Antibiotics = Mycotoxins/What to do about it.-LONG post

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I have plenty of info Heidi, if you want I

can send to all or can send to you privately.

.

Just to give you something to start with:

Hypericin: the active ingredient

in Saint ’s

Wort

Abstract

by A.Y. Oubre

Hypericin, a photochemical extracted from St. s Wort (Hypericum perforatum) and related species,

has been shown to have potent, broad spectrum antimicrobial activity. This compound

is an aromatic polycyclic anthrone, a class of colored or pigmented chemical

substances which have photosensitizing activity. In

both in vitro (laboratory) and in vivo (animal) studies, low, non-toxic doses

of hypericin significantly inhibited the replication of several viruses,

including HIV, influenza A, cytomegalovirus (CMV), Herpes simplex 1 and 2

(HSV-1 and HSV-2), and Epstein-Barr virus (EBV). Hypericin and its

chemical relative, pseudohypericin, produce antiviral activity through a

different mechanism of action than do AZT and other nucleoside antiviral

agents. Hypericin does not appear to directly alter the activity of reverse

transcriptase although it does block the formation of HIV synctium. Recent

findings have shown that the antiretroviral action of this compound disrupts

uncoating of the lipid envelope of both DNA and RNA viruses, thus preventing

infected cells from releasing HIV copies. Theoretically, hypericin and AZT, in

combination, may have synergistic antiviral effects against HIV. On the other

hand, hypericin actually may increase the toxicity of antiretroviral

nucleosides such as AZT, ddI, or ddC.

Traditionally, extracts of St. s Wort (which contain

hypericin) have been used as an antidepressant, possibly by acting as a MAO inhibitor.

The psychotropic effects attributed to hypericin in St. s Wort extract

suggest that the pigment compound can cross the blood brain barrier (possibly

treating neuropsychological symptoms such as dementia). Laboratory

investigations indicate that hypericin may be beneficial as an HIV therapy.

However, its administration should be carefully monitored by a physician. The

levels of hypericin found in most commercially available extracts of St. s

Wort generally are not sufficient to be therapeutically effective against viral

infections.

Liver function should be tested periodically in persons taking

hypericin. Also, extreme photosensitivity has been observed in a few cases of

people taking this high doses (in excess of 10 mg per day) of this compound.

Finally, there is a very small possibility that adverse reactions could occur

on occasion between hypericin and other foods or drugs which interfere with MAO

inhibitors.

Active principles in St. s Wort

The quantity and quality of active principles in Hypericin species

vary according to geographical locale, climate, time of day, and time of year.

St. s Wort contains dianthrone derivatives, mainly in the form of hypericin

and pseudo-hypericin 7, 32, 33 as well as flavonoids 8, 15. Small amounts of coumarins 7, phenolic carboxylic compounds, 7 phloroglucinol derivatives 17, monoterpenes, 7, sesquiterpenes 7, n-alkanes 9, n-alkanols 10, carotenoids 11, and beta-sitosterol 12 are present. The roots contain zanthones 16. Practitioners and consumers should note

that St. s Wort extracts, whether standardized or not, consist of other

active ingredients in addition to hypericin and pseudohypericin.

Pre-clinical studies

Both in-vitro (test tube) and in-vivo (animal) pre-clinical

studies suggest that hypericin (and, to a lesser extent, pseudo-hypericin) may

have therapeutic benefits for HIV infection and other retroviral diseases.

Certain compounds other than hypericin extracted from Hypericum species have antibiotic activity 41, 42, 43. marked antiretroviral effects, however,

have been reported primarily for hypericin 28, 29, 37, 45, 49, 50, 51, 52 which is isolated mainly from Hypericum perforatum. However, synthetic

hypericin has been used in recent studies.

In in-vitro and in-vivo studies, both hypericin and

pseudohypericin (extracted from Hypericum

triquetifolium) had antiviral activity against several retroviruses 28. In one experiment, mice were

simultaneously injected with low doses of the compounds and with Friend

leukemia virus (FV). This aggressive retrovirus

normally causes rapid splenomegaly (swelling of the spleen) and acute

erythroleukemia in mice. However, these symptoms were effectively suppressed by

the addition of hypericin. Splenomegaly had not occurred ten days after

infection at the close of the study. No infectious virus could be recovered

from the spleen. Also, viremia normally associated with FV was absent. Mice treated with hypericin and pseudohypericin

survived a much longer time than mice treated with a toxic antiviral (N3dthd).

Unlike most antiretroviral drugs, hypericin (given in a single dose of low concentration) was

effective without being cytotoxic. Even when it was administered after viral

infection had already started, it still inhibited the onset of disease 28.

In in-vitro studies, mouse cell lines were infected with radiation

leukemia virus (Rad LV) and then incubated with hypericin. The activity of

reverse transcriptase in these cells was suppressed through indirect

mechanisms. In contrast to nucleoside analogues, polycyclic

diones such as hypericin interfere directly with the viral replication

cycle during stages in which virions are assembled or intact virions are

shedded from immature cores. Alternatively, these aromatic compounds may directly

inactivate mature retrovirus that contains normal, assembled cores. Other findings indicate that hypericin is able to

inactivate virions and block viral release from infected cells by interacting

with the cell membrane 28.

Unpublished data show that hypericin disrupts the formation of

synctia in HIV disease as well as in de novo infection of cells 39. In in-vitro studies, hypericin showed

selective activity against HIV and modest inhibition of reverse transcriptase 31. In vitro research also revealed that

hypericin lowered viral activity in whole human blood taken from HIV infected

persons 26, 29. “Wild” strains of HIV taken directly

from infected patients are sometimes more resistant to antiviral agents than

are viral strains bred in the laboratory 51.

Other investigations indicate that the antiviral

effects of hypericin on murine cytomegalovirus (MCMV), Sindbus virus (SV), and

HIV are enhanced by exposure to fluorescent light 37. Hypericin and to some degree,

pseudohypericin, were effective against FV and HSV-1 when the viruses were

first incubated with the compounds for one hour at 37 degrees C before mice

were infected 31. Pre-incubation for one hour at 4

degrees C, however, produced no antiviral effects. The authors of this study (who are scientists at Lilly Research Laboratories)

reported that hypericin and pseudohypericin were effective in vitro against

enveloped viruses such as HSV and influenza when the cultures were

pre-incubated with these agents at 37 degrees C. They also correctly showed that hypericin and its analogue inhibit DNA

and RNA viruses, but not viruses which lack a lipid envelope. The Lilly

researchers, who call AZT a preferred therapy for HIV, however, claim that

single dose administration of hypericin is not efficacious. Human clinical

trials are needed to evaluate the appropriate dose ranges at which hypericin is

therapeutic but nontoxic, and to assess the differences, if any, between

natural and synthetic hypericins. In animal studies, natural sources of

hypericin (in combination with its analogue, pseudohypericin), showed greater

antiviral activity that did synthetic hypericin 51. Preliminary findings thus far strongly

indicate that the wide spectrum antiviral properties of hypericin, its

experimental effectiveness at low concentrations, and its unconventional

mechanisms of antiviral action make it a promising candidate for a new class of

HIV therapies.

Mechanisms of action

Hypericin and pseudohypericin had no effect on purified reverse

transcriptase alone. They did not alter levels of intracellular viral mRNA.

Instead, hypericin lowers the number of mature viral particles without

suppressing intracellular levels of viral mRNA. The concentrations of viral antigens

on the cell surface were also unaffected by hypericin. These findings, as a

whole, imply that the compounds interfere with viral assembly, budding,

shedding or stability at the level of the cell 39 membrane When hypericin was added to

viral-infected cell cultures, red fluorescence appeared at localized areas on

the lipid surface membrane 39.

Unlike nucleoside analogues, polycyclic diones such as hypericin

have no effects on transcription, translation, or transport of viral proteins

to the cell membrane. They are not directly active against reverse

transcriptase even though reverse transcriptase activity was reduced in

infected cells that had first been incubated with hypericin. Cells treated with

hypericin form immature or abnormally assembled cores. This indicates that

hypericin may block the processing of gag-encoded precursor polypeptides 39. Hypericin, whether in the intracellular

medium or bounded to the membrane, is thought to lower the activity of reverse

transcriptase by interfering with protein synthesis 28, 39. (It is noteworthy that the antiviral

effects of harmine, a photoactive alkaloid, involve disrupted kinase activity

in enveloped RNA viruses 47.)

Viral particles are not formed when gag-related polyproteins fail

to be cleaved or synthesized. Gag-related polyproteins, therefore, may play a

decisive role in the virucidal actions of hypericin. Reverse transcriptase

within the core of the assembled virus probably takes the form of an inactive

enzyme or proenzyme. Mechanisms involving viral-encoded proteases or kinases

might be required to activate reverse transcriptase. These mechanisms could

transform the enzyme from a nonfunctional to a functional state. Both hypericin

and pseudohypericin are thought to influence protease activity. In turn,

altered protease activity could disrupt the cleavage or synthesis of

gag-related polyproteins. As a result, immature viral cores would be formed.

Alternatively, by selectively binding to viral polyproteins, hypericin could

interfere with the gag and gag-pol polyproteins needed for viral assembly.

Thus, hypericin could block the process whereby RNA packages encapsulated viral

particles 39.

Some investigators, however, propose that hypericin lyses

infectious virion by interacting directly with the viral envelope instead of

disrupting gag-encoded precursor polyproteins or modifying other proteins 31. In any case, the antiviral properties

of hypericin appear to involve its interactions with the cell membrane or cell

surface recognition sites 26. Molecular modifications at or near the

surface provide a model for rationally designing a new class of anti-HIV

agents. Such therapies may be able to block HIV-encoded protease located in the

gag-pol region. Importantly, drugs of this type would not be toxic like AZT and

other agents whose pharmacological actions are based on direct inhibition of

reverse transcriptase.

The aromatic, ringed structure encircled by six phenolic hydroxy

groups seems critical to the antiviral activity of the hypericin molecule 39. Quinone groups, which often have

antiviral properties, also exert photodynamic effects. Hypericin is thought to

generate singlet oxygen. However, free radical quenchers can interfere with

singlet oxygen reactions involving hypericin thereby reducing its antiviral

properties 35, 37.

Hypericin has a unique molecular structure in which one-half of

the molecule is hydrophilic (water loving) while the other half is hydrophobic

(water repelling). The top, bottom and side (non-polar) of the hypericin

molecule which contains the methyl groups are hydrophobic. It is thought that

the molecule might bond to the outer surface of the cell membrane. Presumably,

the hydrophobic side would be immersed in fat Singlet oxygen, though less

reactive than triplet oxygen, binds with two-electron targets, including, for

example, the double bonds found in polyunsaturated fatty acids. The hydrophilic

sides, in contrast, could hydrogen-bond to the aqueous media 48.

Discrepancies between in vivo findings from different studies on

the antiretroviral effects of hypericin and pseudo-hypericin may be due partly

to variations in light 37. However, differences in hypericin

isolation methods and in the strains of mice used also could account for

variable findings in several investigations. The antiviral effects of hypericin

are largely but not completely, attributed to its photodynamic properties 35, 37, 44. In the presence of light, hypericin

completely inhibited infection of cell cultures of equine infectious anemia

virus (EIAV) 44. On exposure to fluorescent light,

hypericin inactivated MCMV, Sindbis virus (SV), and HIV-1 37. Both membrane virions and

virus-infected cells were more strongly inactivated by visible light 37. (Polyacetylene phenylheptatriyine

(PHY), a substance purified from the plant, Bidens pilosa, also shows antiviral

activity against membrane-bound viruses such as MCMV. The antiviral effects,

which involved interactions between PHY and membrane, occurred in the presence

of long wave ultraviolet light 46). Significant advances in

photobiological research have been made in recent years. New findings

demonstrate clearly that photodynamic action accounts for the antiviral

properties of several natural product derivatives, including hypericin.

Light is required for the photosensitization of hypericin. The

compound absorbs light quanta and generates it in the form of singlet oxygen 35, 37. In so doing, hypericin triggers the

photo-oxidation of cellular components, including, for example, the

photohemolysis of red blood cells 35. The underlying mechanism of

photodynamic reactions is not fully understood. It is thought to involve

interactions between oxygen and light as well as sensitizing pigment which

binds to the cell membrane 35, 37.

In photodynamic reactions mediated by hypericin, singlet oxygen

serves as the main oxidant. Singlet oxygen has a strong affinity for pi

electron-systems found in compounds such as polycyclic diones. The pi

electrons, responsible for the photoactive properties of hypericin, absorb

visible and ultraviolet light and then reemit it within the range of green and

red light. The two hydroxy groups and the two methyl groups flanking each side

of hypericin’s eight ringed structure do not lie within the same plane.

Instead, they repel each other, placing strain on the benzenoid structure. This

causes the hypericin molecule to twist and become unstable. Hypothetically, the

steric strain could increase the energy state of the pi electrons. This would

allow them to form temporary bonds with singlet oxygen which, at a later point,

could be released to disrupt mechanisms of viral replication 48. Pi electrons therefore, seem to play a

major role in the antiviral activity of hypericin.

The “impressive

light-mediated antiviral activities” of hypericin have been shown in several

studies 35, 37, 45. Sindbus virus (SV),

for example, was 99% inhibited in the presence of light. In the dark, however, the antiviral

effects of hypericin were reduced by more than two orders of magnitude 45. On exposure to light (650-700nm.),

hypericin undergoes type II photosensitization in which singlet oxygen and

other reactive molecular species are produced. Though not as destructive as

free radicals (which are generated in Type I photosensitization 35, singlet oxygen could damage viral

membranes, thereby interfering with proteins and nucleic acids. Nonetheless,

hypericin also has some degree of virucidal activity in the dark, though much

less so than in light 37. It is thought that the antiviral

effects produced in the absence of light take place through a different mode of

action than light-mediated virucidal activity 37. Protein kinase C, for example, may

represent an alternative target for hypericin’s antiviral action in the absence

of light 40.

One of the therapeutic advantages of hypericin is that it works by

multiple steps 36. Hypericin is probably able to interrupt

various phases in the replication of enveloped retroviruses. These stages

include polyprotein cleavage and protein alterations as well as assembly,

budding and shedding of viral components. The compound’s disadvantages as an

anti-HIV agent involve its potential toxicity when patients are exposed to

sunlight. Also, it has been reported that in humans, hypericin is more

effective in suppressing HSV-1 and HSV-2 than HIV. Future research is required

to elucidate the mechanisms through which hypericin generates and reacts with

singlet oxygen in triggering antiviral effects.

Dosage

Clinical trials currently being conducted by Dr. Bihari in New York City recommend

the following regimen. For

the first two weeks, patients take one 10 mg. capsule once a day for two weeks.

During the second two weeks, the dosage alternates between one 10 mg. capsule

per day on the first day, two 10 mg. capsules on the second day, one 10 mg.

capsule on the third day, and so forth. The ultimate dosage is given during the

fifth and sixth weeks when patients are given two 10 mg. capsules per day.

Future regimens for optimal dosage are presently being devised by

researchers and clinicians involved in pilot trials of hypericin for the

treatment of HIV. It has been proposed that beta-carotene, a known free radical

quencher, be administered in combination with hypericin. Theoretically, this

might reduce any toxic side-effects associated with hypericin’s generation of

free radicals. Some investigators, however, have warned that quenchers also may

lessen the anti-viral properties of hypericin. The role of beta-carotene and

other free-radical scavengers in hypericin therapy deserves further

clarification.

Conclusions

Hypericin, a pigment

molecule with photodynamic activity, has dramatic antiviral activity,

especially in the presence of light. Like several other plant derived substances, hypericin

only inhibits viruses with membranes. It has antiviral effects against a wide

range of retroviruses, including HSV-1, HSV-2, (murine) CMV, and HIV-1. In

contrast to nucleoside agents such as AZT, hypericin and its chemical relative,

pseudohypericin, do not directly affect the activity of reverse transcriptase.

Rather, these agents seem to disrupt various stages of viral replication,

including assembly, budding, shedding and possibly protein synthesis, all of

which depend on the integrity of the viral membrane.

Hypericin and related compounds, with their alternative targets

for virucidal activity, comprise a new class of potential anti-HIV drugs. It is

not yet known how effective hypericin will be in human AIDS. Preliminary

findings, however, strongly suggest that this compound is one of the most

promising, new anti-HIV prototype molecules currently under investigation.

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Related Articles, Links

Photosensitization

is required for inactivation of equine infectious anemia virus by hypericin.

Carpenter S, Kraus GA.

Department of Veterinary Microbiology and Preventive Medicine, Iowa State University, Ames

50011.

Hypericin, a photoreactive polycyclic quinone, was found to dramatically reduce

infectivity of cell-free stocks of equine infectious anemia virus. However, the

antiviral activity of hypericin was completely dependent on the presence of

light. Short periods of photosensitization resulted in a partial loss of

reverse transcriptase activity and complete inhibition of viral infectivity.

These results suggest that the photodynamic effect of hypericin interferes with

more than one stage in the virus replication cycle.

PMID: 1707176 [PubMed - indexed for MEDLINE]

Immunol

Today. 1990 Sep;11(9):327-33.

Related Articles, Links

Immunologic

issues in anti-retroviral therapy.

Yarchoan R, Mitsuya H, Broder S.

National Cancer Institute, Bethesda,

MD 20892.

A number of drugs acting at different stages of viral replication have been

shown to be effective anti-HIV agents in the laboratory, and several have been

found to be active in patients. It has become evident that inhibition of viral

replication in HIV-infected patients will result in an improvement in their

immune function. However, as Yarchoan, Hiroaki Mitsuya and Broder

point out, complete immunoreconstitution generally does not occur in patients

with established AIDS using currently available therapies. It is important to

understand the factors that limit immunologic improvement in such patients so

that more effective therapy can be devised.

Publication Types:

·

Review

PMID: 1698379 [PubMed - indexed for MEDLINE]

Antiviral activities of hypericin

J. B. Hudsona,

I. -Bazzocchib

and G. H. N. Towersb

a Division of Medical Microbiology, University of

British Columbia, Vancouver, Canada

b Department of Botany, University of British

Columbia, Vancouver, Canada

Received 19 July 1990; accepted 15 October 1990. Available online

12 November 2002.

Abstract

Hypericin, a photodynamic plant quinone, readily inactivated

murine cytomegalovirus (MCMV), Sindbis virus, and human immunodeficiency virus

type 1 (HIV-1), especially on exposure to fluorescent light. Sindbis virus was

significantly more sensitive than MCMV. The inactivated MCMV, when used to

infect cells, was incapable of synthesizing early or late viral antigens. In

addition to this direct virucidal effect, when hypericin was added to cells

infected with viable MCMV, inhibition was also observed, particularly when the

compound was added in the first two hours of infection. Again the antiviral

effect was augmented by visible light. At effective antiviral concentrations,

there were no discernible adverse effects on cultured cells. Thus hypericin appears to have two modes of antiviral

activity: one directed at the virions, possibly on membrane components

(although other virion targets cannot be ruled out), and the other directed at

virus-infected cells. Both activities

are substantially enhanced by light.

Other recent studies on the antiviral activities of hypericin have

not considered the role of light, and it is conceivable that apparent

discrepancies between their results may have reflected different conditions of

light exposure.

Author Keywords: Hypericin; Photosensitization

J

Tradit Chin Med. 1989 Jun;9(2):113-6.

Related Articles, Links

An

experimental study of the anti-HSV-II action of 500 herbal drugs.

Zheng MS.

Experimental assessments were made on the anti-HSV-II action of 500 herbs by

determinations of the virus inhibition logarithm (VIL). 13 highly effective

herbs (VIL greater than or equal to 4.00) were screened cut, providing a

rational basis for clinical therapy. Among these effective herbs, 10 were

aqueous extracts of Artemisia anomala, Centella asiatica, Epimedium Sagittatum,

Hibiscus mutabilis, Hosta plantaginea, Hypericum japonicum, Inula japonica,

Mosla punctata, Rhododendron simsii, and Rhus chinenses, while 3 were alcohol

extracts of Epimedium Sagittatum, Hypericum japonicum, and Mosla punctata.

PMID: 2550706 [PubMed - indexed for MEDLINE]

Arzneimittelforschung.

1987 Jan;37(1):10-3.

Related Articles, Links

[Animal

experiments on the psychotropic action of a Hypericum extract]

[Article in German]

Okpanyi SN, Weischer ML.

Extracts of Hypericum perforatum (Psychotonin M) (St. 's wort) with known

concentrations of hypericin were tested in several models generally accepted as

screening methods in experimental animal studies for the recognition of

psychotropic, and in particular of antidepressant activity. Hypericum extract

enhanced the exploratory activity of mice in a foreign environment,

significantly prolonged the narcotic sleeping time dose-dependently, and within

a narrow dose range exhibited reserpine antagonism. Similar to most other

antidepressants, hypericum extract enhanced significantly the activity of mice

in the water wheel test and after a prolonged daily administration decreased

aggressiveness in socially isolated male mice. The presented data in addition

to the already proven clinical efficacy justify the use of standardised

Hypericum extract in the treatment of mild to moderate depression.

PMID: 3566850 [PubMed - indexed for MEDLINE]

Antiviral

Res. 1990 Jun;13(6):313-25.

Related Articles, Links

Virucidal

activity of hypericin against enveloped and non-enveloped DNA and RNA viruses.

Tang J, Colacino JM, Larsen SH, Spitzer W.

Lilly Research Laboratories, Indianapolis,

IN 46285.

Hypericin is a polycyclic anthrone first isolated from the plant St. s wort and was

shown to have dramatic anti-retroviral activity against Friend leukemia virus

and radiation leukemia virus in mice. Hypericin displayed marginal activity

(IC50 = 6 micrograms/ml) against Moloney murine leukemia virus (Mo-MuLV) in

vitro. Hypericin did not display selective antiviral activity against herpes

simplex virus, influenza A, adenovirus, or poliovirus. The 50% cytotoxic

concentration was approximately 25 micrograms/ml. When virus was incubated with

hypericin before infecting cells, the drug was virucidal to all enveloped

viruses tested (herpes simplex, influenza virus A, and Mo-MuLV) at

concentrations of 1.56 micrograms/ml to 25 micrograms/ml. Hypericin was not

virucidal to the non-enveloped viruses tested (adenovirus and poliovirus).

These data indicate that the mechanism of viral inactivation for hypericin is

dependent upon the presence of a viral lipid envelope. In vivo, hypericin (50

mg/ml) was effective against FLV or HSV-1 if incubated with the virus for 1 h

at 37 degrees C before infecting mice, but was not effective if pre-incubated

with virus for 1 h at 4 degrees C or if administered concurrently with virus.

PMID: 1699494 [PubMed - indexed for MEDLINE]

Studies

of the mechanisms of action of the antiretroviral agents hypericin and

pseudohypericin.

Lavie G, Valentine F,

Levin B, Mazur Y, Gallo G, Lavie D, Weiner D, Meruelo D.

Department of Pathology, Kaplan Cancer Center,

New York University

Medical Center, NY 10016.

Administration of the aromatic polycyclic dione compounds hypericin or

pseudohypericin to experimental animals provides protection from disease

induced by retroviruses that give rise to acute, as well as slowly progressive,

diseases. For example, survival from Friend virus-induced leukemia is

significantly prolonged by both compounds, with hypericin showing the greater

potency. Viremia induced by LP-BM5 murine immunodeficiency virus is markedly suppressed

after infrequent dosage of either substance. These compounds affect the

retroviral infection and replication cycle at least at two different points:

(i) Assembly or processing of intact virions from infected cells was shown to

be affected by hypericin. Electron microscopy of hypericin-treated,

virus-producing cells revealed the production of particles containing immature

or abnormally assembled cores, suggesting the compounds may interfere with

processing of gag-encoded precursor polyproteins. The released virions contain

no detectable activity of reverse transcriptase. (ii) Hypericin and

pseudohypericin also directly inactivate mature and properly assembled

retroviruses as determined by assays for reverse transcriptase and infectivity.

Accumulating data from our

laboratories suggest that these compounds inhibit retroviruses by

unconventional mechanisms and that the potential therapeutic value

of hypericin and pseudohypericin should be explored in diseases such as AIDS.

PMID: 2548193 [PubMed - indexed for MEDLINE]

Antiretroviral activity of synthetic hypericin

and related analogs

A. Kraus*,

Dan Pratt*,

Tossberg#

and Carpenter#

*Department of Chemistry, Iowa State University Ames, IA 50011, USA

#Department of Veterinary Microbiology and Preventive Medicine, Iowa State University Ames,

IA 50011,

USA

Received 8 August 1990. Available online 22 April 2005.

Hypericin and pseudohypericin are

naturally occurring polycyclic quinones which have recently been shown to

inhibit the infectivity of several retroviruses, including human

immunodeficiency virus. To better understand the antiviral mechanisms of these

compounds, hypericin and a series of analogous quinones were synthesized and

tested for anti-retroviral activity against equine infectious anemia virus

(EIAV). Treatment of EIAV-infected cells with hypericin reduced the production of

infectious virus by 99.99%. None of the analogs were found to inhibit virus

replication. These results suggest that the complete ring structure of

hypericin is required, but not sufficient, for antiviral activity

From:

BorreliaMultipleInfectionsAndAutism

[mailto:BorreliaMultipleInfectionsAndAutism ] On Behalf Of Ambitionn01@...

Sent: Monday, March 03, 2008 3:41

PM

To:

BorreliaMultipleInfectionsAndAutism

Subject:

Re: Antibiotics = Mycotoxins/What to do

about it.

This is

interesting about the St. 's

Wart. I will have to do some research into it.

Heidi N

From :

" So the first thing I did was to fix my son ability to detox alkaloids, in

one of my traveling around the world for help and I found the power of

natural red clay to absorb all kind of toxic substances in the gut and the

herbs saint johns worth to turn on the p450 and also is a retroviral

antivirus, in fact it's so strong that it is replacing the cocktail for AIDS

patients and can get rid of herpes viruses 10 times better and safer than

Valtrex! That's right, if you think that stuff is the way to go...SJW it's

10 times more effective, and I did it with great success with my son and

never touched Valtrex or antifungal drugs "

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