Repeat, the origin of the CK and RT activity 11 October 2004
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Eleni Papadopulos-Eleopulos,
Department of Medical Physics, Royal Perth Hospital, Western Australia, 6001,
Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala

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Re: Repeat, the origin of the CK and RT activity

Repeat, the origin of the CK and RT activity

cannot be determined by their "RELATIVE amounts"


In his rapid response, "Relative values", 29 September, Nicholas Bennett wrote:  "The Perth Group have rather missed the point.  If uninfected cells have a value of X and infected cells have a value of Y then surely it's obvious that Y-X is the contribution of viral RT activity…?"


If, to begin with, Nicholas Bennett knows which of his cultures are infected and which are not, then why is he doing the test?


Given that:


(i)                  all cells contain reverse transcriptases;

(ii)                all cells have endogenous retroviruses;

(iii)               the cellular DNA poylmerases beta and gamma can reverse transcribe RNA into DNA (in exactly the same "salts and pHs" conditions as the "HIV" reverse transcriptase)1


Would Nicholas Bennett please tell us how does he know that a high RT activity is due to infection with "HIV" and not to all the other enzymes?


Nicholas Bennett wrote:  "The Perth Group are also apparently unaware of the use of isoenzymes (CK-MB versus total CK) to distinguish myocardial infarction from muscle destruction.  To quote from an online source [2]:  "If the ratio of CK-MB to total CK (relative index) is more than 2.5- 3, the heart is the likely muscle damaged.  A high CK with a very low relative index suggests that other muscles were damaged."  To paraphrase: "Repeat, scientifically it I 2000 S possible to determine what is the cause of reverse transcriptase activity (or raised CK) on the basis of "RELATIVE amount"."


In Nicholas Bennett's reference [2] one reads:  "A high CK, or one that goes up from the first to the second or later samples, generally indicates that there has been some damage to the heart or other muscle.  It can also indicate that your muscles have experienced heavy use….People who have greater muscle mass have higher CK levels than those who don't, and African-Americans may have higher CK levels than other ethnic groups.  Very heavy exercise (such as in weight lifting, contact sports, or long exercise sessions) can also increase CK.


Other forms of muscle damage, such as from a fall, a car accident, surgery, or a shot, can also increase CK.  Several drugs can increase CK levels.  Drinking too much alcohol slightly increases CK.  Rarely, some drugs, particularly cholesterol-lowering drugs (statins), can damage muscle and increase CK".


In an attempt to distinguish between the high levels of CK due to MI and other muscle condition, including heart muscle damage by factors other than MI, another test, CK-MB, is performed.  "CK-MB levels, along with total CK, are tested in persons who have chest pain to diagnose whether they have had a heart attack.  Since a high total CK could indicate damage to either the heart or other muscles, a high CK-MB suggests that the damage was to heart muscle [caused by MI].  If your doctor thinks you have had a heart attack and gives you a "clot-busting" drug (called a thrombolytic), CK-MB can help your doctor tell if the drug worked.  When the clot is broken open, CK-MB tends to rise and fall faster.  By measuring CK-MB in blood several times, your doctor can usually tell whether the drug has worked….If the ratio of CK-MB to total CK (relative index) is more than 2.5-3, the heart is the likely muscle damaged.  A high CK with a very low relative index suggests that other muscles were damaged."  {Emphasis ours}


Note:  The CK-MB/CK ratio only suggest does not prove that the cause of the high CK is MI.  The ratio is not even going to suggest this when the "clot-busting" drug does not work.


In conclusion;  the evidence in Nicholas Bennett's ref. 2 shows that:

(i)                  there are many causes of high  levels of CK activity;

(ii)                it is not possible to determine the cause of the high CK activity by its "RELATIVE amounts"


Nicholas Bennett wrote:  "I'm curious as to the actual basis for their statement that "In Montagnier's 1984 paper the level of RT activity by the DNA polymerases beta and gamma is at least as high as that of the "HIV" polymerase."  According to the methods I use, that clearly is not true.  I'm more inclined to suggest to the reader that, based on their previous track record, the Perth Group are either misunderstanding or misrepresenting the true data."


Would Nicholas Bennett please look at Montagnier's fig 2 and tell us:


(i)                  is the sum of the RT activity by polymerase beta and gamma as high as that of "HIV";

(ii)                are the conditions identical;

(iii)               is it true that the only reason one of the 3 peaks of RT activity obtained in the "infected" cells with poly A oligo dT12-18 is claimed to be "HIV" RT is because the same peak "is also obtained with poly Cm.oligo dG, a reverse transcriptase specific template-primer."


If we are as wrong and dangerous as Nicholas Bennett claims, then he must write to Medical Hypotheses and refute our latest critique of Montagnier's work.2 It goes without saying that Montagnier must do the same.


1.                  Rey MA et al, Characterisation of the RNA dependent DNA polymerase of a new human T-lymphotropic retrovirus (lymphadenopathy associated virus).  Biochem Biophys Res Commun 1984;121:126-33.

2.                  E. Papadopulos-Eleopulos et al.  A critique of the Montagnier evidence for the HIV/AIDS hypothesis, 2004; 63:597-601



Competing interests: None declared