The Perth Group comment on Claus Jensen’s observations re Umber
We agree with everything Claus said. Certainly there is not one simple test, which is routinely used to diagnose "HIV" infection which measures p24. The high amounts of p24 does not necessarily mean high amounts of antibodies.
A few comments regarding the two references.
(a) "HIV-1 regulatory proteins induce a reduction of the expression and the activity of MnSOD, the mitochondrial isoform leading to a sustained generation of super oxide anions and peroxynitrite that represent important mediators of HIV-1 replication in M/M".
The "HIV-1" proteins cannot be at the same time the cause of oxidation (generation of superoxide and peroxynitrite) and the result of oxidation ("HIV-1 replication);
(b) "MnTBAP (Mn(111)tetrakis(4-benzoic acid)porphrin chloride), a synthetic peroxynitrite decomposition catalyst, reduced oxidative stress subsequent to peroxynitrite generation".
"However since according to the same authors the peroxynitrite is a "….by-product of super oxide and nitric oxide, NO", it means that ultimately the effect of MnTBAP is the result of it decreasing the superoxide; the NO or both. Indeed,
the author concluded "Virus production was assessed by p24 ELISA,
Western Blot, and electron microscopy….Results support the role
of superoxide anions in HIV-1 replication in M/M….";
(c) "MnTBAP strongly reduced HIV-1 particles in M/M, as shown by electron microscopy". Regarding the "HIV-1" particles seen by electron microscopy they wrote: "It is known that the HIV-1 particles are accumulated in intracytoplasmic vacuoles in M/M before budding".
by definition, no retrovirus particle (except the type-A
retrovirus-like particles) certainly not lentivirus particles which
"HIV-1" is meant to be, accumulated in intracytoplasmic vacuoles. This means thatAcquaro et al were studying the effects of MnTBAP on something: (P24 is supposed to be a structural protein of the particles) which have nothing to do with retroviruses.
Kalinowski et al
of the donors [of human umbilical vein endothelial cells] took any
drugs regularly, and all were non-smokers and consumed regular
This does not make the two groups (blacks/whites) the same. For example, let us assume that both groups consumed exactly the same amount of caloric/content diet. However:
(i) the blacks obtained it from fish and chips/Kentucky fried chicken. In addition the vast food outlets were changing the oils once or twice every week;
(ii) the whites were obtaining it from backed fish and potatoes/baked chicken breast and potatoes. In addition their meals were accompanied by one or another type of salad or fruit.
These type of differences will have had at least as much an effect on "peroxynitrite" levels as smoking. To extrapolate the findings of this study to the whole black population is to go beyond the evidence;
(b) "We found that decreased NO availability in blacks compared with whites is due to excess O2- produced by NAD(P)H-oxidase that finally yields enhanced formation of ONOO- after stimulation of Enos. This in turn, leads to the eNOS uncoupling, which produced O2- and NO, and may very well contribute to oxidative stress and endothelial dysfunction". In other words, according to Kalinowski the primary culprit is not peroxynitrite but O2-.
According to the Perth Group the main causes of excessive O2- production is the result of: (i)
uncoupling of biological energy production, that is there is a flow of
electrons to oxygen without formation of ATP and reduction of proteins
(SH increase); or (ii) excessive utiliation of ATP and oxidation of protein SHs.
can be the result of exposure to either chemical (drugs, food) or
physical (radiation, excessive exercise) oxidising agents.