HIV immunity mediated by the CCKR5 receptor - UK subject

by trevorskingle | June 5, 2007 at 12:06 am

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In the summer of 1987 I woke
up blind. I went to Moorefields
Eye Hospital
and was diagnosed with toxoplasmosis; one of the indicator illnesses for a
depressed immune system. I was prescribed steroid eye drops and went for an HIV
antibody test which turned out negative.

I moved to Peterborough in 1993 for a job working in the
HIV sector for a local charity. Then in 1994 I developed a subcutaneous herpes infection
in my face which swelled substantially, disfiguring my features. I also had
little white lesions on my tongue which looked like oral hairy leukoplakia, and
bags of skin full of pus grew in profusion in my armpits and groin (I pulled
them off myself). I was prescribed oral zovirax and two months later the
swelling had gone down and the white lesions on my tongue had disappeared. The
bags of pus filled skin eventually stopped growing. I got tested for HIV
antibodies again and again it came back negative.

In 1994, while I was working
in Peterborough,
I saw an advert for a research programme at St. Mary’s Hospital, Paddington, that
was looking for people who had been in relationships with people who were HIV
positive but who were testing negative for HIV antibodies. It was a research
programme looking at the difference between the blood of HIV antibody positive
people, and HIV antibody negative people who may have been exposed to the virus.
I volunteered and travelled to St. Mary’s and visited the Churchill Wing where
bloods were taken by Dr Emma Aarons and I underwent a bronchoscopy, carried out
by Dr Richard Coker, where tissue samples were taken from my lungs and
analysed. HIV was detected in the lung tissue samples using a PCR test (which I
was told is sensitive to 1 in 1,000,000
genome equivalents/ml). The researchers called me up at home in Peterborough to ask if I was OK, was I having
any difficulty with my lungs? I felt fine. Could I come back to St. Mary’s for
follow up tests please? I went back to St.
Mary’s to be given more blood tests; an HIV antibody test which again was
negative for HIV antibodies, a test for p24 antigen which is released when HIV
has infected the cells of the immune system; which was negative, and no
evidence of a continued presence of the virus. The researchers told me they had
then asked themselves if it was as a result of contamination of the equipment
in the bronchoscopy suite? When they went through the records I had been the first
patient in after a weekend, and the last positive person having had a
bronchoscopy in the suite had been six days previously. They then asked themselves
if it had been contamination in the lab? They had sent out five samples to five
different labs with the same results. They asked me to undergo another bronchoscopy,
and this time they could find no virus. Samples of my lung tissue were NASBA RNA (nucleic acid sequence-based amplification) tested (which I was told was sensitive
to 1 in 100,000,000 genome equivalents/ml) where only RNA genome copies are amplified, and a molecular sequencing test
(which I was told was sensitive to 1 viral particle in a 250ml sample) showed
nothing. Next they tested my cyto-toxic T-cells to see if there was a reaction to
HIV. They said that this would indicate that my immune system had encoded for
HIV and programmed my it to attack HIV; this time the result came back positive.
I was then told that I would have to assume that I was somehow infected with
HIV, whilst exhibiting a negative test result for HIV antibodies, and that I
would have to adjust my life and live, ostensibly, as an HIV positive person. I
was then sent for the same counselling that someone newly diagnosed with an HIV
infection would receive. I went into a deep depression and stopped socialising,
becoming more and more isolated as time went by.

Further tests took place
over a two year period. Then, in 1996, I had a telephone call from Emma Aarons
told me that they had taken my bloods to NYC and had found two people in the
USA with the same genetic profile could both trace their ancestry back to Russia
and were descended from Russian Jews. I told them that I was possibly of Polish
or Scandinavian ancestry. The last point proved of interest to the researcher
as the other place that they’d found people who were more likely to have a
similar genetic profile was in Scandinavia, where about 10% of the population
have the same genetic mutation. I was asked by Emma Aarons if I would be
prepared to go public and appear on Hungarian TV’s Tudamanyos Hirado aired on the 28th Oct 96 equivalent of Tomorrow’s
World; of which I have a copy. I was also asked by Emma Aarons if the head of
the research Sarah Rowland-Jones could call me. I said yes. Sarah Rowland-Jones
rang me to say that I was one of the most minutely examined people in the
world. She said that they’d discovered a double mutation in my genetic code
which sequences for a receptor which HIV uses to infect certain cells of the
immune system; something called a CCKR5 receptor, a normal copy of which is
necessary for the virus to lock onto before it can infect the immune cell. They
told me that I had been infected with HIV but because the virus couldn’t lock
onto and hide in the cells in my immune system there had been an immune
response and my immune system had dealt with the infection as it would any
other viral infection and had rid my body of the HIV virus; that I had had what
was called a transient infection. I was also told that there are two types of
mutation, a single mutation which drastically reduces the chances of the
predominant strain of HIV infecting the cells of the immune system and a double
mutation which confers a substantial resistance to infection of the immune
cells from the same predominant strain.

I was subsequently invited
back to St. Mary’s by Richard Coker , who had been the consultant at Jefferis
Wing, the HIV Clinic at St. Mary’s, who had been managing my case, to be shown
around the laboratories in the old wing and have the technical details of my
immune system profile explained to me.

Given that HIV immunity was,
and still is, an anathema for the HIV establishment, I still took it as said
that I was, as the researchers and counselling service had originally
suggested, in some way HIV positive and should live my life as such.

Since I knew that the HIV
establishment was particularly sensitive to claims of immunity I had been
living quietly with this experience since 1994-1996 when the research took
place; only my closest friends knew about what had happened to me. Then the
Stimpson case came to light via the News of the World and the HIV establishment
went on to castigate the paper and Mr Stimpson. I felt very awful, since I work
in the HIV sector, that I didn’t feel able to refute the disparaging remarks
that were made by leading figures in the sector as it would be the cause of
conflict at work, but also that the HIV establishment couldn’t see the news as
encouraging and as adding to the wealth of information that might eventually
lead to the development of an anti HIV drug therapy.

Last November (2006) I went
back to the Jefferis Wing for the first time since the research programme had
ended, and after explaining the situation was tested for HIV antibodies again,
the results of which were negative. I was then told by the clinician, Dr. Simon Portsmouth, that it could only be surmised that
the equipment that had been used in the original tests was contaminated. This
assertion is refuted by the approach used by the original researchers in
analysing multiple reciprocal tests from various laboratories which tested the original
lung tissue samples the results of which tested positive for the HIV virus, as
well as the review that was undertaken on the use of the bronchoscopy suite
when the samples had been taken.

I contacted the scientist,
Sarah Rowland-Jones, who had headed the original research programme who,
contrary to what she had told me on the telephone during the research, she said
in an e mail that none of the test results showed anything out of the ordinary
and there was no evidence of me ever having been infected with HIV. I found
this very odd given that the assertion that I was never infected is refuted by
the original positive test results for the cyto-toxic T cell response to HIV
test which was undertaken right at the start of the research. This had confirmed
I had a genetically programmed immune response to HIV; the evidence for which I
have in my medical case file. Also there’s also the information Sarah
Rowland-Jones gave to me on the telephone in 1996 about the genetic mutation I
have conferring immunity to HIV and that I had had a transient HIV infection.
Additionally the team of researchers at the time were quite happy for me to go
public on Hungarian TV. Since then lots of research has been done on the
particular genetic profile that I have and as a result much time, research and
funding has been invested in developing what are called CCKR5 antagonists,
particularly by Graham Moyle who is based at the Chelsea and Westminster
Hospital , and which could potentially reap a substantial return on that
investment for major pharmaceuticals such as Pfizer (Maraviroc), Schering-Plough
(Vicriviroc), Progenics (Pro 140), Takeda (Tak 652), Corporate Partnership (AK
602), and others coreceptor antagonists such as AMD 070, KRH 3955 and KRH 3140.

See ‘Entry Inhibitors’ and
‘Coreceptor Antagonists’ at

http://www.hivmedicine.com/textbook/haart/horizon.htm

and Graham Moyle’s
presentation on Maraviroc at

http://www.thebody.com/content/art40271.html

Though there are research results
and published papers confirming this type of immunity why is the HIV
establishment so reluctant to acknowledge the experience and case history
evidence of individuals? What gives them so much cause for concern that they
deny everything that happened?

For people who are HIV
positive this is a really sensitive issue but if I, and others like me, had not
volunteered to undergo tests, some of which were quite harrowing (the bronchoscopies
and lymph node aspirations using hypodermics directly into the lymph nodes),
the development of a potential treatments using the results of this research
would not have been possible. Confirmation of this type of immunity was
confirmed when Scientific American ran an article (Sept 1997) which followed a
complicated investigation into the link between exposure to HIV and the
existence of the CCKR5 mutation, which proved a positive correlation that
immunity to HIV is conferred as a result of this particular genetic profile,
and recently another article appeared in another, HIV sector, publication Positive
Nation (June 2007, page 53, ‘Same but Different’) which made the same case.

And the combination of illnesses
I suffered might generally be considered as a sign of a depressed immune system?
Though I have since offered myself as a test subject and had no response I can
only assume in the interim, and as an uneducated guess and until further
research confirms otherwise, that this may have been as a result of the virus
itself rather than the infections that occur as a consequence of the usual
effect of HIV invading the immune cells and destroying the body’s defence
system. The only condition I would make of volunteering as a test subject,
perhaps for one of the large pharmaceuticals, is that, if possible, a donation
be made to a charity of my choice