The Wonderland of “HIV” “tests”
Posted by Henry Bauer on 2009/06/04
“HIV” tests are self-fulfilling prophecies (“HIV” tests are self-fulfilling prophecies, 10 May 2009). Those prophecies are particularly powerful since the actual physical tests are demonstrably invalid (“HIV” tests are demonstrably invalid, 19 May 2009). That’s not all (though it’s surely more than enough). Even as tools for academic research, the application of these tests is fraught. For example, a sub-specialty in HIV/AIDS research is the study of genetic diversity of the innumerable purported strains of “HIV”, including attempts to trace the purported origin of “HIV”. The latter has often relied on the examination of samples preserved from cases described decades ago. Whether those samples can properly be used for this purpose is highly doubtful: “Specimen integrity can have a significant impact on the performance of any assay [nota bene, any]. Manufacturers generally recommend that their kits be used on fresh sera” (p. 158 in Weiss & Cowan, “Laboratory detection of human retroviral infection”, cited in an earlier post (“HIV” tests are self-fulfilling prophecies, 10 May 2009).
A number of other statements in that review article contradict some additional, frequently dogmatic, claims made by defenders of HIV/AIDS theory:
— “virus can usually be recovered from seropositive persons” (p. 148, emphasis added; nota bene, not always). In addition, of course, virus is never “recovered” from anyone — see “Isolation” of “HIV”, below.
— “Only a fraction of initially seropositive newborns are actually HIV-infected” (p. 148) — yet all “HIV-positive” pregnant women and all their babies (at least during birth) are supposed to take the toxic antiretroviral drugs.
— “supplemental testing [is] sometimes referred to colloquially as ‘confirmatory testing’” (p. 155); euphemism again — it’s not “colloquially”, it’s misleadingly. Furthermore, Weiss & Cowan themselves later forget this point and speak of confirmatory assays (e.g., p. 160). They also note that such supplemental or confirmatory tests are not independent of one another since they all look for antibodies, leading to “overestimation of predictive values with most ‘supplementary’ tests”.
— “Early studies [of AIDS patients] . . . characterized immunologic impairment, particularly low CD4 counts, comparatively elevated CD8 counts, and a low CD4/CD8 ratio. Persons without AIDS, but who had similar risk behaviors as those with AIDS, frequently also had similar abnormalities. . . . tests of immune function remained useful for staging patients, but confirmed the expectation that they were not sufficiently accurate to be used to predict if a given individual were infected with HIV” (p. 161).
Hello! One should not use criteria based on CD4 counts for diagnosis? Yet it’s routine — in the United States — to tell “HIV-positive” individuals with CD4 <200 that they have “AIDS”, despite the fact that the “HIV” test itself is an invalid self-fulfilling prophecy.
Note too the admission that immunologic disturbances can result from a range of “risk behaviors”.
— “demonstration that an assay specifically measures viral antigen was a challenging task, insofar as there are no independent laboratory criteria. The specificity of a given assay is likely to prove greater in an acellular sterile body fluid such as cerebrospinal fluid. Moreover, antigen that is detected need not represent viable virus, so care in clinical and epidemiological interpretation may be necessary” (p. 164). Note in passing the euphemisms and weasel words, “challenging” ( = impossible in this context), “need not” (= do not), “care” (impossible, given the lack of definitive guiding criteria), “may be necessary” (God help us!). The substance of this revelation is that if any cellular material is present, then one cannot validly ascribe the presence of “HIV antigen” to the presence of “HIV”; and even in the absence of potentially confounding material, the mere presence of an “HIV antigen” does not mean that actual “HIV” is present.
— How to interpret a positive nucleic-acid test where antibody tests are negative is controversial; it “reflects our still emerging understanding of the biology of retroviral infection” (p. 167). This stands in stark contradiction to the claim made not infrequently by HIV/AIDS dogmatists as early as 1991 that “we probably know more about how HIV produces its pathology than about the pathological mechanism of virtually any other microbe’’ (p. 296 in Gallo, “Virus Hunting”, 1991)”.
— “molecular epidemiological analyses thus remain a research tool, with many theoretical and practical limitations to more generalized use” (p. 167) — something to bear in mind when the media disseminate some laboratory’s proud announcement that they have traced the origin of “HIV” through genetic analysis of its myriad mutants.
A stunningly revealing statement is that “AIDS patients with opportunistic infections have been shown to be significantly less reactive by EIA [ELISA] than AIDS patients with Kaposi’s sarcoma” (p. 159). Yet Kaposi’s is no longer ascribed to “HIV”, it’s “credited” to HHV-8; and moreover Kaposi’s is here implicitly admitted not to be an opportunistic infection. Yet “AIDS” patients who present with Kaposi’s are more likely to test “HIV-positive” than “AIDS” patients who are “really” infected with “HIV”!
But HIV/AIDS theorists can explain anything and everything, even such apparent contradictions. Here, the idea is that since “HIV” infection destroys the immune system, it is less able to generate the “HIV” antibodies that the tests detect. Let’s carry that nice ad hoc hypothesis a little further. By the time AIDS sets in, the immune system has been thoroughly decimated, so few if any antibodies can any longer be generated — thus AIDS patients will no longer test “HIV-positive”. OOPS! The tests were invented on the basis of reactivity of sera from AIDS patients . . . .
Complexities abound. “The relative titers of viral component-specific antibodies vary over time in individuals, leading to systematic differences in EIA reactivity (and, consequently, detection rates) among various populations or patient groups”. Or, in plainer language and exaggerating only somewhat, “HIV” tests are not always “HIV” tests?
Then, too, “in some persons HIV antigen may be produced in sufficient quantities to form immune complexes with corresponding HIV antibodies, potentially reducing the ability of those antibodies to bind to viral antigens in the assay and giving a false negative test result”. A layman’s question: If one is infected with “HIV”, would there not of necessity be “HIV” antigens present? Aren’t they what induce the generation of “HIV” antibodies?
Why Africans and African-Americans test “HIV-positive” more frequently than others:
Several sources of false positives are particularly prevalent in Africa that “may, in effect, systematically shift the standardization curve for African sera as compared to U.S. and European sera” — or, in other words, Africans are more likely to test “HIV-positive” on the tests developed for Europeans. That’s why people of African ancestry test “HIV-positive” at far higher rates than others. The “HIV” tests are racially biased — as I’ve said in 3 chapters of my book and in a number of blog posts.
This review of proper “HIV” testing makes a point at several places of the need to tune the tests to their particular purpose (screening, diagnosis, prognosis, treatment-related) and to the general prevalence in each tested population. That underscores how significant are the demographic constancies that I’ve cited as showing “HIV” to be endemic and not infectious. The same racial disparities — qualitative always, semi-quantitative usually, quantitative in many instances — are found among blood donors, military cohorts, pregnant women, babies, gay men, drug abusers, despite the different testing circumstances. Thus the disparities really are determined by race — they appear to be independent of the particular testing approach, since the differences show up in every type of test, be it of low sensitivity or high sensitivity, low specificity or high specificity.
Nucleic acid tests (NATs):
Weiss & Cowan are no more reassuring about the reliability of NATs than they are about antibody tests or direct tests for “HIV” antigens. (Regarding the latter, they mention “detection of HIV-1 p24 antigen, which can detect HIV-1 approximately 16-17 days following infection” [p. 161]. The uninitiated may not recognize the huge uncertainty underlying this bland assertion, in that there is no way to observe that a new “infection” has occurred; those 16-17 days represent an inference based on indirect evidence and a multitude of assumptions.)
With nucleic-acid detection, potential failings are again legion:
— “The region chosen for detection and amplification requires care”; again that euphemistic “care” standing for “there’s a lack of definitive guidance”.
— “Amplifying pro-viral integrated HIV within the human genome is analogous to finding successfully the proverbial needle-in-a-haystack”.
— “the nucleotides flanking a presumed constant region may vary (primer failure) or the amplified region may vary (probe failure)” — note “presumed”. All NATs presuppose a knowledge of a certain sequence of nucleotides characteristic of “HIV”, and in absence of a gold standard, this is guesswork based on indirect evidence.
— “The exponential amplification [the basis for PCR, used in all NATs] carries great risk of inadvertent contamination”.
— “Viral variation or defective viruses . . . may contribute to indeterminate results”.
(All the above bulleted points are from p. 165).
“Since defective retrovirus variants may be among those amplified, and at least in theory might be the only HIV detected, a positive NAT result (particularly in a seronegative individual) does not necessarily indicate active infection” (p. 166).
— ANTIBODY, ANTIGEN, OR NUCLEIC-ACID —
CAN BE VALIDLY SAID TO DETECT
ACTIVE INFECTION BY “HIV”
Nevertheless, these tests are the basis for informing countless individuals that they are “HIV”-infected.
“Isolation” of “HIV”:
HIV/AIDS enthusiasts like to talk of “isolating” “HIV”, by which they mean something quite different than the usual, normal meaning of “extracting in pure form”. It is actually successive culturing, which involves “the use of carefully selected permissive cell lines . . . or co-cultivation with fresh, normal lymphocytes which have been stimulated with mitogens and maintained with T-cell growth factor (and sometimes alpha-interferon) . . . . HIV isolates with a propensity for growth in specific lines . . . may reflect differences in cellular biology among HIV isolates”; and, once again, “Positive cultures may indicate either active or latent HIV infective states” (p. 167).
Thus, when one reads that “HIV was isolated” from someone, that’s no proof that the person is infected!
There could hardly be a clearer illustration of the dangers of taking technical jargon used by specialists as having the same meaning as the same words when they are commonly used with their dictionary meaning.
This entry was posted on 2009/06/04 at 10:22 am and is filed under experts, HIV and race, HIV risk groups, HIV skepticism, HIV tests, HIV/AIDS numbers. Tagged: “AIDS and Other Manifestations of HIV Infection”, “isolation” of HIV, “Laboratory detection of human retroviral infection”, Elliott P Cowan, HIV tests are demonstrably invalid, Kaposi’s sarcoma and “HIV-positive”, nucleic-acid tests for HIV, Stanley H Weiss. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.