For a very long time, the central belief in HIV/AIDS theory has been that “HIV” kills CD4 cells (albeit by a mechanism that still remains to be identified), thereby wrecking the immune system and allowing opportunistic infections to take over. Measurements of peripheral (in the blood) CD4 cells have been a mainstay in research and treatment. Voices raised to point out the error of this, those of Heinrich Kremer or Juliane Sacher among others, have been studiously ignored. But now it’s become quite official:
“’In both studies, the volunteers who received IL-2 and antiretrovirals experienced notable, sustained increases in CD4+ T cell counts, as anticipated,’ notes NIAID Director Anthony S. Fauci, M.D. ‘Unfortunately, these increases did not translate into reduced risks of HIV-associated opportunistic diseases or death when compared with the risks in volunteers who were taking only antiretrovirals. Although further analyses may help us better understand these findings, the two studies clearly demonstrated that the use of IL-2 did not improve health outcomes for HIV-infected people.’”
That paragraph is from an official release by the National Institute of Allergy and Infectious Diseases (NIAID), “IL-2 immunotherapy fails to benefit HIV-infected individuals already taking antiretrovirals”
Increased CD4 counts do not translate into better health outcomes
for people on HAART —
even though the aim of HAART is supposed to be lower viral load
that supposedly allows rebounding of CD4 counts.
That could already have been inferred, of course, from the publication by Rodriguez et al., “Predictive value of plasma HIV RNA level on rate of CD4 T-cell decline in untreated HIV infection”, JAMA, 296  1498-1506: the predictive value is NIL; viral load doesn’t predict CD4 decline in untreated patients; so why expect that it would do so in HAART-treated patients? But these IL-2 trials had been running since 1999 and 2000 respectively, so why cut them short just because research has shown them to be superfluous or misguided? Or just because the experts who draw up NIH’s Treatment Guidelines have also been sure for some time that CD4, viral load, and patient health do not correlate with one another, they are independent of one another — that’s why the Treatment Guidelines have to distinguish among “virologic failure” (viral load doesn’t decrease under treatment), “immunologic failure” (CD4 counts don’t increase), and “clinical failure” (operation succeeds, viral load down and CD4 up, patient dies).
Mere facts, though, have never been particularly meaningful in HIV/AIDS research. Anything that clearly contradicts HIV/AIDS theory is not accepted as falsification, instead it’s taken as a mystery to be solved. More from the recent NIAID release:
“These are the findings of two large international clinical trials presented today at the Conference on Retroviruses and Opportunistic Infections (CROI) in Montreal. . . .
IL-2 is produced naturally in the body and plays an important role in regulating CD4+ T cell production and survival. As their CD4+ T cell levels drop, people infected with HIV become more vulnerable to AIDS-related opportunistic diseases and death. Earlier research established that giving synthetic IL-2 plus antiretroviral therapy to people with HIV infection boosts their CD4+ T cell counts more than does antiretroviral therapy alone, but it was unknown whether this boost translated into better health [emphasis added]”.
It’s asserted (highlighted sentence above) as though known with certainty that lower CD4 means worse prognosis; yet
“ESPRIT and SILCAAT were designed to test whether giving IL-2 to HIV-infected individuals already on antiretroviral therapy would keep them healthier longer than HIV-infected individuals taking only antiretrovirals.”
If the highlighted assertion above had been right, then these tests were not needed. If they were needed, then the assertion should not have been made.
These clinical trials themselves appear to have been sound; and they looked at CD4 counts in both ranges of interest — there have been long-standing questions about the optimum CD4 counts at which antiretroviral treatment might best begin:
“Together, the ESPRIT and SILCAAT studies involved more than 5,800 HIV-infected volunteers in 25 countries. Participants were assigned at random to receive either combination antiretroviral therapy alone or combination antiretrovirals plus injections of Proleukin (Novartis Pharmaceuticals, Basel, Switzerland), a synthetic form of IL-2, over several five-day cycles. To evaluate the effects of IL-2 treatment at different stages of HIV infection, the ESPRIT study enrolled people with early-stage infection (CD4+ T cell counts at or above 300 cells per cubic millimeter, or mm3), while the SILCAAT study enrolled volunteers with later-stage HIV infection (CD4+ T cell counts between 50 and 299 cells/ mm3).
It is unclear why increased CD4+ T cell counts did not translate into better health outcomes.”
What’s unclear? Increased CD4 doesn’t produce better prognoses. HIV/AIDS theory is wrong. But of course that’s unthinkable:
“James D. Neaton, . . . principal investigator of the global clinical trials network that conducted ESPRIT, offers two possible explanations. ‘It could be that the types of CD4+ T cells induced by IL-2 play no role in protecting the HIV-infected patient, and therefore the administration of IL-2 has no benefit,’ says Dr. Neaton. ‘A second possibility is that the CD4+ T cells are at least somewhat functional or that IL-2 has some modest benefit, but that the side effects of IL-2 may neutralize any possible benefit.’
‘. . .although a person’s number of CD4+ T cells is a key measure of success in the treatment of HIV with antiretroviral drugs, we can’t rely on CD4+ T cell counts to predict whether immune-based therapies such as IL-2 will improve the health of HIV-infected individuals,’ concludes Dr. Levy, the principal investigator of SILCAAT.”
If CD4 counts don’t predict what “immune-based” therapies can do . . .
BUT these CD4s are the immune-system cells that have been accepted for a quarter century as the critical ones in HIV/AIDS, the ones that are supposedly killed off by “HIV” — so isn’t EVERY therapy that seeks to increase CD4 an “immune-based” therapy?
If the problem is with the particular TYPE of CD4 cells, these results would be just as damaging to HIV/AIDS theory and practice, since it would mean that faulty or meaningless measures have been used for more than two decades to make life-or-death decisions as to antiretroviral treatment.
Still, the important thing to note is that these trials, though they failed, were actually successful:
“’The purpose of clinical research is to clearly state and accurately test hypotheses with an ultimate goal of improving patient care,’ notes H. Clifford Lane, M.D., director of clinical research at NIAID and a member of the executive committee of ESPRIT. ‘These two clinical trials successfully reached a definitive answer about the utility of IL-2 therapy for treating HIV infection. NIAID thanks the thousands of dedicated volunteers and investigators who made these studies possible. The results will have significant implications for the future development of immune-based therapies for HIV and studies of HIV pathogenesis.’”
But perhaps this was just official spin for public consumption, for at least one other similar trial was abandoned:
“NIAID has discontinued the use of IL-2 in a separate, 20-country clinical trial known as STALWART (which stands for ‘Study of Aldesleukin with and Without Antiretroviral Therapy’).”
I don’t know about SILCAAT, but I do like those acronyms ESPRIT and STALWART. Perhaps NIAID wordsmiths get their inspiration from the Pentagon.