Oxidation and AIDS: Some Notes from L. Montagnier (2000), Virus; trans. from French by S. Sartarelli (New York, NY: Norton).

(My own notes on Montagnier's discussion of AIDS and oxidation are in brackets.)

 

[Montagnier observes that, when HIV progresses to AIDS, the CDC cells' receptors] . . . are masked by a molecule that is very likely none other than the surface protein of the virus [HIV].

Naturally, while this . . . may explain the apoptosis [cellular death] of the T4 cells, it cannot apply to that of the T8 cells, which do not have a receptor for the virus [and so cannot have the receptor masked by HIV's surface proteins]. Their apopstosis must therefore have another cause.

It might, for example, be explained by the fact that many [lymphoocyte] cells experience a chronic activation [during HIV infection] that cannot be indefinitely prolonged because of a lack of certain growth factors such as interleukin 2. An apoptosis reaction would thus be triggered in the cells.

In HIV-positive patients . . . the phenomenom [apoptosis or cellular death at an increased rate] affects all lymphocyte populations including the B lymphocytes. It may therefore have a more general cause and should be related to another phenomenom . . . so far mentioned only briefly: oxidative stress. (Montagnier, 2000, p. 184.)

We . . . learned very long ago to live in an atmosphere that contains a highly toxic and reactive gas: oxygen. [My note: oxygen is needed for our metabolism to work; it's what burns energy; all higher forms of life on Earth--both plant and animal--need oxygen; but more primitive forms may produce oxygen as a by-product but may not require it and may even be harmed by it!] Many chemical reactions in our metabolism release or create even more reactive chemical compounds--superoxides, free radicals, atomic oxygen--that can cause irreversible damage to the components of our cells: [these components include] proteins, lipids, nucleic acids.

Organisms have therefore developed a number of chemical, enzymatic defenses for detoxifying these molecules: we call them antioxidants. We humans have our own antioxidants, but plants are better than we are in this category. They give us vitamins C, E. and A, powerful anti-oxidants which our bodies are incapable of manufacturing themselves in sufficient quantities.

What happens in patients suffering from AIDS? One notes a significant shortage of anti-oxidants and a rise in oxidation products: the level of gluthathione [which the anti-oxidant, alpha lipoic acid, is thought to help increase] in the lymphocytes decreases, peroxidized lipids appear in the blood, proteins are also oxidized, and for this reason undergo very rapid enzymatic breakdown The phenomenom is massive, and occurs at an early stage [in HIV infection]. . . . The macrophages are an essential source of these oxidation products, which can be lethal to infectious germs.

In addition to the virus [HIV], all opportunistic agents [which are able to cause 'opportunistic' infections] can likewise contribute to oxidative stress . . . . [presumably because these trigger the oxidation processes in cells in an effort to fight germs, and then use up the anti-oxidants faster?]

. . . [T]he products of this [oxidative] stress can trigger cellular apopstosis.

(The above reprinted from Montagnier, 2000: 184-185).



 

The Role of Interferon in Controlling Viruses, and the Ways Chronic Infection Changes Interferon:
More Notes from L. Montagnier (2000), Virus; trans. from French by S. Sartarelli (New York, NY: Norton).

(My note: could interferon be associated with apopstosis in chronic infection? I really do not know; this is a "wild card" I'm throwing.)

 

Montagnier also notes that human interferon plays a role in what happens in AIDS and cancer. Montagnier describes interferon as "a powerful inhibitor of retroviruses," and believes that the inhibitory effect on cancer of "the interferon system" is "particularly effective in humans." Montagnier reported that anti-interferon serum "that neutralized . . . interferon's protective effect" was associated with increased viral infection; however, Montagnier adds that, "[s]ometimes, in a chronic infection, the situation was the reverse. Interferon would become harmful, and one would save the lives of the mice by injecting them with this same anti-interferon serum.

(Information exerpted from Montagnier, 2000: 38.)



 
 

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