Wednesday, February 15, 2012

HIV Tests Are Not HIV Tests. WHAT? part 2

Exploring more from the posting HIV Tests Are Not HIV Tests. WHAT?  dated FEBRUARY 7, 2012. Henry H. Bauer, Ph.D. adds:


HIV tests do not detect HIV. The seminal papers did not demonstrate HIV to be the cause of AIDS. The patent based on this work did not demonstrate that HIV tests are specific for HIV. The progression from “HIV is the probable cause of AIDS” to “HIV antibodies demonstrate active infection by HIV” came by assertion and not evidence. HIV-test-kits do not claim that the test detect infection, and they have never been approved for that purpose. There is no gold standard for an HIV test, and the existing tests are at best adjuncts to clinical diagnosis.
Drastic consequences include that healthy individuals are subjected to iatrogenic harm through life-long intake of highly toxic medication.


So-called “HIV tests” do not detect infection by HIV (human immunodeficiency virus, a retrovirus), even though for more than a quarter century these tests have been widely used precisely as purported diagnosis of such infection. The manufacturers of the test kits do not claim that the tests detect infection, nor has the Food and Drug Administration approved the tests for that purpose, and authoritative discussions of how to detect HIV infection make plain that the tests are insufficient to diagnose infection.

The story behind this circumstance has a number of parts:
1.     The initial claimed discovery or identification of a retroviral cause of AIDS.
2.     The patented method for detecting antibodies claimed to be specific to human immunodeficiency virus.
3.     A progression from claiming to find antibodies to presuming that presence of antibodies signifies active infection --- without the benefit of any specific evidence to that effect and in the face of evidence to the contrary.
4.     In absence of any gold standard test, the first (unproven, unvalidated) antibody test has been the basis for supposed validation of all later tests.
The consequences of the mistaken equating of “HIV-positive” with “infected by human immunodeficiency virus” could not be more serious. Healthy individuals who happen at some time to test “HIV-positive” have suffered physical, psychological or financial damage as a result of such a “diagnosis”; particularly harmed have been gay men and people of African ancestry.
In the following, when citing early work that employed the nomenclature of HTLV-III and LAV, those terms are used rather than the now-agreed term “HIV.”

ANNOUNCEMENT of an AIDS-causing retrovirus

HTLV-III was the probable cause of AIDS, the Secretary for Health and Human Services announced on 25 April 1984 at a press conference, introducing the purported discoverer, Robert Gallo. Four later publications in Science repeated that claim.

Popovic et al. 1 described an immortalized T-cell line in which large quantities of HTLV-III could be obtained by co-culture with putatively infected T-cells. Retrovirus was detected through the presence of “particle-associated RT [reverse transcriptase]”, and RT activity was also the criterion for choosing a sucrose density of 1.16 g/ml as the “band” in which retrovirus would be found under ultracentrifugation. However, reverse transcriptase activity is present in normal cells, which vitiates a central element in this work as well as in much subsequent research on HIV: the “particles” with which RT activity was associated could just as well have been cellular debris and not virions. Electron microscopy claiming the presence of large amounts of “extracellular viral particles” was not supported by evidence that these particles were in fact virions. The virus was also said to be detectable via antigen-antibody reaction, but this involved a tautology, see in the next section “Isolation is not isolation; purification is not purification.”

It was further stated that HTLV-III proteins had been found in 85% of sera from AIDS patients and that HTLV-III is related to HTLV-I and -II, retroviruses previously discovered by Gallo, whereas by contrast the lymphadenopathy-associated retrovirus LAV described earlier by Barré-Sinoussi and Montagnier was not related to HTLV-I or -II and was reactive to only 37.5% of sera from AIDS patients. Those claims were soon shown to be false. HTLV-III in fact was LAV, a sample of which Montagnier had sent to Gallo; and the 2009 Nobel Prize for discovering the virus went to Barré-Sinoussi and Montagnier to the exclusion of Gallo. Numerous flaws have been uncovered in the work reported from Gallo’s laboratory, and it was owing only to a technicality that Gallo himself failed to be charged formally with scientific misconduct 2.

In an article immediately following that of Popovic et al. 1, Gallo et al. 3 claimed to have isolated HTLV-III from 26 of 72 AIDS patients, 18 of 21 individuals with pre-AIDS, 3 of 4 healthy mothers of children with AIDS, and 1 of 22 “normal male homosexual subjects.” However, as an illness becomes more severe, one might expect to find more of the pathogenic agent at work rather than less, so it seems strange that “the primary cause of AIDS” could be found in only 36% of those suffering from the active disease when it could be found in 86% of those merely with pre-AIDS. Moreover, the symptoms of “pre-AIDS” were fever and chronically swollen lymph nodes, seen in many illnesses and not specifically precursors to AIDS; those symptoms were presumed to be such precursors only when encountered in people belonging to the groups in which AIDS had appeared, gay men or injecting drug abusers. Beyond that, “isolated” is drastically misleading, see “Isolation is not isolation; purification is not purification” in the next section.

The third article published at the same time 4 again asserted that HTLV-III is “a true member of the HTLV family” yet “clearly distinguishable from HTLV-I and -II.” There were somewhat confused claims about which antigens are associated with which of these retroviruses. Thus p61 and p65 are “encoded by HTLV-I” yet often recognized by sera from AIDS patients. Antigens of HTLV-III are “similar in size” to those of other HTLVs but include three “serologically unrelated” groups: p55 and p24 which are “group-specific”; p65 is “envelope-related”; and the third group is “of unknown affiliation.” In one place it is said that “antibodies to the structural proteins of HTLV, notably p24 and p19 (15), are not detectable in most AIDS patients (16)”, yet later p24 is included among the “most prominent . . . antigens” of HTLV-III, namely p65, p60, p55, p41, p24; less prominent were said to be p88, p80, p39. p32, p28, p21. Some cross-reaction of p65 with HTLV-I was acknowledged, as well as cross-reactions with unspecific gag-related antigens. Nevertheless, specificity was claimed for p65, p55, p41, p39, p32, p24 as “newly expressed after viral infection”; but of course this does not preclude the possibility that these antigens might be found also in association with other agents than HTLV-III. It is pertinent that the immunological abnormalities seen in AIDS patients are also present in people suffering from, for instance, tuberculosis, diabetes, malaria, macroglobulinemia, aplastic anaemia, or thalassaemia, and that they can be induced by (for example) adrenalin, prednisone, or Epstein-Barr virus 5.

The fourth article 6 reported antigens of HTLV-III to be reactive with sera of 88% of AIDS patients and 79% of gay men with pre-AIDS symptoms as well as with under 1% of “heterosexual subjects.” This time the major reactivity was said to be against p41, a presumed viral-envelope antigen.
These papers fall far short of demonstrating that HTLV-III is a necessary and sufficient cause of AIDS. That has often been remarked, for example, “the evidence does not constitute proof of the isolation of a retrovirus, that the virus is exogenous or that the virus is causally related to AIDS” 7. All that the Gallo opus showed is that antibodies in sera from AIDS and pre-AIDS subjects react with material obtained from cultures infected with agents present in sera from AIDS and pre-AIDS subjects, a circular procedure 8 that does not clarify the nature of the “isolated” materials; nor had it been shown that similar reactivity is not present in other physiological conditions or in other illnesses than AIDS.

PAtent for detecting the virus

U.S. Patent 4,520,113 granted to Robert Gallo and co-workers Mikulas Popovic and Mangalasseril G. Sarngadharan, dated 28 May 1985, claims that “antigens associated with the infection of human cells by this virus are specifically recognized by antibodies from AIDS patients. Specifically, HTLV-III isolated from AIDS patients and transmitted by cocultivation with an HT cell line is specifically detected by antibodies from human sera taken from AIDS patients.”

Claimed test is non-specific
This nascent test was hardly foolproof, since sera from only 88% of AIDS patients and from 79% of pre-AIDS gay men showed positive and since positive reactions were also seen in some presumably uninfected blood donors 6. From the very beginning, the test was anything but specific.
One reason may be the claim of p41 as the most characteristic and prominent HIV-specific antigen, and that p65, p60, p55, and p24 too were “not detected in normal sera.” However, antibodies to p24 are found in substantial proportions of patients with multiple sclerosis, T-cell lymphoma, and generalized warts 9. Moreover, in about 15% of healthy blood donors, p24 was “the predominant band” on Western Blot tests, and p41 has also been found in blood platelets of healthy individuals 7. Far from being specific to HIV or AIDS patients, then, p24 and p41 are not even specific to illness.

Isolation is not isolation; purification is not purification
In the patent as well as in the earlier articles in Science, and in the HIV/AIDS literature overall to date, “isolation” and “purification” do not have the meaning those terms convey in common parlance or when used by chemists or physicists. For the latter scientists and for most people, isolation means to extract solely the pertinent entity free from all other material. Purification means, similarly but not identically, to remove all contaminants to leave only the pertinent entity.
In HIV/AIDS parlance, however, “isolation” and “purification” do not mean getting pure HIV from an AIDS patient: that has never been shown to be done in the only possible way, which would be to detect by electron microscopy actual virions of HIV and nothing else in a purified sample taken directly from a patient. Instead, HIV “isolation” means that serum from a patient is cultured together with various cells and reagents and that a later extract from that culture reacts “HIV-positive.” It is assumed that the culturing amplifies already-present HIV, but one cannot exclude that the culturing actually produced ab initio whatever was generating a positive test-response. Indeed, human genomes include some DNA sequences homologous with “HIV”, and these may be expressed by culturing techniques like those used in HIV/AIDS research 7.

“Purification” in HIV/AIDS parlance means that material thought to contain HIV is ultracentrifuged in a specified medium, and what sediments at a particular density is regarded as “HIV.” In point of fact, published electron micrographs of such “purified” “isolates” show a motley mixture of cellular debris, by far not pure virions 10.

Gallo has even asserted that there is no need to purify HIV since his method of culturing produces so much of it that it did not matter what else might have been present:
You have to purify. . . . [A] retrovirus comes out of chromosome membrane. In so doing, it incorporates some cellular proteins in the virus. . . . [B]y putting it through a sucrose gradient it would do hardly anything when you have very little virus. So the ratio of cellular material to virus, I don’t want to say this is an accurate number but I will give an example. Let’s say it would be a thousand to one but when we succeeded in mass producing the virus in a continuous culture, you have got an enormous purification far beyond the sucrose gradient alone because you are now producing loads of virus with little amounts of cell. 11

It is far from obvious why each virion would incorporate less cellular protein in mass culture, but in any case the presence of even tiny amounts of some unknown, undetected, active agent can confound experiments. There can be no substitute for complete purification, literal isolation.

No longer operative
A number of assertions in the patent have since been quietly forgotten, for example that there is a certain cross-reactivity with Gallo’s HTLV-I and HTLV-II retroviruses. Gallo had earlier reported isolation of HTLV-I from an AIDS patient 12 and described HTLV-I and -II as  the only known specific co-factors for AIDS” (emphasis in the original) 13.

The patent assigns the main specificity of the test to p41, with some reactivity also to p65, p60, p55, and p24. But the contemporary criteria for Western Blot tests call for any 1 or 2 of p160, p120, p41, not necessarily the “most prominent” p41; and some 2 or 3 among p68, p55, p53, p39, p32, p24, p18. Only 3 of the 5 antigens said by Gallo to be specific for HIV are among the 10 now supposedly Western-Blot specific for HIV 14.

 Arbitrary criterion for “positive”
The primary antibody test (ELISA) measures a color intensity. Controls are not perfectly colorless, however; what intensity of color shall be judged “positive”?

The patent’s Example 1 reports that “absorbance readings greater than three times the average of 4 normal negative control readings were taken as positive.” Under that criterion, 88% of AIDS patients, 79% of pre-AIDS individuals, 60% of intravenous drug abusers, and 27% of gay men tested positive; 0.5% of controls also tested positive. That is hardly foolproof, specific detection of whatever might be uniquely characteristic of AIDS.

In other ways, too, the patent is less than impressive. Example 1 and Example 4 both refer to the data in Table 1 and describe the same procedure, though in somewhat different words; why they are given as distinct separate examples is puzzling. In a single paragraph, Example 5 asserts a finding of specificity without stating how many experiments were carried out.

 Not an HIV test
In effect, the manner in which this test was developed makes it at best an AIDS and pre-AIDS test, not an HIV test, and more sensitive to and specific for pre-AIDS and not AIDS. Moreover, since the symptoms of pre-AIDS --- swollen lymph nodes, fever --- are seen also in many other illnesses, the test is nothing more than a nonspecific illness test. That is why over the years the Centers for Disease Control and Prevention (CDC) added dozens more illnesses to the list of “AIDS” diseases: patients with many illnesses may react “HIV-positive.”

antibodies as denoting infection

The scientific publications and the patent claiming HTLV-III to be the probable cause of AIDS were clearly insufficient to establish the claim. How then did it come about that a less-than-specific antibody test became a basis for asserting actual infection by HIV?

Rodney Richards, who worked on the development of the first ELISA HIV test (marketed by Abbott Laboratories), has described in chronological detail how this unprecedented equating of antibodies with active infection came about 15. The story would be literally incredible were it not fully documented by authoritative material in the public domain.

Initially, in 1984, the CDC had quite properly acknowledged the possibility of false-positive antibody tests owing to “an antigenically related virus or nonspecific test factors.” In people at high risk of AIDS, it “probably” meant prior exposure, however, “Whether the person is currently infected or immune is not known . . . . the frequency of virus in antibody-positive persons is yet to be determined” 16.
Six months later, CDC admitted that there would be a high proportion of false positives when screening low-risk populations: no one should be informed of testing positive before the test had been duplicated 17.

Three months beyond that, the Food and Drug Administration approved Abbott’s ELISA test for blood screening. Obviously it makes sense to take all possible precautions against the presence of a possible pathogen in blood that is to be used for transfusions: better to discard 100 donations of good blood than to allow 1 infected sample to be transfused. It is very different, however, to inform someone on the basis of a highly unreliable test that they are infected with a deadly pathogen for which there is no cure. The package insert with the Abbott test had the appropriate caveats: “there is no recognized standard for establishing the presence or absence of HIV-1 antibody in human blood. . . . The risk of an asymptomatic person with a repeatedly reactive serum sample developing AIDS or an AIDS-related condition is not known.” The same caveats apply to the Western Blot antibody-test approved in 1987 and widely used as supposed confirmation of duplicate positive ELISA tests 15, p.339. Similar disclaimers from various manufacturers are found in more recent test-kit inserts 18.

Some months after the Abbott test had been approved for blood screening, data from blood donors revealed that 44% of samples strongly positive for “HIV” antibody contained no virus detectable by culture. Similarly, 40% of gay men testing antibody-positive had no detectable virus 19. In nearly half of all cases, then, both in a high-risk group and in a low-risk group, a positive “HIV” test came in absence of HIV.

Then CDC stood this evidence on its head. The data showed that absence of virus accompanied antibody-positive in almost half of all cases. Looking instead at the other half, CDC asserted that “Since a large proportion of seropositive asymptomatic persons have been shown to be viremic (5), all seropositive individuals, whether symptomatic or not, must be presumed capable of transmitting this infection” 20 [reference (5) 17 admitted that it was not known what proportion of seropositive donors was actually infected].

Perhaps CDC was so concerned to prevent transmission of HIV that it used the same reasoning as with blood screening: better that some large number of actually non-infected people be warned against passing on a possibly fatal infection than that a small number of infected persons unwittingly infect others. But that ignores the devastating psychological effect on the many uninfected people who were thereby doomed to believe that they were harboring an incurable, inevitably fatal infection.
CDC then went even further than “presuming” that seropositive might mean infection: in 1986, in an article in the journal of the American Medical Association --- much more widely read than the Mortality and Morbidity Reports in which the “presumption” had been stated --- CDC researchers defined seropositive as equivalent to infection 21. As Richards points out 15, all the cited data reported that virus could not be cultured from a high proportion of seropositive individuals. By asserting that seropositive equals infection, CDC was dismissing evidence from culture, implying that there was something ineffective in the virus-culturing procedure and substituting for that a test which had never been validated.

CDC has continued to dispense with all caveats, asserting that “presence of antibody indicates current infection” 22: not as a precautionary measure in screening blood, not as a precautionary measure to prevent transmission, not when the seropositive individuals are in a high-risk rather than low-risk population, and irrespective of whether they are symptomatic or asymptomatic; it is asserted dogmatically without any exception that seropositive means infected. Surely this constitutes public-health malpractice based on junk science.

Furthermore, Richards 15 points out that CDC was actually transgressing its mission to safeguard public health by this assertion which dictates what doctors should do on the basis of a particular test, even in the face of what the Food and Drug Administration, charged with protecting consumers, had said just a few months earlier: “The significance of antibodies in an asymptomatic individual is not known” 23.
Some twenty years later, it is clear that the CDC’s dogmatic insistence that “HIV-positive” equals infection has resulted in widespread iatrogenic harm, in many cases death, through the administering of toxic antiretroviral drugs to uninfected individuals.

NO gold standard for HIV tests

The work just reviewed dates from the 1980s. Were the deficiencies corrected by later work?
Unequivocally and simply, “No.”

For one thing, all later work has built on and presumed the soundness of the seminal articles. For another, it remains understood by the actual experts that a positive “HIV” test does not in itself signify infection, be the test an ELISA, a Western Blot, a “viral load” measurement, or a culture; but this understanding is not broadcast outside the technical literature.

The following is taken from Weiss and Cowan 24, which can be regarded as authoritative on several grounds: Weiss has worked in this field since the beginning, having published since 1984 including with Gallo; and this is a chapter in the fourth edition (2004) of a monograph that has been favorably accepted and reviewed (e.g. the 3rd edition in JAMA 25 and the 4th in Clinical Infectious Diseases 26 or JAMA 27).

In terms of substance, really no more need be said than that
In the absence of gold standards, the true sensitivity and specificity for the detection of HIV antibodies remain somewhat imprecise (p. 150).

Obviously enough, “somewhat imprecise” is a euphemism: the lack of gold standard makes everything highly doubtful. Pure virions of HIV, the sine qua non for establishing a veritable gold standard, have never been obtained from an AIDS patient or from an “HIV-positive” individual. Twenty-five years of HIV/AIDS research have not brought unequivocally valid HIV tests.
Weiss and Cowan make clear that inferring HIV infection is a matter of probability, not certainty, and that the assessment of probability requires interplay of laboratory testing with clinical information, very much including individual medical history and risk-category classification:

A pre-test probability assessment is required whenever test results are to be meaningfully interpreted (p. 149; emphasis in original)

An essential part of the testing process takes place even before testing is done; that is, the estimation of the probability of infection (the ‘pre-test’ probability). This is necessary in order to interpret a test result appropriately, whatever the purpose --- whether it is clinical, counseling or research --- and can dramatically impact the predictive value after testing (or ‘post-test’ probability) (p. 159)
No test, per se, should be the basis for diagnosis on its own, but rather a test is merely an aid in correct diagnosis. The practitioner must use test results in the context of a clinical picture to reach an accurate diagnosis (p. 172)

The import of these uncertainties is illustrated in a table 24, p.149 showing that in low-risk populations (prevalence of “HIV” 0.1%), a “positive” “HIV”-test-result has only about 1 chance in 6 of being a “true” positive; 5 out of 6 would be false positives. Conversely, at a prevalence of 99.9%, a negative test-result would have only about 1 chance in 6 of truly being negative --- once an individual has been designated “high risk”, even a negative “HIV” test may not be accepted as definitively showing lack of infection, further testing is recommended.

This illustration is based on a hypothetical test that is 99.5% sensitive and 99.5% specific, but the principal point is independent of the actual numbers --- and no test, of course, is 100% sensitive or specific. Thus the initial belief that a person is high or low risk biases interpretation of the laboratory tests to becoming self-fulfilling prophesies.


There is no gold standard for HIV tests. Positive tests do not prove infection by HIV. Nevertheless, current practice is to take positive tests as proof of active infection. As a result, healthy people are unwarrantedly doomed to lifelong administration of toxic drugs. This applies particularly to people in groups traditionally regarded as “high risk”: gay men and injecting drug users; but in recent years African Americans have come to be regarded as being at high risk, and positive tests are also common among TB patients and as a result of pregnancy. Only the slightest indication of ill health --- or indeed just routine “HIV” testing --- suffices for individuals in any of those groups to be told they are infected and are then assigned to antiretroviral treatment .


I am very grateful to Rodney Richards for clarifying discussions, particularly the crucial insight that the “HIV” test was really an AIDS test.

Henry H. Bauer, Ph.D., is Professor Emeritus of Chemistry & Science Studies and Dean Emeritus of Arts & Sciences at the Virginia Polytechnic Institute & State University (Virginia Tech).
1306 Highland Circle, Blacksburg VA 24060-5623. E-mail:

POtential COnflict of Interest

I am the author of the book, The Origins, Persistence and Failings of HIV/AIDS Theory, which claims to show that HIV is not the cause of AIDS.


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 2       Crewdson J. Science Fictions: A Scientific Mystery, a Massive Coverup, and the Dark Legacy of Robert Gallo.  Boston etc.: Little, Brown; 2002.
 3       Gallo RC, Salahuddin SZ, Popovic M, et al. Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with  AIDS and at Risk for AIDS. Science 1984;224:500-503.
 4       Schupbach J, Popovic M, Gilden  RV, et al. Serological analysis of a subgroup of human T-lymphotropic  retroviruses (HTLV-III) associated with AIDS. Science 1984;224:503-505.
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 7       Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Has Gallo proven the role of HIV in AIDS? Emergency Medicine [Australia] 1993;5:113-123.
 8       Hodgkinson N. Why an HIV test may not provide proof positive at all. The Business, May 9/10, 2004:1,6; HIV diagnosis: a ludicrous case of circular reasoning. ibid., May 16/17, 2004:1,4.
 9       Ranki A, Johansson E, Krohn K. Interpretation of antibodies reacting solely with human retroviral core proteins. N Engl J Med 1988;318:448-449.
10 Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. Cell membrane vesicles are a major contaminant of gradient-enriched human  immunodeficiency virus type-1 preparations. Virology 1997;230:125-133; Bess JW, Gorelick RJ, Bosche WJ, et al. Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. ibid. 134-144.
11 Transcript of Gallo testimony is available at Accessed 27 November 2009.
12 Gallo RC, Sarin  PS, Gelmann EP, et al. Isolation of human T-cell leukemia virus in Acquired Immune Deficiency Syndrome (AIDS). Science 1983;220:865-867.
13 Gallo RC. Virus Hunting: AIDS, Cancer, and the Human Retrovirus. New York: BasicBooks; 1991; p.248.
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15 Richards R. The birth of antibodies equals infection. App. II, pp. 333-340 in Farber C. Serious Adverse Events: An Uncensored History of AIDS. Hoboken NJ: Melville House; 2006.
16 Antibodies to a retrovirus etiologically associated with Acquired Immunodeficiency Syndrome (AIDS) in populations with increased incidences of the syndrome. Morb Mortal Wkly Rep, July 13, 1984;33:377-379.
17 Provisional Public Health Service inter-agency recommendations for screening donated blood and plasma for antibody to the virus causing Acquired Immunodeficiency Syndrome. Morb Mortal Wkly Rep, January 11, 1985;34:1-5.
18 Zip file of test-kit inserts, Accessed 27 November 2009.
19 Current trends update: Public Health Service Workshop on Human T-Lymphotropic Virus Type III antibody testing --- United States. Morb Mortal Wkly Rep, August 9, 1985;34:477-478.
20 Current trends: Additional recommendations to reduce sexual and drug abuse-related transmission of Human T-Lymphotropic Virus Type III/ Lymphadenopathy-Associated Virus. Morb Mortal Wkly Rep, March 14, 1986;35:152-155.
21 Ward JW, Grindon AJ, Feorino PM, et al. Laboratory and epidemiologic evaluation of an enzyme immunoassay for antibodies to HTLV-III. JAMA 1986;256:357-361.
22 Perspectives in disease prevention and health promotion. Public Health Service guidelines for counseling and antibody testing to prevent HIV infection and AIDS. Morb Mortal Wkly Rep, August 14, 1987;36:509-515.
23 Cruzan S. FDA News, April 30, 1987:p.87-11; cited in Richards xv.
24 Weiss SH, Cowan EP. Laboratory detection of human retroviral infection. Chapter 8 in Wormser GP (ed.). AIDS and Other Manifestations of HIV Infection. London etc.: Academic Press; 2004 (4th ed.).
25 Panwalker AP. JAMA 1999;281:1757.
26 Johnson SC.  Clin Inf Dis 2005;40:1866-1867.
27 Manfredi R. JAMA 2005;293:1393-1394.

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