I was introduced to the work of the Perth Group and also Peter Duesberg at a party more than 20 years ago, during a conversation with a couple other gay men. One started talking to me about the problems with the theory and I was stunned. I began reading everything I could get my hands on and managed to read through the technically demanding papers by the Perth Group.
I was shocked when I discovered that 50% of dogs have antibodies that cross react on the 'HIV' antibody tests. If 50% of dogs have cross-reacting antibodies, why don't 50% of gay men have equally non-specific antibody reactions I remember wondering?
Or the research they pointed to that looked at research into the 'HIV' antibody tests at 'sentinel' hospitals where upwards of almost 22% of non-risk group men were 'HIV' positive but who weren't dying of AIDS? To me this pointed to an epidemic of repeated testing and not to the spread of a new communicable agent in a population.
There are so many weird things like this in the world of AIDS research, but I think the biggest problem is gay men don't want to know this, by and large. They want to believe that the government has clear poppers as being ok to use, and that the pharmaceutical industry is doing them a favor by having them use PrEP.
I actually think Covid has breathed new life into this debate given that so many people are now seeing the light of day regarding Fauci, the pharmaceutical industry and how the government perpetuated a narrative that has fallen apart over time. In fact there's significant interest in questioning germ theory altogether with people like Dr. Sam Bailey and her husband being very vocal about dismantling not only 'HIV' but many other commonly received STDs and other pathogens.
I am one of those whom the HIV/AIDS issue was brought to light after covid. I am 60 and never gave HIV/AIDS a second thought until I saw Rebecca's interview with Dr Breggin not too long ago. I remember some of the fear of AIDS back in the 80s but I was neither gay nor did intravenous drugs so I wasn't concerned. I never even knew of Fauci (I won't give him the Dr) until March of 2020. Since HIV only affected a small percentage of the population I think there are many like me but now with covid everyone is affected so more are seeing the light. Interesting times indeed.
I think anything to do with Gallo can be ignored. The only 'virus' he obtained was the one he was sent by the French in September, which he then (very publicly backed by the US govt) passed off as his own in April 1984.
But what did the French have?
Their 'seminal' paper 'Isolation of a T-lymphotropic retrovirus from a patient (Patient BRU) at risk for acquired immune deficiency syndrome (AIDS)' is one of the most cited papers in the 20th century.
It is one the prime 'origin of AIDS' papers.
One of the first problems with the paper is that it was sent to Gallo for peer review. He added his own abstract and the first sentence clearly bears his stamp, describing Montagnier's discovery as 'a retrovirus belonging to the family of recently discovered human T-cell leukemia viruses (HTLV).'
A second problem refers to 'reproducibility'. On p57 of Montagnier's autobiography he writes,
'We tried...to redo the the (BRU) procedure on biopsies of patients at the same stage of illness. The results were either negative or created confusion.'
The third and biggest problem with the paper is that what actually became called 'HIV' in 1986, and what had been sent to Gallo in September 1983, was not taken from Patient BRU at all but from a Patient LAI. No formal research paper exists that links 'LAI' to AIDS.
Montagnier clarified the position in 'A History of HIV Discovery', published in Science, November 2002.
‘We tried (unsuccessfully) to grow the BRU isolate in different T cell lines. If we had tried the LAI isolate instead, we would have been able to grow the virus without any trouble. In October 1983, we were finally able to grow the BRU isolate in Epstein-Barr virus-transformed B cell lines, although we discovered later that the LAI virus had contaminated our BRU culture. At least six laboratories (including Gallo in Bethesda and Weiss in London) received the LAI sample (under the name BRU) from our group and experienced the same contamination. We think that the LAI virus readily contaminated the BRU culture because it associates with a mycoplasma species, Mycoplasma pirum, usually present in T cell lines. This physical association makes a fraction of the LAl virus highly infectious, and, in fact, this fraction can be neutralized with antibodies against M. pirum. As mycoplasmas are common contaminants of cultured cells, an infectious pseudotype virus (LAI associated with M. pirum) may have caused several contaminations between 1983 and 1984 in different laboratories' (including Gallo in Bethesda, Weiss in London and the CDC in Atlanta).
So, what the world knows as HIV-1, was a double contaminant, an infectious pseudotype virus (LAI associated with Mycoplasma pirum). That makes it worthless in scientific terms and renders everything connected to it, all AIDS research, AIDS test kits etc, invalid.
One of the major ‘canons’ of the ‘HIV causes AIDS’ orthodoxy was that AIDS was a new disease caused by a new virus.
Just how new was AIDS? My research quickly told me it wasn’t new at all. The only new thing about AIDS was the affected demographics and the branding.
Let me explain.
I have already mentioned that in the first five cases reported in the June 5th 1981 MMWR of PCP pneumonia, all five cases had evidence of CMV infection.
The Lancet of 12 December 1981 published details of a 49 year old homosexual man (a frequent visitor to Florida), who had reported to Brompton Hospital. He was diagnosed with PCP and cytomegalovirus (CMV) but had no underlying immune deficiency. This is widely regarded as the first report of a UK AIDS case. The paper’s headline was ‘Primary Pneumocystis Carinii and Cytomegalovirus Infections.’
Twenty years before this, October 29th 1960, another paper in the Lancet was published with the headline: ‘CYTOMEGALIC INCLUSION DISEASE AND PNEUMOCYSTIS CARINII INFECTION IN AN ADULT.’
‘In adults, cytomegalic inclusion disease is rare and takes a different form. It may be confined to a single organ in association with other diseases, notably those of the reticuloendothelial system. In a more generalised form, it is often accompanied by other systemic diseases.’ (For ‘other systemic diseases’ read opportunistic infections.)
The patient’s ‘general health was good until December, 1958; he then gradually developed breathlessness on exertion, nocturnal sweats, anorexia, loss of weight, tiredness, and fever. He had a cough, producing mucopurulent sputum.
He was wasted, febrile, and ill. There was moderate generalised gingivitis. A few scaly brownish lesions were seen on the skin of his back and shoulders.’ (Kaposi’s sarcoma?)
Post-death, ‘the body was severely emaciated. Numerous small lesions, some pustular, others dry and encrusted, were distributed irregularly over the skin of the thorax, abdominal wall, scapular regions, and inner aspects of thighs.
The main pulmonary lesion was a severe interstitial pneumonia associated with cytomegalic inclusion disease and a patchy Pneumocystis infection.
Generalised cytomegalic inclusion disease in the adult has been described in association with toxoplasmosis, Pneumocystis carinii infection and severe systemic diseases. (AIDS in all but name)
‘Steroid therapy…probably contributed to a decreased host resistance in this case, thus encouraging extension of the infections, and possibly allowing these saprophytic organisms to adopt a pathogenic role.
The pattern of generalised cytomegalic inclusion disease may vary, but the lungs, adrenals, liver, spleen, and kidneys are most commonly involved.
The association (of CMV) with Pneumocystis carinii infection was of further interest. Hamperl (1956) demonstrated the infection in a case of fatal inclusion (CMV) pneumonitis reported by McMillan (1947) and suggested the probability in two similar cases of Wyatt et al. (1953). Simultaneous Pneumocystis and cytomegalic inclusion infections have also been described by Berdnikoff (1959)i n a n infant. The association of these two apparently separate and normally saprophytic infections is interesting, and perhaps not entirely fortuitous, especially since the nature o f the Pneumocystis organism has not yet been determined. In due course a closer relationship may be established. It is important to recognise their potential pathogenicity and their ability to produce, either alone or in combination, fatal infections in man.
There is some evidence that this danger is increased by prolonged treatment with steroids and antibiotics. Possibly more cases will occur because of the increasing use of these drugs. At present, there is no effective treatment.
Very rarely both infections described have been found together in adults in association with serious underlying diseases; no underlying disease was identified in this patient.
The nature of the infections is discussed and reference is made to the risk of converting these saprophytes into pathogenic organisms by prolonged treatment with steroid drugs and antibiotics.’
There was no lack of either steroid or antibiotic usage amongst gay males in the 1970s.
Next time, in part five of ‘Hiding In Plain Sight - The CMV / AIDS connection’ , I will continue exploring the association between PCP pneumonia and CMV in the 1960s.
I was introduced to the work of the Perth Group and also Peter Duesberg at a party more than 20 years ago, during a conversation with a couple other gay men. One started talking to me about the problems with the theory and I was stunned. I began reading everything I could get my hands on and managed to read through the technically demanding papers by the Perth Group.
I was shocked when I discovered that 50% of dogs have antibodies that cross react on the 'HIV' antibody tests. If 50% of dogs have cross-reacting antibodies, why don't 50% of gay men have equally non-specific antibody reactions I remember wondering?
Or the research they pointed to that looked at research into the 'HIV' antibody tests at 'sentinel' hospitals where upwards of almost 22% of non-risk group men were 'HIV' positive but who weren't dying of AIDS? To me this pointed to an epidemic of repeated testing and not to the spread of a new communicable agent in a population.
There are so many weird things like this in the world of AIDS research, but I think the biggest problem is gay men don't want to know this, by and large. They want to believe that the government has clear poppers as being ok to use, and that the pharmaceutical industry is doing them a favor by having them use PrEP.
I actually think Covid has breathed new life into this debate given that so many people are now seeing the light of day regarding Fauci, the pharmaceutical industry and how the government perpetuated a narrative that has fallen apart over time. In fact there's significant interest in questioning germ theory altogether with people like Dr. Sam Bailey and her husband being very vocal about dismantling not only 'HIV' but many other commonly received STDs and other pathogens.
This is a super interesting period we're in.
I am one of those whom the HIV/AIDS issue was brought to light after covid. I am 60 and never gave HIV/AIDS a second thought until I saw Rebecca's interview with Dr Breggin not too long ago. I remember some of the fear of AIDS back in the 80s but I was neither gay nor did intravenous drugs so I wasn't concerned. I never even knew of Fauci (I won't give him the Dr) until March of 2020. Since HIV only affected a small percentage of the population I think there are many like me but now with covid everyone is affected so more are seeing the light. Interesting times indeed.
Re - Is there an HIV “reproducibility crisis”?
Thank you for the post Rebecca.
I think anything to do with Gallo can be ignored. The only 'virus' he obtained was the one he was sent by the French in September, which he then (very publicly backed by the US govt) passed off as his own in April 1984.
But what did the French have?
Their 'seminal' paper 'Isolation of a T-lymphotropic retrovirus from a patient (Patient BRU) at risk for acquired immune deficiency syndrome (AIDS)' is one of the most cited papers in the 20th century.
It is one the prime 'origin of AIDS' papers.
One of the first problems with the paper is that it was sent to Gallo for peer review. He added his own abstract and the first sentence clearly bears his stamp, describing Montagnier's discovery as 'a retrovirus belonging to the family of recently discovered human T-cell leukemia viruses (HTLV).'
A second problem refers to 'reproducibility'. On p57 of Montagnier's autobiography he writes,
'We tried...to redo the the (BRU) procedure on biopsies of patients at the same stage of illness. The results were either negative or created confusion.'
The third and biggest problem with the paper is that what actually became called 'HIV' in 1986, and what had been sent to Gallo in September 1983, was not taken from Patient BRU at all but from a Patient LAI. No formal research paper exists that links 'LAI' to AIDS.
Montagnier clarified the position in 'A History of HIV Discovery', published in Science, November 2002.
‘We tried (unsuccessfully) to grow the BRU isolate in different T cell lines. If we had tried the LAI isolate instead, we would have been able to grow the virus without any trouble. In October 1983, we were finally able to grow the BRU isolate in Epstein-Barr virus-transformed B cell lines, although we discovered later that the LAI virus had contaminated our BRU culture. At least six laboratories (including Gallo in Bethesda and Weiss in London) received the LAI sample (under the name BRU) from our group and experienced the same contamination. We think that the LAI virus readily contaminated the BRU culture because it associates with a mycoplasma species, Mycoplasma pirum, usually present in T cell lines. This physical association makes a fraction of the LAl virus highly infectious, and, in fact, this fraction can be neutralized with antibodies against M. pirum. As mycoplasmas are common contaminants of cultured cells, an infectious pseudotype virus (LAI associated with M. pirum) may have caused several contaminations between 1983 and 1984 in different laboratories' (including Gallo in Bethesda, Weiss in London and the CDC in Atlanta).
So, what the world knows as HIV-1, was a double contaminant, an infectious pseudotype virus (LAI associated with Mycoplasma pirum). That makes it worthless in scientific terms and renders everything connected to it, all AIDS research, AIDS test kits etc, invalid.
https://cascades.substack.com/p/cascaids-655?utm_source=profile&utm_medium=reader2
Hello and welcome to my eleventh ‘CascAIDS’ post.
One of the major ‘canons’ of the ‘HIV causes AIDS’ orthodoxy was that AIDS was a new disease caused by a new virus.
Just how new was AIDS? My research quickly told me it wasn’t new at all. The only new thing about AIDS was the affected demographics and the branding.
Let me explain.
I have already mentioned that in the first five cases reported in the June 5th 1981 MMWR of PCP pneumonia, all five cases had evidence of CMV infection.
The Lancet of 12 December 1981 published details of a 49 year old homosexual man (a frequent visitor to Florida), who had reported to Brompton Hospital. He was diagnosed with PCP and cytomegalovirus (CMV) but had no underlying immune deficiency. This is widely regarded as the first report of a UK AIDS case. The paper’s headline was ‘Primary Pneumocystis Carinii and Cytomegalovirus Infections.’
Twenty years before this, October 29th 1960, another paper in the Lancet was published with the headline: ‘CYTOMEGALIC INCLUSION DISEASE AND PNEUMOCYSTIS CARINII INFECTION IN AN ADULT.’
New disease?
Let me quote extensively from the 1960 paper https://www.penroseinquiry.org.uk/finalreport/pdf/LIT0013977.PDF
‘In adults, cytomegalic inclusion disease is rare and takes a different form. It may be confined to a single organ in association with other diseases, notably those of the reticuloendothelial system. In a more generalised form, it is often accompanied by other systemic diseases.’ (For ‘other systemic diseases’ read opportunistic infections.)
The patient’s ‘general health was good until December, 1958; he then gradually developed breathlessness on exertion, nocturnal sweats, anorexia, loss of weight, tiredness, and fever. He had a cough, producing mucopurulent sputum.
He was wasted, febrile, and ill. There was moderate generalised gingivitis. A few scaly brownish lesions were seen on the skin of his back and shoulders.’ (Kaposi’s sarcoma?)
Post-death, ‘the body was severely emaciated. Numerous small lesions, some pustular, others dry and encrusted, were distributed irregularly over the skin of the thorax, abdominal wall, scapular regions, and inner aspects of thighs.
The main pulmonary lesion was a severe interstitial pneumonia associated with cytomegalic inclusion disease and a patchy Pneumocystis infection.
Generalised cytomegalic inclusion disease in the adult has been described in association with toxoplasmosis, Pneumocystis carinii infection and severe systemic diseases. (AIDS in all but name)
‘Steroid therapy…probably contributed to a decreased host resistance in this case, thus encouraging extension of the infections, and possibly allowing these saprophytic organisms to adopt a pathogenic role.
The pattern of generalised cytomegalic inclusion disease may vary, but the lungs, adrenals, liver, spleen, and kidneys are most commonly involved.
The association (of CMV) with Pneumocystis carinii infection was of further interest. Hamperl (1956) demonstrated the infection in a case of fatal inclusion (CMV) pneumonitis reported by McMillan (1947) and suggested the probability in two similar cases of Wyatt et al. (1953). Simultaneous Pneumocystis and cytomegalic inclusion infections have also been described by Berdnikoff (1959)i n a n infant. The association of these two apparently separate and normally saprophytic infections is interesting, and perhaps not entirely fortuitous, especially since the nature o f the Pneumocystis organism has not yet been determined. In due course a closer relationship may be established. It is important to recognise their potential pathogenicity and their ability to produce, either alone or in combination, fatal infections in man.
There is some evidence that this danger is increased by prolonged treatment with steroids and antibiotics. Possibly more cases will occur because of the increasing use of these drugs. At present, there is no effective treatment.
Very rarely both infections described have been found together in adults in association with serious underlying diseases; no underlying disease was identified in this patient.
The nature of the infections is discussed and reference is made to the risk of converting these saprophytes into pathogenic organisms by prolonged treatment with steroid drugs and antibiotics.’
There was no lack of either steroid or antibiotic usage amongst gay males in the 1970s.
Next time, in part five of ‘Hiding In Plain Sight - The CMV / AIDS connection’ , I will continue exploring the association between PCP pneumonia and CMV in the 1960s.
regards,
Paul
I'm glad to hear that you have a lot of new readers!