Re: AIDS

On 15 Jul 2006 08:15:55 -0700, monty1945@xxxxxxxxx wrote:

I agreee with Mr. Carter about the BMJ debate. Take a look at it and
decide for yourself. One link is:
http://www.rethinking.org/bmj/response_31507.html

LOL...right. A one-sided view of the debate. Why not try the original
source. That is
http://bmj.bmjjournals.com/cgi/eletters/326/7387/495#32532

There is plenty of back-and-forth with the Perth group, which also
further underscores that denialist nonsense has NOT been silenced.
They've had the opportunity to air the tawdry laundry of their tiny
minds and been left flailing.

Sigh. It pisses me off, obviously--as it does you, I'm sure. But for
me it is personal. I do not want to see more people infected. I do not
want to lose more of my friends to AIDS. I've known hundreds of people
who have died of AIDS--very many dear and close friends. A tiny
fraction of the millions who have died.

For this stupid fucking debate to carry on like this in 2006 is simply
obscene. It is ridiculous and again, it deflects from the seriously
fucked up problems our world faces while you womble off into your
psychotic fantasy la-la land.

The problem with saying that the Perth Group has not done an experiment
is that they seek funding but only those who agree with the "HIV/AIDS"
claim can get that amount of funding.

Oh, horse***. They wrote in Nature Biotechnology. They simply do not
have the ABILITY to do that kind of research.

However, this does not preclude
them from using human reason to point out that if you never find the
virus, but only "markers" that can be generated by totally non-viral
phenomena, then your "theory" is in big trouble.

This statement is gobbledy-gook. It means nothing. The reference I
provided above gives AMPLE resources.

HIV has been isolated. It is found in people with HIV infeciton and
AIDS. It is not found in people who do lots of recreational drugs, for
example, but do not have or develop AIDS.

Notice that Mr.
Carter does not provide a citation for an experiment that detected
particles of the correct size and shape in those said to be HIV
infected or dying of AIDS.

Are you claiming that such does not exist?

This is a patently false claim. See, for example,
http://hiv-web.lanl.gov/content/hiv-db/REVIEWS/Gelderblom.html

Of course, if you wish to rely on criteria that are impossible to
meet, then of course you will be satisfied with your conclusion. This
is what the Perth Group does. Brian Foley notes: " The criteria that
the Perth group claim are needed are impossible to meet. No virus has
ever met them and none ever will. Density gradient ultracentifugation
can only "enrich" a virus preparation up to 80% to maybe 98% purity,
it can never produce a 100% "pure" virus preparation free of all other
materials. Several groups have made such preparations of HIV (as they
have for FIV, SIV, EIAV and other lentiviruses) and shown that there
is some cellular debris and microvessicles derived from the cell
culture in these preparations. Even 100% virus particles will contain
some cell-derived proteins, because lentiviruses are enveloped viruses
and the lipid bilayer envelope carries with it some cellular proteins
such as MHC molecules.

"Infectious molecular clones on the other hand can be made 100% pure,
free of even viral proteins, they are just naked DNA copies of the
viral genome. There are thousands of other advantages of cloning, over
crude density preps of viruses. Molecular genetics offers a whole
world of research that was not available with pre-1970 techniques."

In short, by Perth's standards, NO viruses exist. It's ridiculous--and
underscores why they are intellectually bankrupt.

I really have to laugh that Perth, in its vapid embrace of only ONE
method of sucrose-gradient density centrifugation that is acceptable
methodology in their little pea-brained minds, they cite Sinoussi F,
Mendiola L, Chermann JC, Jasmin C, Raynaud M. (1973) Purification and
Partial Differentiation of the Particles of Murine Sarcoma Virus (M.
MSV) According to their Sedimentation Rates in Sucrose Density
Gradients. Spectra 4:237-243.

Do you know who the first author is?

One guess.

The woman that discovered LAV, later known as HIV-1.

You'd think she might know a wee bit about viral isolation, wouldn't
you?

This is the kind of evidence that would be
necessary in order to begin to formulate a hypothesis that might blame
a virus.

Bull***. There are more data that you will willfully ignore as that
is the tautology of denialism that you suffer from:
amie Mills asks:
"Did either Bess et al. or Gluschankof et al. approach 80% or even 98%
purified virus, or what looks like purified virus?"

And the answer is YES. In the Bess paper, the HIV-1 isolate MN, clone
4 virus grown of CEM-SS cells produced a preparation that was more
than 99% pure. They discuss why there are differences in purity
depending on which cell line and which virus is used.

Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ.
Cell membrane vesicles are a major contaminant of gradient-enriched
human immunodeficiency virus type-1 preparations.
Virology. 1997 Mar 31;230(1):125-33.
PMID: 9126268

Bess JW Jr, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO.
Microvesicles are a source of contaminating cellular proteins found in
purified HIV-1 preparations.
Virology. 1997 Mar 31;230(1):134-44.
PMID: 9126269

"...how is that proof of an exogenous and infective retrovirus?"

No single experiment is "proof" of anything, really. There are whole
textbooks written about virology and retroviruses. I can't spell it
all out here. Endogenous retorviruses do exist, they are found in the
genomes of nearly all eukaryotes. If the virus in not found in the
germ-line DNA of an organism, it is not defined as endogenous, it is
exogenous. No complex retrovirus (such as the lentiviruses and the
T-cell leukemia viruses) which carry regulatory genes (tat, rev, nef,
vif, vpu, vpx etc) in addition to the gag pol and env retroviral
genes, have ever been found in an endogenous state in any host. A few
endogenous viruses have one or two potenital open reading frames in
addition to gag, pol and env, but none are truly complex. The closest
relative to lentiviruses found in the human genome are endogenous
retroviruses such as HERV-K, and these retroviral elements are very
clearly not HIV-1 or any other lentivirus.
As for infectious, the global pandemic of infections with many
different subtypes and circulating recombinant forms derived from the
HIV-1 M group of viruses pretty much answers that question. Whether
one studies infectious molecular clones of HIV-1, or transmission
chains such as the case of Nushawn Williams who infected 13 young
women, or local or country-wide epidemics, the answer is always
consistent.

"... our local laboratories use proteins isolated from sucrose
gradients,(as mentioned in accompanying leaflets), ..."

How were those proteins grown before the sucrose gradient prpearation?
Was it clone whole virus grown on human cells? Or was it just viral
genes grown in E. coli? Do you observe a large false-positive rate
with the tests you are using? Just because sucrose gradients of HIV-1
whole virus particles are contaminated with varrying levels of
cellular vessicles when the virus is grown on human cell lines, does
not mean that all sucrose gradients are useless for all purposes.

"...If we then move on to western blots as a means of confirming a
diagnosis, how many bands and which do you need to confirm a
diagnosis? This varies considerably around the world and means a
person may be HIV positive in Africa but hop on a plane and have the
same test in Australia and be HIV negative! What does that mean for
our patients? ..."

No test of tests for any infection or any other medical condition
(such as pregnancy for an example) is always 100% perfect. What this
means for any patient, is that some human intelligence is required in
interpretting results. There are dozens of possible logical reasons
for either a false negative (very recent infection is the major one)
or false positive (the patient has elevated levels of some antibody or
antibodies that bind to HIV proteins) HIV ELISA test. This is why a
single ELISA is not the recommended standard for diagnosis. A person
truly cannot be HIV positive in one country and HIV negative in
another. They can be "officially" diagnosed as such, but they are
either infected or not regardless of that diagnosis. If a gets a
positive pregnancy test result with one test and negative with
another, it doesn't mean she is "partially pregnant", and the same
principles hold true for diagnosing HIV infection or any other
infection. More than 99% of people who are infected with HIV-1 develop
antibodies to many different HIV-1 proteins over time, such that some
bands on the western blot typically appear first, followed by others.
Also, very late in AIDS progression antibodies to some ands on the
western blot are prone to decline. The end result is that we should
expect a temporal variance in the number of reactive bands within any
one infected individual. It should also be noted that "reactivity" to
a protein band on a western blot is not a binary condition (wither
"yes" or "no") but an analog condition varying from weak to strong.

The end result is that both patients and doctors need to use other
data besides the ELISA and WB tests and human intelligence to
interpret that data. If a person has never had sex, never had a
transfusion, never injected drugs and has a weakly positive ELISA and
two weakly positive western blot bands, the sensible thing to do is to
wait a few months and re-test to see if this was just a spurious
problem. If the results are identical months later, then it might be
worth finding out what is causing them (perhaps infection with HTLV,
which is one of the closest relatives of the lentiviruses). On the
other hand if reactivity has increased to a strong ELISA positive plus
3 or 4 strongly reactive western blot bands, there is little (but
still some) doubt that the person is truly infected, and further tests
should be done to find out for sure, and if so, to find out how this
person could have become infected (perhaps they were not fully honest
about sex, or IV drug use, or perhaps they will be the clue that
uncovers a new route of transmission as Kimberly Bergalis was in the
famous "Florida Dentist" case).


Moreover, if you look at the literature written by the "virus
huinters" themselves, they point to the inflammatory response and the
dangerous element, and that would take hours or days, not more than a
decade, to happen. I have numerous quotations from these virus hunters
on my web site essays, for those interested.

LOL...more nonsense. Chronic inflammatory responses cause disease in a
variety of settings from Hepatitis B or C chronic infections to
rheumatoid arthritis.

However, due to the way "HIV/AIDS" is defined (in a way antithetical to
the scientific method) and also the fact that people who "test
positive" most likely are leading very unhealthy lives (and let's not
forget how many "AIDS patients" die of livers damaged by the
"medicines" today), it's no surprise that one can say something like,
"look at all the people dying of AIDS who tested positive many years
ago." I'm surprised the numbers are not higher, actually.

That's the point. If "lifestyle" caused AIDS, there would be a HELL Of
a lot of dead straight people in the US who died from infections like
pneumocystis. And a lot of LIVING people--many whom I have personally
known--men, women, children, straight, gay, whatever -- who did NOT
have a particularly hardcore lifestyle. They DID have HIV and too many
of my friends have died of AIDS.

Your ongoing dithering bull*** is a distraction from the fight
against AIDS--and the political nightmare that arises in terms of
healthcare access that affects EVERYONE in the US--including 47
million of us lacking insurance, as an example.

Supposedly,
this terrible infectious pandemic "HIV/AIDS" kills hardly any female
prostitutes in the USA who don't do IV drugs, and in fact only
supposedly kills about 14,000 a year in the USA these days - not on the
top of the list by any means.

More unsupported, declarative statements. Back this nonsense up.

Hospital infections, which are
completely avoidable, kill 90,000 or so each year. Avoidable accidents
at work kill around 40,000 or so, and just think about how many are
killed in automobile accidents. "HIV/AIDS" has become a big business,
and those who tell you that you need to fear a "retrovirus" 12 years
later are mostly totally conflicted, making money and/or holding
positions of power in the "industry" that "HIV/AIDS" has become.

LOL. I'm not and most of the people I know in the fight against
HIV/AIDS are not. That's just a pathetic dodge in the first part to
say other things kill people (duh) and an attack the messenger lie on
the second part that puts you on a par with Karl Rove.

More abstracts below.

George M. Carter

***
Regier DA, Desrosiers RC.
The complete nucleotide sequence of a pathogenic molecular
clone of simian immunodeficiency virus.
AIDS Res Hum Retroviruses. 1990 Nov;6(11):1221-31.
PMID: 2078405

Takeuchi H, Suzuki Y, Tatsumi M, Hoshino H, Daar ES,
Koyanagi Y.
Isolation and characterization of an infectious HIV type 1
molecular clone from a patient with primary infection.
AIDS Res Hum Retroviruses. 2002 Oct 10;18(15):1127-33.
PMID: 12402946

Mochizuki N, Otsuka N, Matsuo K, Shiino T, Kojima A, Kurata
T, Sakai K, Yamamoto N, Isomura S, Dhole TN, Takebe Y,
Matsuda M, Tatsumi M.
An infectious DNA clone of HIV type 1 subtype C.
AIDS Res Hum Retroviruses. 1999 Sep 20;15(14):1321-4.
PMID: 10505681

Novelli P, Vella C, Oxford J, Daniels RS.
Construction and characterization of a full-length HIV-1(92UG001)
subtype D infectious molecular clone.
AIDS Res Hum Retroviruses. 2002 Jan 1;18(1):85-8.
PMID: 11804560

Ndung'u T, Renjifo B, Novitsky VA, McLane MF, Gaolekwe S,
Essex M.
Molecular cloning and biological characterization of
full-length HIV-1 subtype C from Botswana.
Virology. 2000 Dec 20;278(2):390-9.
PMID: 11118362

Ndung'u T, Renjifo B, Essex M.
Construction and analysis of an infectious human
Immunodeficiency virus type 1 subtype C molecular clone.
J Virol. 2001 Jun;75(11):4964-72.
PMID: 11333875

Takahoko M, Tobiume M, Ishikawa K, Ampofo W, Yamamoto N,
Matsuda M, Tatsumi M.
Infectious DNA clone of HIV type 1 A/G recombinant
(CRF02_AG) replicable in peripheral blood mononuclear cells.
AIDS Res Hum Retroviruses. 2001 Jul 20;17(11):1083-7.
PMID: 11485626

Earlier papers:

Adachi A, Ono N, Sakai H, Ogawa K, Shibata R, Kiyomasu T,
Masuike H, Ueda S.
Generation and characterization of the human
immunodeficiency virus type 1 mutants.
Arch Virol. 1991;117(1-2):45-58.
PMID: 1706590

Kuwata T, Igarashi T, Ido E, Jin M, Mizuno A, Chen J,
Hayami M.
Construction of human immunodeficiency virus 1/simian
immunodeficiency virus strain mac chimeric viruses
having vpr and/or nef of different parental origins and their in vitro
and in vivo replication.
J Gen Virol. 1995 Sep;76 ( Pt 9):2181-91.
PMID: 7561755

Collman R, Balliet JW, Gregory SA, Friedman H, Kolson DL,
Nathanson N, Srinivasan A.
An infectious molecular clone of an unusual
macrophage-tropic and highly cytopathic strain of human
immunodeficiency virus type 1.
J Virol. 1992 Dec;66(12):7517-21.
PMID: 1433527

Dirckx L, Lindemann D, Ette R, Manzoni C, Moritz D, Mous J.
Mutation of conserved N-glycosylation sites around the
CD4-binding site of human immunodeficiency virus type 1
GP120 affects viral infectivity.
Virus Res. 1990 Dec;18(1):9-20.
PMID: 2082620

Fisher AG, Collalti E, Ratner L, Gallo RC, Wong-Staal F.
A molecular clone of HTLV-III with biological activity.
Nature. 1985 Jul 18-24;316(6025):262-5.
PMID: 2410792

Popovic M, Sarngadharan MG, Read E, Gallo RC.
Detection, isolation, and continuous production of
cytopathic retroviruses (HTLV-III) from patients
with AIDS and pre-AIDS.
Science. 1984 May 4;224(4648):497-500.
PMID: 6200935

Ghrayeb J, Kato I, McKinney S, Huang JJ, Chanda PK,
Ho DD, Sarangadharan MG, Chang TW, Chang NT.
Human T-cell lymphotropic virus type III (HTLV-III)
core antigens: synthesis in Escherichia coli and
immunoreactivity with human sera.
DNA. 1986 Apr;5(2):93-9.
PMID: 3011373

Heidecker G, Lerche NW, Lowenstine LJ, Lackner AA, Osborn
KG, Gardner MB, Marx PA.
Induction of simian acquired immune deficiency syndrome
(SAIDS) with a molecular clone of a type D SAIDS retrovirus.
J Virol. 1987 Oct;61(10):3066-71.
PMID: 3041028

Fisher AG, Ratner L, Mitsuya H, Marselle LM, Harper ME,
Broder S, Gallo RC, Wong-Staal F.
Infectious mutants of HTLV-III with changes in the 3'
region and markedly reduced cytopathic effects.
Science. 1986 Aug 8;233(4764):655-9.
PMID: 3014663

Adachi A, Gendelman HE, Koenig S, Folks T, Willey R,
Rabson A, Martin MA.
Production of acquired immunodeficiency syndrome-associated
retrovirus in human and nonhuman cells transfected
with an infectious molecular clone.
J Virol. 1986 Aug;59(2):284-91.
PMID: 3016298

Sakai K, Dewhurst S, Ma XY, Volsky DJ.
Differences in cytopathogenicity and host cell range
among infectious molecular clones of human
immunodeficiency virus type 1 simultaneously
isolated from an individual.
J Virol. 1988 Nov;62(11):4078-85.
PMID: 3172338

Sakai K, Ma XY, Volsky DJ.
Low-cytopathic infectious clone of human immunodeficiency
virus type I (HIV-I).
FEBS Lett. 1988 Oct 10;238(2):257-61.
PMID: 2458968

More papers related to serological analysis of the products
of cloned HIV genes, etc.

Chandra A, Gerber T, Kaul S, Wolf C, Demirhan I, Chandra P.
Serological relationship between reverse transcriptases from
human T-cell lymphotropic viruses defined by monoclonal
antibodies. Evidence for two forms of reverse
transcriptases in the AIDS-associated virus, HTLV-III/LAV.
FEBS Lett. 1986 May 12;200(2):327-32.
PMID: 2423366

Chakrabarti LA, Ivanovic T, Cheng-Mayer C.
Properties of the surface envelope glycoprotein associated
with virulence of simian-human immunodeficiency virus
SHIV(SF33A) molecular clones.
J Virol. 2002 Feb;76(4):1588-99.
PMID: 11799153

Gorny MK, Williams C, Volsky B, Revesz K, Cohen S, Polonis
VR, Honnen WJ, Kayman SC, Krachmarov C, Pinter A,
Zolla-Pazner S.
Human monoclonal antibodies specific for conformation-
sensitive epitopes of V3 neutralize human
immunodeficiency virus type 1 primary isolates from
various clades.
J Virol. 2002 Sep;76(18):9035-45.
PMID: 12186887

Zhang PF, Bouma P, Park EJ, Margolick JB, Robinson JE,
Zolla-Pazner S, Flora MN, Quinnan GV Jr.
A variable region 3 (V3) mutation determines a global
neutralization phenotype and CD4-independent infectivity
of a human immunodeficiency virus type 1 envelope
associated with a broadly cross-reactive, primary virus-
neutralizing antibody response. J Virol. 2002 Jan;76(2):644-55.
PMID: 11752155

Ball JM, Payne SL, Issel CJ, Montelaro RC.
EIAV genomic organization: further characterization by
sequencing of purified glycoproteins and cDNA.
Virology. 1988 Aug;165(2):601-5.
PMID: 2841805

Rekosh D, Nygren A, Flodby P, Hammarskjold ML,
Wigzell H.
Coexpression of human immunodeficiency virus envelope
proteins and tat from a single simian virus 40 late
replacement vector.
Proc Natl Acad Sci U S A. 1988 Jan;85(2):334-8.
PMID: 2829181

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