p24 is a designation that refers to the size of a protein (24,000
daltons, more or less). So it may refer to different proteins. In the
case of HIV, p24 refers to a core protein.

However, here I don't understand. If you look up p24 and
neuroblastoma, you get some interesting citations, mostly referring to
in vitro conditions under which HIV, via infected macrophages or glial
cells, induces production of toxic metabolites and by products that
can damage neurons.

I do see one reference to CD9 as p24. Not the same as HIV-p24.

As to being p24 reactive and HIV-negative, that would refer I imagine
to HIV's p24. It would suggest you were exposed to the virus but not
productively infected. Where did you get this test result? What test
was used?
George M. Carter


On 20 Aug 2003 15:26:08 -0700, bphata@intermind.net (Bill Patterson)
wrote:

On 21 Aug 2003 13:55:16 -0700, bphata@intermind.net (Bill Patterson)
wrote:

By the context of the discussion. The same way we know which "Bill"
we're talking about!

HTLV I/II is NOT the same as HIV. I don't know a lot about it, but it
appears to have a p24 protein as well.

It may be that you are infected with an HTLV? Do you have any
symptoms?

LOL...I'd say it takes the Prostate out of PSA!! Unless there's
something new about women' anatomy that slipped by me...I haven't been
keep up with the One True Gospel of God, the Weekly World News...

Likewise!

Wow--no, for me it was nothing so dramatic. I was home when it
happened and they were out at 4:10 pm and back up at 4:30 am. We were
lucky!


George--

***


Int J Hematol. 2003 May;77(4):412-3. Related Articles, Links

Seroindeterminate HTLV-1 prevalence and characteristics in blood
donors in Taiwan.

Lu SC, Chen BH.

Tainan Blood Center, Tainan, Taiwan.

Human T-cell leukemia virus type 1 (HTLV-1) is commonly accepted
as the cause of adult T-cell leukemia and tropical spastic
paraparesis/HTLV-1-associated myelopathy. Screening of blood donors
for HTLV-1 and HTLV-2 was implemented in Taiwan in February 1996. From
February 1996 to December 1998, we investigated the seroprevalence of
HTLV-1 in all unpaid blood donors in Taiwan. Of 2,578,238 donors in
all 6 blood centers, 1793 (0.06%) were seropositive for HTLV-1, and
605 (0.023%) were indeterminate for HTLV-1. Among these indeterminate
donors, 359 (59.3%) were male. The most common HTLV-1-indeterminate
pattern by Western blot in our study was GD21 alone (34.6%) followed
by p24 alone (7.8%), p53 alone (6.5%), and gp46 + GD21 (6.0%). That
GD21 pattern was found in 59.6% of indeterminate results in this study
suggested that the majority of nonspecific enzyme immunoassay
reactions were probably precipitated by viral envelop glycoprotein
GD21.

On Thu, 21 Aug 2003, GMCarter wrote:

Sounds like an ELISA - some of the endogenous RVs might well spike a p24
antibody enough to turn an ELISA positive but you'd not show up on a WB.

With all the work I've done with HIV Gag proteins I wouldn't be surprised
if I spiked an ELISA :-P

Bennett

On 27 Aug 2003 15:51:21 -0700, bphata@intermind.net (Bill Patterson)
wrote:

snip
What the ELISA and Western blot test for is the presence of an immune
response to HIV. If you are infected, the body produces antibodies.
That's what they detect.

Now, I suspect they will do a PCR which looks for the presence of
virus itself. It is not usually used as a diagnostic.

Say--the other test was HTLV-I --have you spent time in Japan? These
are different types of viruses.
George M. Carter

GMCarter wrote:
No PCR can test for the virus itself.
PCR is actually worse than Elisa an WB for looking
for the "real virus" . What am I saying : on all
three test leaflets it says : "this test cannot be
used as an indicator for the presence of hiv."


Different types of fantasies ?

Hayek.

gmc0@ix.netcom.com (GMCarter) wrote in message news:<3f4dcf70.2808177@news.verizon.net>...
George,
As you know I am a Viet Nam veteran and the Agent Orange, and 13 other
toxic chemicals they exposed us to, pretty much messed up our immune
systems. Example; Dr. John Martin tested me for the Stealth Virus,
when I asked him how the test came out the said that I grew the virus
three times as much, three times as fast as his normal cultures.

I have had the same remarks by other drs. on EBV, Herpes I, II, VI.

Take a look at my Photos page, when I get sores, I GET SORES.
http://www.intermind.net/~bphata/pictures.htm
Thanks much for your responses,
Bill Patterson
LV, Nev
*

On Thu, 28 Aug 2003 17:13:12 +0200, Hayek <hayektt@nospam.xs4all.nl>
wrote:

snip.
Nonsense.

George M. Carter

GMCarter wrote:
No, science.

Pcr tests for relatively small sequences, not for
whole virus.

You have proven again the shallowness of the
believers.

Hayek.

Hayek <hayektt@nospam.xs4all.nl> wrote in message news:<3F54E175.6060005@nospam.xs4all.nl>...
Could you tell me what part is false in the below quote from the SA?

"Scientific American:
Polymerase Chain Reaction (PCR)
....
Beginning with a single molecule of the genetic material DNA, the PCR
can generate 100 billion similar molecules in an afternoon."

This sounds like good science, can you point out where it goes a
stray? I'm really interested in what you have to say.

My eyes are about to fall out from trying to decipher all this stuff.
Thanks to both of you,
Bill Patterson
bphata@intermind.net
*

On 2 Sep 2003 18:14:12 -0700, bphata@intermind.net (Bill Patterson)
wrote:

Correct.

Incorrect.

This is correct. It can also be amplified RNA.

The denialist argument is that the piece of DNA (or RNA) that is
amplified is irrelevant and intrinsically meaningless. It is not an
intrinsically bad argument, except that the data accumulated over some
significant amount of time show that they are wrong.

Now, when you amplify a piece, or sequence, of DNA, it could be a bit
that is ALSO found on some other protein. Either something the body
already uses or another infection. So you could get a false positive
reading. Indeed, this CAN and occasionally DOES happen. Indeed, one
study, below, does suggest that in the hands of the researchers,
individuals with TB may have a positive PCR without HIV infection (see
below). However, even in this case, the HIV-negative controls do not
come up positive.

The sequences that have been selected are derived from the gag (core
HIV proteins) and env (envelope)/ regions. Similar efforts are
undertaken for determining Hepatitis C viral load.

Some have observed sequence homologies between different regions of
HIV genes and endogenous human ones as well as other genes. These
sequences do not necessarily overlap with the primers selected for
amplification. The thing is, one does not see these PCR results in
people who are NOT infected.

Thus, the specificity of PCR is really quite good, especially when
taken in context with other serological evaluation and the clinical
picture. It's sensitivity, though, under certain conditions, can be
found wanting (see the abstract from Turkey below).

The PCR technology is being utilized to more rapidly detect a variety
of other infections. It is NOT generally used as a diagnostic tool on
its own due to the limited sensitivity, however, with established HIV
infection based on antibody tests, it serves quite well.

George M. Carter

***
PS-here's an interesting one from 1996, Bill:

[Pub.C.1112] PROFILES OF CD4 CELL STATUS, HIV SUBTYPE PREVALENCE AND
OTHER VIRAL COINFECTIONS IN A STUDY POPULATION OF BOMBAY, INDIA

Joshi Pheroze J, Bhave GG*, Maniar JK**, Mukhopadhyaya R. Virology
Laboratory, Cancer Research Institute, KEM Hospital*, GT Hospital**,
Bombay, India.

Objective: To determine the CD4 (and CD8) cell percentage in the
peripheral blood mononuclear cells (PBMC) and PCR based evaluation of
HIV-1 and HIV-2 prevalence along with co-infection with HHV-6, HTLV-1
and II in the HIV positive population.

Methods: PBMC were derived from a total of 126 HIV ELISA positive
cases either in healthy asymptomatic stage or in different stages of
the disease and the CD4/CD8 subset analysis was carried out using an
indirect immunofluorescent assay. A total of 124 PBMC derived DNA were
tested by PCR amplification of HIV gag region, HIV-1 env region (V3
loop and flanks) and HIV-2 env region (gp 36). Also using PCR we
studied the presence of HHV-6, HTLV-I and II. All amplified products
were tested for specificity by end labeled oligo probe hybridisation.

Results: The CD4/CD8 subset analysis showed that advancing clinical
stages correlated with progressive depletion of CD4 cells. All 124
samples were positive for HIV gag amplification (115 bp), 97 were
positive for only HIV-I (422 bp), 2 for only HIV-2 (785 bp), and 20
were double positive. HHV-6 amplification (223 bp) was detected in 30
samples and HTLV-I (570 bp) in 3 cases HTLV-II was not detected in any
case.

Conclusions: CD4 depletion profile in the Indian HIV infected
population reflects the universal pattern. The dominant infection is
with HIV-1 (78.2%) with a relatively small size population (1.6%) with
only HIV-2 but a significant population (16%) showing presence of both
HIV-1 and 2. Apparently only HTLV-I and not HTLV-II has entered in but
a small number of the HIV infected population of Bombay though the
high HHV-6 infection level warrants further study.

P.J.Joshi, Virology Laboratory, Cancer Research Institute, Parel,
Bombay-400012., India.

Tel.: 91-22-4147360 Fax:91-22-4146089 email:cri3@soochak.ncst.ernet.in

***
Taci N, Yurdakul AS, Ceyhan I, Berktas MB, Ogretensoy M. Detection of
Mycobacterium tuberculosis DNA from peripheral blood in patients with
HIV-seronegative and new cases of smear-positive pulmonary
tuberculosis by polymerase chain reaction. Respir Med. 2003
Jun;97(6):676-81.

Ataturk Chest Disease and Thoracic Surgery Education and Research
Hospital, Ankara, Turkey.

Tuberculosis is still one of the most important cause of mortality and
morbidity in many countries and there is a need for new methods for
accurate and rapid diagnosis of tuberculosis. To determine the
sensitivity and specificity of polymerase chain reaction (PCR) method,
we have evaluated Mycobacterium tuberculosis DNA in peripheral blood
samples with PCR technique in adult patients with human
immunodeficiency virus (HIV)-negative and new cases of smear-positive
pulmonary tuberculosis. We investigated the relationship between
characteristic of the patients, radiological extension of the disease,
sputum smear grade, presence of cavity, body-mass index (BMI) serum
albumin level, total delay time and PCR positivity. Forty patients (33
male and 7 female; mean age 37.8 +/- 14.1) and 20 healthy control
subjects (13 male and 7 female; mean age 35.6 +/- 7.3) were enrolled
in this study. PCR was positive in 16 of 40 (40%) patients with
pulmonary tuberculosis and negative in 24 of 40 (60%). None of the
healthy controls had positive PCR results. The overall sensitivity
specificity and accuracy of the PCR assay was 40, 100 and 60%,
respectively. We found the positive correlation between PCR positivity
and sputum smear grade (r=0.46, P=0.003) radiological extension of the
disease (r=0.69, P=0.001), presence of cavity (r=0.90, P=0.001). We
conclude that the detection of M. tuberculosis DNA from peripheral
blood by PCR technique is useful for the rapid diagnosis of
tuberculosis patients with HIV-negative. Hematogenous dissemination
was important in tuberculosis patients and peripheral blood samples
were suitable and easy materials. However, standardization of the PCR
method must be ensured for the diagnosis of tuberculosis.

***
Young NL, Shaffer N, Chaowanachan T, Chotpitayasunondh T, Vanparapar
N, Mock PA, Waranawat N, Chokephaibulkit K, Chuachoowong R, Wasinrapee
P, Mastro TD, Simonds RJ; The Bangkok Collaborative Perinatal HIV
Transmission Study Group. Early diagnosis of HIV-1-infected infants in
Thailand using RNA and DNA PCR assays sensitive to non-B subtypes. J
Acquir Immune Defic Syndr 2000 Aug 15;24(5):401-7f

HIV/AIDS Collaboration, Nonthaburi, Thailand. nly0@cdc.gov

OBJECTIVES: To evaluate the sensitivity and specificity of RNA and DNA
polymerase chain reaction (PCR) for early diagnosis of perinatal HIV-1
infection and to investigate early viral dynamics in infected infants.
DESIGN: A cohort study of 395 non-breastfed infants born to
HIV-infected mothers in a randomized clinical trial of short-course
antenatal zidovudine. METHODS: Infant venous blood specimens collected
at birth, 2 months, and 6 months of age were tested by qualitative DNA
and quantitative RNA PCR (Roche Amplicor). To determine sensitivity
and specificity of DNA and RNA PCR, results were compared with later
DNA PCR results and to antibody results at 18 months. The HIV-1
subtype of the mother's infection was determined by peptide
serotyping. RESULTS: In the study, 92% of mothers were infected with
subtype E. DNA PCR sensitivity was 38% (20 of 53) at birth, and 100%
at 2 months (53 of 53) and 6 months (47 of 47). RNA PCR sensitivity
was 47% (25 of 53) at birth and 100% (53 of 53) at 2 months. All
samples that tested DNA-positive tested RNA-positive. Specificity was
100% for both DNA and RNA testing at all timepoints. For infected
infants, the median viral load of RNA-positive specimens was 407,000
copies/ml (5.6 log10) at birth, 3, 700,000 copies/ml (6.6 log10) at 2
months, and 1,700,000 copies/ml (6.2 log10) at 6 months. Infant RNA
levels at 2 and 6 months did not differ by maternal zidovudine
exposure, or RNA level at birth. CONCLUSION: This RNA PCR assay
performed well for diagnosing perinatal HIV subtype E infection,
detecting nearly half of infected infants at birth, and 100% at 2 and
6 months, with 100% specificity. Infected infant viral RNA levels were
very high at 2 and 6 months, and were unaffected by maternal
zidovudine treatment.

On Tue, 2 Sep 2003, Hayek wrote:

Sequences which are physically part of the virus structure, indeed are
the core of the virus, indeed what makes the virus what it is and
specifically amplified, unlike an antibody test which detects the bodies
reaction. Yes PCR does detect the virus as opposed to a marker for it. You
can do enough reactions and get a complete overlapped sequence for the
thing and get the whole sequence if you want - this is how cosmid based
sequencing was done for any number of viruses.

You are detecting the virus itself - your introduction of the word 'whole'
virus is arguing against something that George did not say.

Tim
--
When playing rugby, its not the winning that counts, but the taking apart
ICQ: 5178568

Bill Patterson wrote:
It multiplies a sequence of guanine, adenine,
thymine, cytosine, like in ...GATTACA..., but
then, lets say a few thousands long.

They warm and cool down the test tube, and each
time the sequences copy themselves.

This leads to 2x2x2x2x2x2... copies.
log(base 2) 100 billion = 37 cycles and you have
more than 100 billion copies of a sequence.



Look for dr "Nicholson" and "Mycoplasma" on
google. I will send you a document, I am sure you
will like reading this.

Hayek.

Tim Fitzmaurice wrote:
A lot of handwaving for a fauly argument.

Hayek.

In article <3F54E175.6060005@nospam.xs4all.nl>,
Hayek <hayektt@nospam.xs4all.nl> wrote:
There may be reasons not to use PCR to test for HIV, but this isn't one
of them. Cat hair is evidence of a cat. Bear tracks are evidence of a
bear. You don't need to see the "whole animal" to know it's around.

--
David Canzi

In article <3F59F730.E323F2A8@sfo.com>,
Brian Mailman <bmailman@sfo.invalid> wrote:
We were talking about PCR. Checking for Liquid Plumber is more like an
antibody test.

--
David Canzi

bphata@intermind.net (Bill Patterson) wrote in message news:<7b900a11.0308201426.7042d9e6@posting.google. com>...
A lot of nice answers can someone send me to a page that doesn't say
p24 is a core protein to HIV or ALTERNATE NAMES p24 are CD9, DRAP-27,
MRP-1, p24. I mean a p24 refers to a protein of a certain weight, how
does one know if they have found a p24 from an HIV or a p24 of an
HTLV-II, III, or a p24 of a cancer marker? If you find a p24 on an
HTLV-II test, and you don't find any of the other HTLV marker bands,
then it obviously isn't a p24 associated with an HTLV-II, which means
it must be a p24 of something else. Correct? And if you test for HIV
and you find a p24 for a HTLV.... Does anybody see what I am saying.
Thanks in advance,
Bill Patterson
LV, Nev

On 15 Sep 2003, Bill Patterson wrote:

If they find a "p24" in an ELISA kit they aren't looking at the weight,
oddly enough. They are looking at the antibody reactivity to that
protein. Sadly antibodies aren't completely perfect at recognising their
targets, and sometimes cross-reactions do occur. This is why they'll have
to look in some instances for other proteins to confirm the original
finding.

As for what those other proteins are, they could be anything! Well, not
really anything, but there's certainly no reason why they have to be 24
kilodaltons in size. As an example, my p24 antibodies in the lab will
react with the full-length Gag protein of HIV that contains p24, but is
itself about 55kD in size (p55). It's still a "p24" antibody though
because that's what it was created to bind to.

The problem has arisen because people are referring to a specific protein
"The Core Antigen of Human Immunodeficiency Virus Type 1" as "p24". So
the false positive is really a cross-reaction to another protein, not
detecting of anything that is 24kD in size. The problem isn't unique by
any means to HIV - science in general suffers from people shortening names
and giving them acronyms and abbreviations.

If the p24 was from an HTLV I test then it'll be "The Core Antigen of
Human T-Cell Lymphotrophic Virus Type I" rather than any old thing
weighing 24kD.

As for what could give a false-positive reaction to a p24 antigen: there
are plenty of endogenous viruses that humans carry that also have Core
Antigens similar to HIV and HTLV, and some people will have antibodies
that will cross-react. Welcome to the wonderfully clean and precise world
of immunology :-P

Bennett

Nick Bennett <njb35@cam.ac.uk> wrote in message news:<Pine.SOL.4.44.0309161248120.28602-100000@red.csi.cam.ac.uk>...
<snipped>
So Bennett, how does one find out which viruses have a p24, I've been
searching but to no avail. And so has my Infectious Disease Doc, my
Hematologist... The ID doc thinks it is AIDS, he just is having
trouble finding the illusive HIV env. Right now I'm battling a
fungi/bact. infection in my mouth, there isn't one part of me that has
turned into raw meat from time to time. You've probably seen my med
probs page. But I won't ever give up until I get an answer.

When I look at the NIH stuff on the HIV (graphics) I have to ask
myself, did it create it or did it collect it? Just a thought.

Thanks very much for you great answer,
Bill Patterson
LV, Nev.

On 16 Sep 2003, Bill Patterson wrote:

Blimey, well, that again depends on what you're trying to find:

A protein weighing 24 kilodaltons
A protein similar to a retroviral core antigen

If it's been detected with an ELISA-type test (i.e. using antibodies) then
it's probably the second. The answer to which is many-fold, but we can
narrow down the options.

Human viruses likely to have a p24-like protein are: HIV-1, HIV-2, HTLV-I,
HTLV-II and the endogenous viruses, of which there are probably over a
dozen. I only know this having been taught virology and worked in the
field of human retroviruses (albeit for only a few years) and I'm not sure
of an easy place to look it up. There are tests for all the exogenous
viruses mentioned above, and the endogenous viruses are almost certainly
harmless (i.e. I've never heard of them causing disease in anyone). You
and every other human being has been carrying them around for the past few
millenia without any apparent harm.

And so has my Infectious Disease Doc, my
Okay, having trouble finding env (or probably antibodies to env, but
PLEASE correct me if I'm making an incorrect assumption here!) probably
means it's simply not there.

It would be silly to struggle to find something that isn't there while
ignoring other possibilities. Now, that's not to say it isn't possible!
HIV-1 group O was discovered despite the index case not having responses
to env - the reason being that group O env is different from group M and N
and the tests weren't able to detect it. They can now.

Most current HIV tests look for HIV-1 group O, M, N and HIV-2 so you
should be pretty much covered. What tests exactly were run?

A blip on the ELISA (p24) followed by a failed detection of env antibodies
(on the Western Blot) means a negative diagnosis - you're clear. But of
course that still leaves your symptoms to explain.

Right now I'm battling a
I don't think I have actually - can you post a link up again? Knowing a
history would help as much as (if not more than) a bunch of test results
:-) Knowing what tests _haven't_ been done yet would also help.

I'm willing to bet it's a false positive reaction to that one protein and
you have something else funky going on.

Glad to help where I can, I just hope I'm making sense and not talking in
jargon too much.

Cheers

Bennett

Nick Bennett <njb35@cam.ac.uk> wrote in message news:<Pine.SOL.4.44.0309170908520.16140-100000@red.csi.cam.ac.uk>...
<snipped>
Thanks Bennett, my list is:
http://www.intermind.net/~bphata/medprobs.htm
and getting longer by the day. As I said now I'm loosing the gums,
bone and teeth. With the bone going I'm going to have big problems
soon, so I must find the answer soon.

All herpes, I, II, VI, EBV, Stealth, Hepatitis C (hep. B ok now),
fungi, bact., Hypertension, osteoporosis, osteoarthritis, Rheumatoid
Arthritis, and now I'm living in Las Vegas with its mold and Valley
Fever nipping at my heels. I'm about to give up on the govenment docs
and go back to the civilian docs next week. Like I said last week, the
oncologist was sure it was CML, but it was my impression from the last
visit the bone marrow was negative. He also is changing my diagnosis
from Polycythemia Vera to Erythrocytocis, hehe from black to gray.

I really do appreciate your excellent answers,
Sincerely,
William Patterson
Las Vegas, Nev.

PS: You might enjoy seeing the numbers from the last round of civilian
doctors.
http://www.intermind.net/~bphata/P3.htm