering how much
harm can be done if causes are not determined. I have proposed various
experiments that would be on point and would settle the "HIV/AIDS"
notion, but these are not going to be done by those in authority today,
and so all I can do is to ask for the evidence, and an explanation
about how this evidence demonstrates that there is a specific
retrovirus doing specific kinds of harm. If you don’t feel those who
make such claims have a responsibility to provide this much, then you
are allowing them to preside over this area of "disease" in a
manner very similar to the religious cult leader. You are the one who
asks others to believe!
As to DavidT, yes, I’m sure the gentleman believes he is seeing "HIV" –
nobody is disputing that point. The question concerns what he actually
found. He found a few particles that corresponded to what he thought
the textbooks said a retrovirus might look like. He did not
demonstrate viremia, nor did he demonstrate that these particles are
both the correct shape and size. Furthermore, there are no experiments
done to determine if those who are ill from other "diseases" have the
same kinds of particles in their bodies. These are just some things
that the scientific method demands before claims of a specific
retrovirus causing a deadly disease over a decade later, after many
years of no symptoms, should be entertained by anyone of sound mind.
monty1…@lycos.com wrote:
<snip waffle>
> As to DavidT, yes, I’m sure the gentleman believes he is seeing "HIV" –
> nobody is disputing that point. The question concerns what he actually
> found. He found a few particles that corresponded to what he thought
> the textbooks said a retrovirus might look like. He did not
> demonstrate viremia, nor did he demonstrate that these particles are
> both the correct shape and size. Furthermore, there are no experiments
> done to determine if those who are ill from other "diseases" have the
> same kinds of particles in their bodies. These are just some things
> that the scientific method demands before claims of a specific
> retrovirus causing a deadly disease over a decade later, after many
> years of no symptoms, should be entertained by anyone of sound mind.
Have you looked at the paper yet.
Look at fig 1b. Nice core. Nice knobs. 100nm scale for size reference.
Chris Noble
On 31 Aug 2006 09:22:25 -0700, monty1…@lycos.com wrote:
>I don’t want anyone to "believe" anything; I want the scientific
>method to be followed.
Oh what a complete fucking load of crap. You want nothing of the sort.
You want to pontificate and snort and bellow and make bold statements
that say nothing while utterly ignoring all evidence presented to you.
In short, you’re a bullshit blowhard.
George M. Carter
The "evidence," Mr. Carter?
Quote from David Rasnick:
In ’85 I was at a research meeting where HIV was being discussed. An
AIDS specialist was asked how much HIV was present in an infected AIDS
patient. He was asked, "What’s the titer of HIV?"
The titer is the number of infectious virus particles in a blood or
tissue sample. A titer of live virus is easily obtainable from the
particular tissue that the virus infects. If you have herpes, the
sample comes from a cold sore; if it’s polio, it’s from the intestine;
if it’s smallpox, it’s a pustule; if it’s a cold, it’s the throat.
When you’re infected with a virus, it infects and kills about 30
percent of the specific tissue that it targets before you get any
symptoms. You can take a titer of any infected area, put it under a
microscope and see millions of living viruses.
So, the virologist was asked, "What’s the titer?"
He answered, "Undetectable. Zero."
UNQUOTE.
Source: http://www.pharmharm.com/controversial.html
When you find the "pathogen," do be kind enough to inform the rest of
us, Mr. Carter. Until then, I will rely upon the evidence that makes
sense and is consistent with physical and biochemical reality, down to
the molecular level. For example, even something as "trite" as protein
energy malnutrition can cause the changes that are characteristic of
"HIV/IDS." But you go ahead and put your faith in the great men of our
time, like Mr. Gallo, and see where that gets you.
I thought, how is that possible? How can you be made sick from
something that isn’t there? With polio, researchers threw away a
hundred viruses before they found the right one. I assumed Gallo had
simply gotten the wrong virus, and we’d have to start over.
On 10 Sep 2006 06:42:30 -0700, monty1…@lycos.com wrote:
>The "evidence," Mr. Carter?
>Quote from David Rasnick:
That’s not really evidence. It’s just the ditherings of a discredited
idiot that are really pretty old.
Data have accumulated since 1985. Technologies have improved. It is
quite an easy matter to find HIV, to measure viral load, to assess the
impact of viral load on immune function, and so forth.
If that’s what constitutes "evidence" for you, you are in sad shape,
dear. Try to be a bit more up-to-date.
George M. Carter