Re: HIV EM and purification 1 July 2004
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY 13084

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Re: Re: HIV EM and purification

In response to Robert Da Prato's questions, I am afraid that I have little personal experience with EM methodology. However, it should be born in mind that a viral load of 1 million per ml still equates to a relative volume of 9*10^-16. In other words, a million virus particles make up less than one thousandth of a trillionth of the total volume of the blood. Trying to find a virus particle in that situation would be a complete waste of effort.

That however hardly detracts from any argument of causality. It is perhaps sad that a respected EM researcher such as de-Harven didn't appreciate this simple fact of impossiblity. His particular problem with using RT-PCR also shows a lack of faith in the extensive internal and external controls used throughout the world of molecular biology when employing quantitative PCR methods. Trying to match these to visual pictures directly would be no more possible than trying to kiss one's elbow.

In addition, one viral particle is more than capable of killing a cell which is far larger than itself: in the world of virology size hardly matters.

They have been however attempts made to match PCR detection of virus from cultures of viruses. Ho et al managed to optimise a culture system that may well have been able to detect infectious virus with 100% sensitivity from peripheral blood.

In addition, this work along with that of Pantaleo et al showed the huge disparity between peripheral and central virus quantitation. Peripheral cells showed an infection rate of approximately 1 in 40, and yet in lymph nodes more than 25% of the cells showed demonstrable infection with HIV. Any criticisms of causality of HIV causing AIDS relying on peripheral data alone show only a shocking ignorance of the current proposed mechanisms of AIDS pathogenesis and the simple observed facts described above. Early criticisms made by such highly accomplished retrovirologists as Duesberg have been since soundly refuted by excellent work, which goes largely ignored or discounted by those arguing against HIV/AIDS causality.

Duesberg's original argument also relied on the assumption, entirely reasonable, that T cell replacement rates would be more than adequate to replace those lost to HIV infection. However, along with the massive underquantitation of HIV using peripheral measurements, later work by Hellerstein et al and other groups looking at T cell kinetics showed that T cell replacement rates were severely affected by HIV infection, a situation that was remedied by administration of antiretroviral therapy.

As such, there is no need (and arguably never was) to make a case against HIV causing AIDS based upon "low" levels of virus (25% infection of lymph node cells, which make up the vast majority of total body lymphocytes) and "adequate" T cell replacement rates (when T cell half- lives are in fact about a third as long in HIV-infected people). Such early criticisms are clearly untenable in the face of current evidence.

Refs:

Hellerstein, M. et al Nature Medicine (01/99) Vol. 5, No. 1, P. 83; "Directly Measured Kinetics of Circulating T Lymphocytes in Normal and HIV -1-Infected Humans"

Ho et al. N Engl J Med. 1989 Dec 14;321(24):1621-5 "Quantitation of human immunodeficiency virus type 1 in the blood of infected persons."

Pantaleo et al Nature 1993 Mar 25;362(6418):355-8 "HIV infection is active and progressive in lymphoid tissue during the clinically latent stage of disease. "

Competing interests: None declared