Excretion of GI mucus

[Guest guest]

Hi everyone!

Sorry about this description, but I need some suggestions here- My son

is unwell again after being very well for 2 weeks- Now he has some

mucus, clear transparent but yellowish in color coming out of his

bottom (without stools); it is smelly.

I am not sure if this is an infection or a die off- he has started to

take a E3Live product, which is a preparation of blue bacteria (which

basically amount to low doses vitamins, minerals, fatty acids, lots of

chlorophyll, amino acids (rich) and supposedly a protein with

anti-viral activity. (see below). So I suppose a die off is possible,

although somehow I rather doubt it. He is also on LDN since 7 weeks now.

Has anyone seen this before? Any suggestions comments on what I should do?

Thanks

Lorene

Apparently E3Love product contains cyanovirin-N (CV-N); this seems

very interesting indeed- I'd love to know of much of this protein is

present in the E3Live product? It seems that people are developing

various expression system and purification for topical use (and

possibly injection as seen in mice with Ebola virus), in E. coli and

even in transgenic plants. Would be nice to know if it could be

effective in the gut, before being digested?

I read this: Since CV-N may be immunogenic in humans, methods for

using CV-N for ex vivo inactivation of HIV in blood, plasma, or

putative vaccines preferably would allow for its exclusion from

biologicals for parenteral use. I suppose to have this ex-vivo plasma

treatment could potentially be the last resort of treatment to

inactivate viruses in individuals known to be infected (the the

symptoms of that individuals will have to be serious and clearly

identified to this infective agent to consider this sort of treatment,

I think).

I see also that this protein may be active against several viruses,

including measles and herpes, but not vaccinia virus (see below).

Anyhow, certainly very interesting, Please Perri let me know if you

have any idea of the amounts of such proteins in your Algae product.

Regards

Lorene

Antimicrob Agents Chemother. 2003 Aug;47(8):2518-25. Related

Articles, Links

Click here to read Click here to read

Potent anti-influenza activity of cyanovirin-N and interactions with

viral hemagglutinin.

O'Keefe BR, Smee DF, Turpin JA, Saucedo CJ, Gustafson KR, Mori T,

Blakeslee D, Buckheit R, Boyd MR.

Molecular Targets Development Program, Center for Cancer Research,

Frederick, land 21702, USA.

The novel antiviral protein cyanovirin-N (CV-N) was initially

discovered based on its potent activity against the human

immunodeficiency virus (HIV). Subsequent studies identified the HIV

envelope glycoproteins gp120 and gp41 as molecular targets of CV-N.

More recently, mechanistic studies have shown that certain

high-mannose oligosaccharides (oligomannose-8 and oligomannose-9)

found on the HIV envelope glycoproteins comprise the specific sites to

which CV-N binds. Such selective, carbohydrate-dependent interactions

may account, at least in part, for the unusual and unexpected spectrum

of antiviral activity of CV-N described herein. We screened CV-N

against a broad range of respiratory and enteric viruses, as well as

flaviviruses and herpesviruses. CV-N was inactive against

rhinoviruses, human parainfluenza virus, respiratory syncytial virus,

and enteric viruses but was moderately active against some herpesvirus

and hepatitis virus (bovine viral diarrhea virus) strains (50%

effective concentration [EC(50)] = approximately 1 micro g/ml) while

inactive against others. Remarkably, however, CV-N and related

homologs showed highly potent antiviral activity against almost all

strains of influenza A and B virus, including clinical isolates and a

neuraminidase inhibitor-resistant strain (EC(50) = 0.004 to 0.04 micro

g/ml). When influenza virus particles were pretreated with CV-N, viral

titers were lowered significantly (>1,000-fold). Further studies

identified influenza virus hemagglutinin as a target for CV-N, showed

that antiviral activity and hemagglutinin binding were correlated, and

indicated that CV-N's interactions with hemagglutinin involved

oligosaccharides. These results further reveal new potential avenues

for antiviral therapeutics and prophylaxis targeting specific

oligosaccharide-comprised sites on certain enveloped viruses,

including HIV, influenza virus, and possibly others.

J Virol. 2000 May;74(10):4562-9. Related Articles, Links

Click here to read Click here to read

Multiple antiviral activities of cyanovirin-N: blocking of human

immunodeficiency virus type 1 gp120 interaction with CD4 and

coreceptor and inhibition of diverse enveloped viruses.

Dey B, Lerner DL, Lusso P, Boyd MR, Elder JH, Berger EA.

Laboratory of Viral Diseases, National Institute of Allergy and

Infectious Diseases, National Institutes of Health, Bethesda, land

20892-0445, USA.

Cyanovirin-N (CV-N) is a cyanobacterial protein with potent

neutralizing activity against human immunodeficiency virus (HIV). CV-N

has been shown to bind HIV type 1 (HIV-1) gp120 with high affinity;

moreover, it blocks the envelope glycoprotein-mediated membrane fusion

reaction associated with HIV-1 entry. However, the inhibitory

mechanism(s) remains unclear. In this study, we show that CV-N blocked

binding of gp120 to cell-associated CD4. Consistent with this,

pretreatment of gp120 with CV-N inhibited soluble CD4 (sCD4)-dependent

binding of gp120 to cell-associated CCR5. To investigate possible

effects of CV-N at post-CD4 binding steps, we used an assay that

measures sCD4 activation of the HIV-1 envelope glycoprotein for fusion

with CCR5-expressing cells. CV-N displayed equivalently potent

inhibitory effects when added before or after sCD4 activation,

suggesting that CV-N also has blocking action at the level of gp120

interaction with coreceptor. This effect was shown not to be due to

CV-N-induced coreceptor down-modulation after the CD4 binding step.

The multiple activities against the HIV-1 envelope glycoprotein

prompted us to examine other enveloped viruses. CV-N potently blocked

infection by feline immunodeficiency virus, which utilizes the

chemokine receptor CXCR4 as an entry receptor but is CD4 independent.

CV-N also inhibited fusion and/or infection by human herpesvirus 6 and

measles virus but not by vaccinia virus. Thus, CV-N has broad-spectrum

antiviral activity, both for multiple steps in the HIV entry mechanism

and for diverse enveloped viruses. This broad specificity has

implications for potential clinical utility of CV-N.