The pharmaceutical giant has refused to distribute a safer formulation of its anti-HIV drug Truvada so that it can make more money on the original, more toxic version of the drug
By February 2021, eight months into my HIV/AIDS research, I had come to the conclusion that the ‘HIV causes AIDS’ narrative was a house built on sand. Robert Gallo sciencefictions.net in Bethesda had nothing in his lab apart from what he had been given by the French. The French in Paris had nothing in their lab but a double contaminant. penroseinquiry.org.uk/finalreport/pdf/L…
As Montagnier himself wrote:
‘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.’
‘A History of HIV Discovery’ - Luc Montagnier, SCIENCE, VOL 298, 29 NOVEMBER 2002.
If HIV was not the cause of AIDS then what was? Also in February 2021 I began reading ‘And The Band Played On’, the ‘definitive history of the spread of AIDS throughout the USA in the 1980s.’ I was struck by how many patients, despite Don Francis protestations that the virus had not killed anyone (p73 paperback edition), in the first 124 pages, were stricken by severe CMV infections.
I thought AIDS has to be caused by something, why not check this virus, and its connection with the syndrome, out.
I soon hit a rich seam.
On June 4, 1981, MMWR published a cdc.gov/mmwr/preview/mmwrhtml/00043494.… ‘Pneumocystis Pneumonia -- Los Angeles’, about Pneumocystis carinii pneumonia in homosexual men in Los Angeles. This was the first published report of what, a year later, became known as acquired immunodeficiency syndrome (AIDS).
The paper co-authored by Michael Gottlieb and Wayne Shandera, begins with:
‘In the period October 1980-May 1981, 5 young men, all active homosexuals, were treated for biopsy-confirmed Pneumocystis carinii pneumonia at 3 different hospitals in Los Angeles, California. Two of the patients died. All 5 patients had laboratory-confirmed previous or current cytomegalovirus (CMV) infection and candidal mucosal infection.’
The Editorial Note expanded upon the possibility CMV had a role to play in AIDS.
‘All 5 patients described in this report had laboratory-confirmed CMV disease or virus shedding within 5 months of the diagnosis of Pneumocystis pneumonia. CMV infection has been shown to induce transient abnormalities of in vitro cellular-immune function in otherwise healthy human hosts. A high prevalence of CMV infections among homosexual males was recently academic.oup.com/jid/article-abstract/1…179 (94%) of 190 males reported to be exclusively homosexual (and sexually active) had serum antibody to CMV. In another study of 64 males, 4 (6.3%) had positive tests for CMV in semen, but none had CMV recovered from urine. Two of the 4 reported recent homosexual contacts. These findings suggest not only that virus shedding may be more readily detected in seminal fluid than in urine, but also that seminal fluid may be an important vehicle of CMV transmission. All the above observations suggest the possibility of a cellular-immune dysfunction related to a common exposure that predisposes individuals to opportunistic infections such as pneumocystosis and candidiasis.’
‘Common exposure?’ 94% sounded like common exposure to me. That report, published in February 1981, concluded that ‘homosexual men are at greater risk for CMV infections than are heterosexual men.’
Just four days before the MMWR report came out, another paper, pubmed.ncbi.nlm.nih.gov/6262407 was published on June 1st 1981.
In the abstract was this CMV/AIDS smoking gun:
‘Acute CMV infection is associated with a reversal in the normal ratio of helper to suppressor T lymphocytes with relative and absolute decreases in T helper cells and corresponding increases in T suppressor cells.’
This ‘reversal in the normal ratio of helper to suppressor T lymphocytes’ was the immune system marker of AIDS patients. The abstract to the June 1st 1981 paper stated that: ‘During convalescence, helper T lymphocytes increase, suppressor T lymphocytes decrease, and Con A responses return to normal.’
I thought about AIDS patients. There was no ‘convalescence’ for them, and therefore no return to normality for their T (for Thymus)-cells, or their immune systems.
Within a short space of time I had discovered that, no matter what Don Francis thought, CMV had the means and the opportunity to be a major factor behind the new ‘mystery’ immune system syndrome in sexually active gay males.
Thanks for reading CascAIDS post number nine. Please let me know what you think about my posts so far.
Next time, in part two of ‘Hiding In Plain Sight - The CMV / AIDS connection’ cascades.substack.com/publish/post/1353…, I will examine another paper co-authored by Michael Gottlieb, nejm.org/doi/full/10.1056/nejm198112103…, published in December 1981, which examines in some detail the relationship between CMV and AIDS.
Great work Rebecca. The reporting and exposes of folks like you, Celia Farber and others has opened many eyes (including mine) and surely saved many lives.
cascades.substack.com/p/cascaids-acd?ut…
Hello and welcome to my ninth ‘CascAIDS’ post.
By February 2021, eight months into my HIV/AIDS research, I had come to the conclusion that the ‘HIV causes AIDS’ narrative was a house built on sand. Robert Gallo sciencefictions.net in Bethesda had nothing in his lab apart from what he had been given by the French. The French in Paris had nothing in their lab but a double contaminant. penroseinquiry.org.uk/finalreport/pdf/L…
As Montagnier himself wrote:
‘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.’
‘A History of HIV Discovery’ - Luc Montagnier, SCIENCE, VOL 298, 29 NOVEMBER 2002.
If HIV was not the cause of AIDS then what was? Also in February 2021 I began reading ‘And The Band Played On’, the ‘definitive history of the spread of AIDS throughout the USA in the 1980s.’ I was struck by how many patients, despite Don Francis protestations that the virus had not killed anyone (p73 paperback edition), in the first 124 pages, were stricken by severe CMV infections.
I thought AIDS has to be caused by something, why not check this virus, and its connection with the syndrome, out.
I soon hit a rich seam.
On June 4, 1981, MMWR published a cdc.gov/mmwr/preview/mmwrhtml/00043494.… ‘Pneumocystis Pneumonia -- Los Angeles’, about Pneumocystis carinii pneumonia in homosexual men in Los Angeles. This was the first published report of what, a year later, became known as acquired immunodeficiency syndrome (AIDS).
The paper co-authored by Michael Gottlieb and Wayne Shandera, begins with:
‘In the period October 1980-May 1981, 5 young men, all active homosexuals, were treated for biopsy-confirmed Pneumocystis carinii pneumonia at 3 different hospitals in Los Angeles, California. Two of the patients died. All 5 patients had laboratory-confirmed previous or current cytomegalovirus (CMV) infection and candidal mucosal infection.’
The Editorial Note expanded upon the possibility CMV had a role to play in AIDS.
‘All 5 patients described in this report had laboratory-confirmed CMV disease or virus shedding within 5 months of the diagnosis of Pneumocystis pneumonia. CMV infection has been shown to induce transient abnormalities of in vitro cellular-immune function in otherwise healthy human hosts. A high prevalence of CMV infections among homosexual males was recently academic.oup.com/jid/article-abstract/1…179 (94%) of 190 males reported to be exclusively homosexual (and sexually active) had serum antibody to CMV. In another study of 64 males, 4 (6.3%) had positive tests for CMV in semen, but none had CMV recovered from urine. Two of the 4 reported recent homosexual contacts. These findings suggest not only that virus shedding may be more readily detected in seminal fluid than in urine, but also that seminal fluid may be an important vehicle of CMV transmission. All the above observations suggest the possibility of a cellular-immune dysfunction related to a common exposure that predisposes individuals to opportunistic infections such as pneumocystosis and candidiasis.’
‘Common exposure?’ 94% sounded like common exposure to me. That report, published in February 1981, concluded that ‘homosexual men are at greater risk for CMV infections than are heterosexual men.’
Just four days before the MMWR report came out, another paper, pubmed.ncbi.nlm.nih.gov/6262407 was published on June 1st 1981.
In the abstract was this CMV/AIDS smoking gun:
‘Acute CMV infection is associated with a reversal in the normal ratio of helper to suppressor T lymphocytes with relative and absolute decreases in T helper cells and corresponding increases in T suppressor cells.’
This ‘reversal in the normal ratio of helper to suppressor T lymphocytes’ was the immune system marker of AIDS patients. The abstract to the June 1st 1981 paper stated that: ‘During convalescence, helper T lymphocytes increase, suppressor T lymphocytes decrease, and Con A responses return to normal.’
I thought about AIDS patients. There was no ‘convalescence’ for them, and therefore no return to normality for their T (for Thymus)-cells, or their immune systems.
Within a short space of time I had discovered that, no matter what Don Francis thought, CMV had the means and the opportunity to be a major factor behind the new ‘mystery’ immune system syndrome in sexually active gay males.
Thanks for reading CascAIDS post number nine. Please let me know what you think about my posts so far.
Next time, in part two of ‘Hiding In Plain Sight - The CMV / AIDS connection’ cascades.substack.com/publish/post/1353…, I will examine another paper co-authored by Michael Gottlieb, nejm.org/doi/full/10.1056/nejm198112103…, published in December 1981, which examines in some detail the relationship between CMV and AIDS.
regards,
Paul
Great work Rebecca. The reporting and exposes of folks like you, Celia Farber and others has opened many eyes (including mine) and surely saved many lives.