The loose ends of the HIV hypothesis were finally thought to have been tied in 1995 with two papers by a team of AIDS researchers led by Dr.David Ho of the Aaron Diamond Research Center and Dr.George Shaw of the University of Alabama.  Ho and Shaw offered what they characterized as indisputable evidence that HIV is active from the moment of infection, and present in quantities sufficient to cause massive T cell destruction.138  They claimed to find an average of over 100,000 HIVs per mL of blood in AIDS patients by using a virus counting method based on the new technology of polymerase chain reaction (PCR).

Their papers asserted that HIV has always been present and active in enormous quantities, but that its presence and activity could not be measured by standard means, and that scientists were looking for the wrong thing to measure.  Until 1995, the method for finding and quantifying a virus was by isolation of the virus.  This simple, direct method has been successfully applied to every virus except HIV.  Instead, proponents of viral load assert that scientists must look for fragments of genetic materials rather than isolating the virus.

PCR is an innovative technique that enables scientists to take a sample of blood containing an otherwise undetectable number of DNA or RNA molecules and produce detectable quantities of fragments from these few original molecules.  Forbes magazine described PCR as “biotechnology’s version of the Xerox machine”.  Dr.Kary Mullis, who won a Nobel Prize for this revolutionary creation, explains the “PCR makes it possible to identify a needle in a haystack by turning the needle into a haystack.”139 While PCR has provided many realms of science and industry with an effective new tool, its application to AIDS research has been far more misleading than useful.

Ho and other researchers employed PCR to find, not HIV, but fragments of RNA, the genetic material in the viral core.  Using the logic that each HIV virus particle contains two HIV RNAs, they assumed that every two RNA pieces indicated by PCR must correspond to one HIV viral particle, and they called the sum of what is copied, multiplied, counted, and divided, “viral load.”

Viral load has been celebrated in the press as an astounding breakthrough in AIDS research, and has won Dr.David Ho numerous awards including Time magazines’s 1996 Man of the Year.  Viral load is also the measure by which new AIDS drugs are deemed effective.  Protease inhibitors were approved for use based solely on their alleged ability to reduce “viral load”.  The media, AIDS organizations and most AIDS doctors have uncritically accepted the viral load hypothesis as fact.

According to the viral load hypothesis, billions of HIV are busy infecting CD4 T cells every day from the moment a person is exposed, and killer immune cells (CD8 T cells) continuously destroy billions of CD4 cells that host active HIV infection, while new, uninfected CD4s quickly replace the billions destroyed by the killer cells.140 Eventually, after one to 15 years of this microscopic battle, the virus wears out the immune system allowing AIDS-defining illnesses to develop.  Proponents of viral load claim that the reason this incredible activity was never noticed before is that the CD4s replicate so quickly, few HIV infected T cells ever make it into the blood where they can be measured.140

However, the viral load hypothesis fails to answer two important and unsettling questions: If billions of HIV are present, why is PCR necessary to find them?  And if PCR is the only way HIV can be detected, how is it possible for scientists to verify the results of PCR?

Another problem with viral load is that PCR detects and multiplies single genes, not virus, and most often only fragments of genes.  When it detects two or three genetic fragments out of a possible dozen complete genes, this is not proof that all the genes or the complete genome are present, or that a complete HIV viral particle is present.141 Further, a person can carry a whole retroviral genome in their cells for an entire lifetime without ever producing a single virus.

The FDA has not approved PCR viral load for HIV screening or for diagnostic purposes.  The CDC acknowledges that the specificity and sensitivity of PCR are “unknown” and that “PCR is not recommended and is not licensed for routine diagnostic purposes.” 142 The viral load test manufacturers’ literature warn “the test is not intended to be used as a screening test for HIV or as a diagnostic test to confirm the presence of HIV…” 143

Although, no research has specifically studied PCR tests on HIV negative subjects, the medical literature records many incidents of detectable levels of viral load found in persons who are HIV negative.144

A group of AIDS researchers from the Johns Hopkins School of Public Health recently lamented the inaccuracies of PCR viral load, describing the test as unreliable and expensive when several attempts to verify PCR produced conflicting results.145  A recent paper by AIDS reappraiser Dr.David Rasnick published in the Journal of Biological Chemistry demonstrates that at least 99.8% of what viral oad tests measure are noninfectious virus particles, and notes that PCR should be replaced by a test that measures actual HIV in blood plasma.146

PCR measurements do not correlate with amounts of T cells, with clinical symptoms of AIDS, or with levels of co-culturable HIV.147  In the only published study that compares viral load results with the detection of HIV by co-culture, a process that can artificially induce production of virus even when the patient’s blood contains no virus, 53% of HIV positive AIDS patients with detectable levels of viral load – many with loads topping 200,000 and 300,000 – had zero co-culturable HIV.147

A number of mainstream AIDS experts refute Ho’s portrait of wildly multiplying and abundant HIV.  Their objections have been published in Nature, Lancet and other science journals.  Some like former government AIDS researcher Dr.Cecil Fox dismiss Ho’s ideas as “unconfirmed mathematical speculation”.148   Another prominent AIDS specialist, Dr.Mario Roderer, considers the viral load model of HIV pathogenesis a dead issue since “several well-designed and informative studies provide the final nails in the coffin for…the two Nature papers,”  while noted AIDS researcher Dr.Jay Levy warns that “medicine suffers when one is misled by numbers that are not relevant to the clinical problem involved…”149  Other critics have been more blunt, characterizing this new hypothesis of HIV as “a viral load of crap.”150

References

138. Ho D, et al 1995 Rapid Turnover of Plasma Virions and CD4 Lymphocytes in HIV-1 Infection Nature 373: 123-126; Wei X, et al 1995 Nature 373:117-122.

139. Kary Mullis at HEAL Los Angeles, October 25 1995.

140. Philpott P. Johnson C 1996 Viral Load of Crap Reappraising AIDS Vol 4:10 p2

141. Johnson C Viral Load and the PCR Continuum Vol 4:4 November/December 1996

142. CDC faxback document #320320 sent in reply to an inquiry by Christine Johnson

143. Roche Amplicor PCR Diagnostics HIV-1 Monitor test kit pamphlet

144. Defer C, et al 1992 Multicenter Quality Control of PCR Detection of HIV DNA AIDS 6:659-663; Bush, et al 1992, Journal of AIDS 5:872; Gerberding J 1994 Incidence and Prevalence of HIV, Hepatitis B, and CMV Among Health Care Personnel at Risk for Blood Exposure  Journal of Infectious Disease 170:1410-1417; de Mendoza, et al 1998 False Positive for HIV Using Commercial Viral Load Quantification Assays  AIDS 12:2076-2077; Rich J, et al 1999 Misdiagnosis of HIV Infection by HIV-1 Plasma Viral Load Testing: A Case Series, Annals of Internal Medicine 130:37-39

145. Schwartz D, et al 1997 Extensive Evaluation of a Seronegative Participant in an HIV-1 Vaccine Trial as a Result of False-Positive PCR, Lancet Vol 350 No 9073 p256

146. Rasnick D 1997 Kinetics Analysis of Consecutive HIV Proteolytic Cleavages of the Gag-Pol Polyprotein Journal of Biological Chemistry March 7 p6348-6353.

147. Piatak M, et al 1993 Science 259:1749-53

148. Roderer M 1998 Getting to the HAART of T Cell Dynamics Nature Medicine Vol 4:2 p145-146; Levy J 1996 AIDS Surrogate Markers: Is There Truth in Numbers? JAMA Vol 276 p161-162

149. Levy J 1996 AIDS Surrogate Markers: Is There Truth in Numbers? JAMA Vol 276 p161-162

15. Philpott P, Johnson C 1996 Viral Load of Crap Reappraising AIDS Vol 4:10 p2

What’s Up With Viral Load ? 

Dr. Valendar Turner Takes a Critical Look at
RT-PCR, NASB and bDNA Viral Load Assays

Measurement of HIV RNA is deemed particularly valuable because it is said to predict disease progression and determine the effects of treatment.  In regard to HIV RNA, every HIV/AIDS patient and their physicians should carefully examine the table here.

The three assays frequently used to quantify the “viral load” are reverse transcription-polymerase chain reaction (RT-PCR), nucleic acid sequence-based amplification (NASBA) and branched chain DNA (bDNA).  To assess the impact if the assays used and of “genetic variability in HIV-1 RNA quantification,” researchers from France “evaluated three commercial kits by using a panel of HIV-1 isolates representing clades A to HS.

These isolates were expanded in culture.  Virus was collected by ultracentrifugation and re-suspended in HIV-seronegative plasma.  To standardize the quantities of virus to similar levels in each preparation, the p24 antigen was determined and the volume adjusted so that each specimen contained approximately 10pg of p24 antigen per ml.”  The “HIV-1 RNA copies” per ml of plasma obtained were as follows (where <400 is considered zero RNA):

If this test is measuring one and the same thing, that is, the amount of HIV RNA in a patient’s plasma, all the numbers in the rightmost three columns should be of identical order.  Their gross variability should not be excused on the basis of “quantification of HIV-1 RNA is highly influenced” by the “HIV-1 strain” and the test kit used.

One can only marvel that such a test could be used to quantify anything at all let alone a deadly microbe.  If “viral load” were a pregnancy test there would be cries of joy or woe emanating simultaneously from the same mouth as the same sample was reported.

Reference : Coste J, Montes B, Reynes J, et al. (1997).  Effect of HIV-1 genetic diversity on HIV-1 RNA quantification in plasma:  comparative evaluation of three commercial assays. J. Acquir.  Immun. Def. Syndr. Hum. Retrovirol., 15,174.