Re: sackie B3, selenium, and CFS - Palamara refs

[Guest guest]

Here's a couple of references from Palamara et al describing in more

detail what Rich speaks about, the inhibiting effect of endogenous

glutathione on HIV:

J Leukoc Biol. 1997 Jul;62(1):54-9.

Intracellular GSH content and HIV replication in human macrophages.

Garaci E, Palamara AT, Ciriolo MR, D'Agostini C, Abdel-Latif MS,

Aquaro S, Lafavia E, Rotilio G.

Department of Experimental Medicine, University of Rome, Tor

Vergata, Italy.

In vitro HIV-1 infection induced a significant decrease in

intracellular reduced glutathione (GSH) in human macrophages. Such a

decrease was observed at the time of infection corresponding to

maximum release of virus from infected cells and was not related to

cell cytotoxicity. GSH los was not related to its oxidation or

leakage through the cell membrane. Inhibition of intracellular GSH

synthesis by buthionine sulfoximine (BSO) did not further decrease

GSH levels with respect to the decrease caused by HIV alone.

However, treatment of macrophages with BSO significantly increased

the HIV yield in the supernatant. Exogenous GSH strongly suppressed

the production of p24 gag protein as well as the virus infectivity.

Previous observations with other RNA and DNA viruses consistently

showed that GSH antiviral effect occurred at late stages of virus

replication and was related to the selective decrease of specific

glycoproteins, such as gp120, which are particularly rich in

disulfide bonds.

PMID: 9225993 [PubMed - indexed for MEDLINE]

AIDS Res Hum Retroviruses. 1996 Nov 1;12(16):1537-41.

Glutathione inhibits HIV replication by acting at late stages of the

virus life cycle.

Palamara AT, Perno CF, Aquaro S, Bue MC, Dini L, Garaci E.

Department of Experimental Medicine and Biochemical Sciences,

University of Rome, Italy.

We investigated the effect of glutathione on the replication of

human immunodeficiency virus (HIV) in chronically infected

macrophages, a known reservoir of the virus in the body. We found

that exogenous GSH strongly suppresses the production of p24gag

protein as well as the virus infectivity. This is related to a

dramatic decrease in both budding and release of virus particles

from chronically infected cells (either macrophages or lymphocytes),

together with a selective decrease in the expression of gp120, the

major envelope glycoprotein, rich in intrachain disulfide bonds and

thus potentially sensitive to the effect of a reducing agent such as

GSH. Overall data suggest that GSH can interfere with late stages of

virus replication. This would be in agreement with data obtained in

cells exposed to herpesvirus type 1 (a DNA virus) or to Sendai (an

RNA virus), showing that the suppression of virus replication by GSH

is related to the selective inhibition of envelope glycoproteins.

These results suggest a potential role of GSH in combination with

other antivirals in the treatment of virus-related diseases.

PMID: 8911579 [PubMed - indexed for MEDLINE]

> Hi, all.

>

> It is well-known that people with chronic fatigue syndrome (PWCs)

> often test positively for various viral infections. In the U.S.,

> these commonly include the herpes family viruses Epstein--Barr,

> cytomegalovirus and HHV-6A. There are reports in the literature

of

> sackie B3 viral infections being found in PWCs as well, but

these

> reports appear to originate primarily from the U.K. and from other

> European countries, not from North America. I have been puzzling

> over this apparent difference for some years.

>

> Recently I learned of the work of Prof. Harold D. of the

> University of in Canada (http://www.hdfoster.com). Among

> other things, Prof. has advanced a recommendation for the

> treatment of AIDS that is based on supplementing selenium and

three

> of the amino acids (tryptophan, cysteine and glutamine). The

basis

> for this treatment is his theory that the HIV virus produces full-

> blown AIDS by depleting the body of these nutrients. In his view,

> the virus does this by expressing the enzyme glutathione

peroxidase,

> which is encoded in its genome. This enzyme requires these

> nutrients for its synthesis. I think this is a very promising

> approach to the treatment of AIDS, as his initial testing has

shown

> (Journal of Orthomolecular Medicine 20(2), pp. 67-69 (2005)).

>

> Prof. notes, based on the work of E.W. (Journal of

> Orthomolecular Medicine 12(4), pp. 227-239 (1997)) that not only

the

> HIV virus, but also several other viruses are known to encode for

> selenoproteins in their genomes, and he suggests that these

viruses

> may produce infections by depleting their hosts of selenium,

also.

> These viruses include sackie B3, Ebola Zaire, Molloscum

> contagiosum, and hepatitis C.

>

> It is known that the intake of selenium by the populations of the

> U.K. and other European countries has been dropping in recent

years

> since the formation of the European Union and the consequent

greater

> proportion of the wheat consumed in these countries coming from

> Europe rather than North America. Wheat from Europe is known to

be

> significantly lower in selenium content than that from Canada and

> the U.S., because of differences in the soil contents in these

areas

> (Rayman, M.P., British Medical Journal 314, p. 387 (1997)).

>

> Putting these propositions together, it occurs to me that perhaps

> the reason for the occurrence of sackie B3 infections in PWCs

in

> the U.K. and other European countries, but for the most part not

in

> the PWCs in North America, may be a result of greater selenium

> deficiency in the populations of the former countries as a result

of

> differences in food sources. sackie B3 may be more prevalent

in

> general in these populations because of the generally lower levels

> of selenium in them.

>

> This is not to say that selenium deficiencies are not also present

> in PWCs in North America. In fact, it is known that mercury forms

> stable complexes with selenium in the body, taking it out of

> bioavailability. When glutathione depletion occurs, as it does in

> many PWCs, the body is not able to rid itself of mercury with

normal

> efficiency. PWCs who are exposed to mercury from dental fillings,

> fish consumption, or nearby environmental sources such as coal-

fired

> power plants, therefore experience a buildup of mercury in their

> bodies, and this can deplete the bioavailable selenium, impacting

> not only the activity of the glutathione peroxidase enzymes, but

> also those that convert the thyroid hormone T4 to the more active

> hormone T3, as well as the other selenoenzymes.

>

> Nevertheless, sackie B3 appears to be much less prevalent among

> PWCs in North America. Again, perhaps this is a result of a

smaller

> general prevalence of this virus in this population because of its

> generally higher selenium levels.

> As I noted in my poster paper at the most recent AACFS meeting

last

> October

> http://www.cfsresearch.org/cfs/research/treatment/15.htm

>

> the herpes family viruses that are found to be producing

infections

> in PWCs are highly prevalent in their latent state in the general

> U.S. population, and they are reactivated at the onset of CFS. It

> appears, based on work at the University of Rome which I cited in

> that paper (Palamara, A.T. et al., Antiviral Research 27, pp. 237-

> 253 (1995)), that the reactivation of these viruses in PWCs is a

> direct result of glutathione depletion.

>

> I would appreciate receiving comments on these hypotheses.

>

> Rich