HIV immunity mediated by the CCKR5 receptor UK subject

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 1995 for a job working in the HIV sector for a local charity. Then I

developed a subcutaneous herpes infection in my face which swelled substantially, disfiguring my

features till I looked a bit like the Elephant Man. 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.

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 NA (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 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 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; the equivalent of the UK's 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 (heterozygote) which drastically reduces the

chances of the predominant strain of HIV infecting the cells of the immune system and a double

mutation (homozygote) 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 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 awful, since I was working 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.

In 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 PCR tests of my lung tissue samples from various laboratories which

tested the original lung tissue samples the results of which tested positive for the HIV virus, as well as

the cyto-toxic T-cells test revealing that my immune system had encode for HIV and 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. These 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

homozygous delta base 32 pair double gene mutation of the genetic mutation to the CCKR5 receptors

which 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 (AK602), 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? Perhaps they, and the pharmaceutical companies that fund their research are worried

about previous research subjects laying claim to some of the profits that might emerge from the

production and distribution of the coreceptor antagonists? That’s not why I joined the research

programme. I got involved hoping any benefit might filter down to those who needed it the most not to

try to benefit from the increased profits of pharmaceutical companies!

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 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.