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thank you. you are right - it is absolutely fantastic that the hiv=aids

hypothesis is still being entertained, given the magnitude of evidence that

discredits it. it is also amazing to me how often the rules change (ie: take

meds forever faithfully or we'll have monstrous strains of hiv upon us - to:

drug holidays are good for you) and how people are accepting this as

science. i guess the machine needs to keep rolling, but i can hear the

misfiring of pistons within that machine as of late . . . it is music to my

ears!

love your attitude - keep it up!

>From: freelightexpress@...

>Reply-cures for AIDSegroups

>cures for AIDSegroups

>Subject: davids response to john

>Date: Wed, 6 Dec 2000 14:01:05 -0800

>

>Hi david,

>

>good reply there. Its just amazing that all this " monopoly " exists around

>HIV......the 'culprit virus'....if indeed the little booger just hasnt

>been scientifically proven to exist or isolated. My friend who has been

>'poz' for 15 years say it does exist! - his rationale being that

>......'theres something out there killing people'.(he has by the way gone

>back on some of the 'meds' - seems like a lot of people go on and off of

>them for periods). Hmmm. Well.......disease manifests in zillions of ways

>by zillions of factors. You know it just had to happen that some 'virus'

>has to be blamed for the condition called " aids " - which is so broad a

>term as to include anything. I tested poz two times in a row which tells

>me that my immune system is up and running. Good news. I think it boils

>down to this - people have to have a 'culprit' ..........a virus, a bug,

>a germ, whatever. The whole hiv=aids equation is perfect for the mass

>market of multiple forums. I am quite healthy taking my Body Balance(a

>whole food liquid supplement made from sea vegetables and aloe vera

>juice), plenty of antioxidants.......garlic, herbs, fresh air, sunshine,

>and distilled water. A positive mind and a radiant spirit do wonders for

>ones well-being.

>

>Hope all are well and staying well.

>

>blessings,

>

>paul

________________________________________________________________________________\

_____

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PARASITES As Cofactors For AIDS

Excerpts from the work of

Dr. Bowman Pearce

Chronic Non-Opportunistic Parasitism as a Co-Factor for AIDS © 1997

Bowman Pearce rpearce@...

The growing body of evidence is supporting the idea that parasitic

disease may be an essential factor for AIDS. The theory was based

upon three lines of evidence :

all the risk groups for AIDS had evidence for chronic " pan-

immunosuppression " prior to HIV/AIDS

the epidemic of parasites in homosexuals preceded AIDS by a few

years. That was a common factor with African and Haitian risk Groups.

parasites exert immunosuppressive, antigenic and mitogenic effects on

T cells.

Between 80 and 100 percent of sexually active homosexual men

worldwide are infected with one or more species of intestinal

parasite.

The epidemic of parasites in gay men preceded AIDS by a few years.

In separate studies, the parasites gay men carry -- E. dispar

(formerly E. histolytica), other so-called " nonpathological " amebae

and Giardia -- have been shown to be specifically associated with a

suppression of cell mediated immunity, elevation of IgM, depressed

CD4:CD8 ratios, and increased risk for seroconversion to - and

seropositivity for - HIV.

Parasites explain why AIDS develops among men and women alike in

Africa and other tropical regions (Southeast Asia, the Caribbean,

India) where parasites infect men and women indiscriminately. By

contrast, in developed countries and urban settings, male homosexuals

are the principal risk group for chronic parasite infection and AIDS.

Malaria appears to predispose to HIV in central and eastern Africa.

Malaria has long been regarded as a co-factor for EBV-induced

Burkitt's lymphoma.

E. histolytica extract activates latent HIV in T cells in culture. In

mice, parasites activate HIV transgenes, depress anti-HIV and anti-

adenoviral CTL activity, and promote a Th2 predominant state (which

may favor retroviral replication). Mice with malaria are much more

susceptible to leukemia caused by Moloney Murine Leukemia Virus than

non-parasitized mice.

Logistic regression analyses of factors predisposing to KS in gay men

show that the leading independent risk is exposure to feces. The

intestinal parasites that colonize gay men are transmitted

exclusively through the fecal-oral route. One early survey of

Kaposi's Sarcoma in Africa showed an exact geographical confluence

between KS and onchocerciasis, a chronic parasitic disease. Thus, the

development of KS in gay men without HIV may be related to chronic

immunodepression by parasites that permits the emergence of the KS

associated herpes virus, HHV8.

Only feral cats that are parasitized naturally acquire FIV and

develop feline AIDS. Pathogen-free cats do not transmit FIV when

housed together, and when inoculated with FIV undergo an acute phase

response but fail to develop feline AIDS characterized by severe CD4

depletion, opportunistic infection, and death.

Monkeys housed in the nation's primate centers, including those used

in SIV studies, are universally infected with intestinal parasites

and the animals in which the first reported cases of immunodeficiency

appeared had been previously infected with malaria.

Cattle with trypanosomes are significantly more likely to be infected

with Bovine Leukemia Virus (BLV) and to develop leukosis than

parasite-free herds.

Progression to fulminant AIDS is more rare in groups such as sex

partners of hemophiliacs and health care workers with occupational

exposures to HIV than other risk groups whose immune systems are

chronically activated. Such persons may seroconvert to HIV and/or

develop anti-HIV cell-mediated activity, but lacking parasites or

other chronic immune stimulus, do not progress to fulminant AIDS at

the high rates observed in the major risk groups.

In 1987, it was predicted that HIV and AIDS would most likely spread

by heterosexual transmission beyond Africa into other parasite

endemic regions of the world, especially rural South America,

Southeast Asia, and India. This, in fact, has occurred. If parasites

were not an obligatory cofactor for AIDS, heterosexual transmission

of HIV and AIDS would theoretically have occurred at an equally high

rate in parasite-free regions of North America, Europe, and

Australia. The comparatively low rate of HIV infection and AIDS

progression among heterosexuals in these temperate regions is

consistent with the idea that environmental cofactors are important

determinants of HIV transmission and pathogenesis.

Not widely known is the fact that 80% or more of sexually active gay

men currently carry Entamoeba dispar, E. coli, E. hartmanni, I.

bütschlii, D. fragilis, and Giardia intestinalis among other protozoa

(compared to an incidence in the general population of a 1-3%). The

epidemic of parasites in gay men began in the mid 1970s and grew

exponentially becoming pandemic in this group by 1979, a year or two

before AIDS began to take its toll. E histolytica lectin stimulates

HIV production in vitro while E. dispar and other " non-pathogenic "

amebae in HIV(-) gay men are independently associated with skin

anergy, chronically elevated IgM, and an increased risk for

seroconversion to HIV.

In gay men, oral-anal contact is an independent risk factor for KS.

KS can develop in HIV negative homosexual men, suggesting that some

other immunodepressing agent besides HIV-1 can predispose to the

putative KS virus, HHV8. This other source of immunodepression could

be parasites since, in Uganda, KS (but not other tumors) has been

found to be in exact and narrow geographical confluence with the

chronic parasitic disease onchocerciasis. In Africa and other

tropical areas as well as in Belle Glade, Florida, AIDS affects women

as frequently as men.

In the U.S., between 1 and 2 million gay men are currently multiply

infected with protozoa, yet very few are even aware of the fact. No

other putative cofactor for AIDS, (e.g. mycoplasma, alcohol and drug

abuse, HHV-6A) has such a uniformly high incidence rate in the gay

and tropical risk groups for AIDS.

Epidemiological Association between Intestinal and Other Non-

opportunistic Parasites and HIV/AIDS

Largely unappreciated, but by no means unknown, is the fact that 60%

to 100% of sexually active gay men currently harbor one or more

species of intestinal parasite, including Entamoeba dispar, E. coli,

E. hartmanni, Iodamoeba butschlii, Dientamoeba fragilis, and Giardia

intestinalis among others (Law et al, 1991, Esfandiari et al., 1995).

A recent surveillance for Giardia in New York City shows that the

spread of this parasite through sexual means, i.e. as a STD among

mostly gay men, continues to the present time. The highest rates are

among hispanic children (mostly Dominican immigrants) and gay men,

both HIV(+) and HIV(-) (NYC Department of Health,

Ymilko@...).

Like sexually active gay men, the tropical risk groups for AIDS also

have a high prevalence of non-opportunistic parasites. In addition to

enteric infections by nematodes and protozoa, these include

schistosomiasis, strongyloidiasis, onchocerciasis and malaria

(Climent, et al., 1994; and Buster, 1984; Bouree, et al., 1995;

Plumelle and Edouard, 1996).

The triad of HIV, non-opportunistic parasites, and AIDS is now

reported for Haiti, the Republic of Congo (formerly Zaire), Uganda,

Rwanda, Tanzania, Ethiopia, Puerto Rico, Jamaica, ique, Papua

New Guinea, India, Pakistan, Southeast Asia, Belle Glade, Florida and

South Los Angeles. Indeed, lymphotropic retroviruses, which require

immune activation to reproduce successfully, may have co-evolved with

parasites in the tropical regions of the world whence HIV and HTLV

emerged.

Parasites Are Agents of Chronic Immunosuppression

Even the so-called " non-pathogenic " (i.e. non-invasive) ameba can

depress cell-mediated immunity. They found that anergy significantly

and independently associated with the presence of E. histolytica [now

termed E. dispar], E. coli, and Iodamoeba bütschlii but not with

other parasites (P< 0.005). The authors concluded:

" Our main findings were that intestinal parasites and systemic

deficiency of cell-mediated immunity correlate within the group of

healthy homosexual men and that this correlation specifically

involves the 3 amoebas, E. histolytica, E. coli, and I. bütschlii. [O]

ur data support the hypothesis that parasites may cause AIDS or act

as a cofactor to facilitate HIV infection and/or its progression to

AIDS. "

For gay men, parasitic infections are multiple, repeated (weekly

exposures are not uncommon), and encountered for the first time in

the second and third decades of life. This sudden and sustained

onslaught of antigens and protozoa may have considerable impact on

immune responses and the state of immune activation not only in the

gut, but systemically as well.

Bentwich and colleagues of the Weizman Institute in Rehovot Israel

have reported that Ethiopian Jews with and without HIV-1 also carry

several species of intestinal parasite including helminths

(Kalinkovich et al., 1996 XI ICA). These patients are being followed

for possible changes in the in rate of progression to AIDS but it is

these authors' opinion that progression to AIDS is slower in

Ethiopians treated for parasites. They have shown that lymphocytes

from parasitized individuals are highly susceptible to HIV infection

in vitro (persona lcommunication).

Speaking at a recent conference, Dr. Bentwich reported that in

Africa, Ethiopians with HIV died two to three times more quickly than

those infected in the West and who were without parasites. In an

article appearing in the Jewish Bulletin of Northern California

Bentwich was quoted as saying:

The Epidemic of Parasites in Gay Men Preceded AIDS

The incidence of gastrointestinal parasites rose exponentially in gay

men during 1977-1983 (Figure 2). The transmission of parasites was

associated with sexual activity that exposed partners to feces,

particularly oral-anal sex or " rimming. " By 1980, the prevalence of

parasites was 60% or greater for homosexual men attending STD clinics

or private practice (Pearce, 1983; Markell and Kuritsubo, 1981;

et al., 1981; , et al., 1978; Schmerin, et al., 1977;

Mildvan et al., 1977). HIV was apparently introduced into Western

societies in the 1970s or even earlier.

One possible reason the virus didn't proliferate and produce

fulminant disease until the early 1980s might be the absence of a

suitable pool of parasitized hosts. By that time parasite epidemic in

gay men had reached its height. Even well before 1980, clinicians had

warned about the emerging parasite epidemic in gays. The first to

report a homosexual case cluster of E. histolytica was Harry Most who

dubbed Manhattan a " tropical isle " (Most, 1968). This concern was

echoed by another leading infectious disease specialist who in in

1979 warned:

Evidence indicates that an epidemic of intestinal protozoan infection

exists in the homosexual male population in New York City. The

difficulty in making a diagnosis, inadequate therapy, failure to

alert potential victims,and official neglect of the epidemic have

combined to create a dangerous situation. (Kean et al., 1979)

The parasite theory led to the prediction that AIDS would spread

beyond Africa and Haiti into other regions of the world where

parasites are holoendemic (Pearce, 1986, 1989). In contrast, and

contrary to the warnings of some researchers (Redfield, 1986), AIDS

has not emerged as an overwhelming epidemic among heterosexuals in

the developed (and largely parasite-free) countries of North America,

Europe and Australia. This strongly suggests an environmental

component to AIDS is present in the tropical regions of the world.

Unlike Other Putative Cofactors for HIV (e.g. HTLV-1, CMV, HHV-6A,

Adenoviruses, Mycoplasma), Parasites Are Chronic, Multiple,

Recurrent, Antigenically Highly Variable, and Present in 80-100% of

the Gay and Tropical Risk Groups but Only 1-2% of the General

Population

Table 2. Frequency of intestinal parasites in ARC patients with

lymphadenopathy syndrome (LAS), thrombocytopenia (ITP) compared to

healthy gay controls and mostly heterosexuals in the San Francisco

Bay Area in 1982. [From Pearce and Abrams 1987].

Parasite LAS ITP Gay Mainly Heterosexual

Any 80% 82% 59% 14%

Endolimax nana 61% 59% 38% 7%

Entamoeba histolytica 37% 41% 27% 1%

Entamoeba hartmanni 37% 41% 25% 2%

Entamoeba coli 21% 24% 17% 4%

Iodamoeba bütschlii 7% 6% 18% 1%

Giardia intestinalis 1% 0% 5% 2%

Dientamoeba fragilis 1% 6% 1% 3%

Parasitism Has Been Etiologically Linked to Other Lymphotropic

Retroviral Diseases Including ATLL, Burkitt's Lymphoma, and BLV-

induced Bovine Leukemia, and Feline Immunodeficiency Virus (FIV)

Induced AIDS in Cats and MAIDS in Mice.

Strongyloides, filaria, malaria and other parasites are thought by

several researchers to predispose to adult T cell leukemia (ATLL) by

chronically activating the HTLV-1 provirus (Nakada et al., 1983;

Patey et al., 1992; Plumelle Y, et al. 1997).

Strongyloides has also been frequently observed in association with

HTLV-1 and ATLL. Nakada et al. reported that 60% of 166 chronic

Strongyloides sterocoralis carriers were HTLV-1 seropositive compared

to only 20% of nearly 3000 controls consisting of persons not

carrying the worm at the time of the study (Nakada et al., 1983).

Denis Burkitt originally postulated that malaria caused Bukitt's

lymphoma by chronically activating B cells and depressing anti-EBV

immune responses (Burkitt, 1969). If true, one would expect less

lymphoma in Africans with sickle cell anemia since such individuals

resist malaria.

A survey of the literature reveals one study, published in 1970,

showing that Nigerians with the sickle cell trait were significantly

(P<0.03) less likely to develop Burkitt's lymphoma than persons with

wild type hemoglobin ( A, 1966).

Primates with SAIDS are also infected with parasites. According

published reports and to L. Blanchard, DVM Ph.D., Head

Veterinarian at the Tulane Regional Primate Research Center, all new

world and old world monkeys used in research, including those

currently used in AIDS research, are infected with several species of

intestinal protozoa including E. histolytica and Giardia (van Riper,

et al., 1966; JLB, personal communication).

Cattle with trypanosomes are significantly (P<0.001) more likely to

be infected with BLV, a virus related to HTLV-1, than non-parasitized

herds (Hare et al., 1970). Previously, in a USDA study, it was

observed that 100% of overtly leukemic cattle were trypanosomized

(Malmquist, 1965).

In contrast to pathogen-free experimental cats, nearly all outdoor

and feral cats carry parasites including Isospora felis, I. rivolta,

Dupylidium canium, Toxocara cati, Toxascaris leonina, Ancylostoma sp

and Toxoplasma gondii (Lin et al., 1990).

More recently, a group from the Colorado State University was able to

induce AIDS in cats raised and housed under pathogen-free conditions.

By infusing plasma pooled from cats with FIV infection, more than 50%

of recipient kittens developed AIDS by 6-12 weeks (Diehl, et al.,

1995). The model is reminiscent of transfusion cases of AIDS in

humans where allogeneic proteins may stimulate the immune system and

predispose to HIV infection and progression to AIDS.

These observations in cats, cattle, and mice merely reflect what

veterinarians have long known: animals with intestinal parasites are

much more susceptible to other infections, particularly viruses.

Confluence of Onchocerciasis and KS in Uganda

In 1966, and reported a closely defined

geographical confluence between KS and onchocerciasis (a filarial

parasite) in the Western Nile District of Uganda ( and

1966). In contrast, other tumors such as cervical and breast

cancers were present throughout the entire district which is heavily

populated. A second report on the distribution of onchocerciasis in

Africa confirms the existence of specific foci for the parasite as

reported by and (Oomen, 1969). It is possible that

black flies (Simuliidae) that are the insect vector for

onchocerciasis also transmits the viral agent of KS. However, HHV8,

the probable agent of KS is readily transmitted by sexual contact so

clearly an insect carrier is not obligatory for transmission. A more

likely scenario is that the immunosuppression caused by chronic

ochocerciasis allows for HHV8 expression just as all herpes viruses

express during periods of protracted immunosuppresion.

Based on the African Paradigm and Independent Risk Associated with

Anilingus, Parasites Explain the " Mystery " of KS in HIV-negative Gays

HIV seronegative gay men with only slightly depressed or normal

numbers of CD4 cells can develop KS (Chuck et al., 1996). The virus

that most likely causes KS, HHV8, is easily transmitted sexually

since up to 25% of random blood donors are seropositive for HHV8

(Lennette, et al., 1996). The KS virus apparently disseminated

through the homosexual community by sexual contact. However, in

several studies, anilingus ( " rimming " ), was found to be a strong and

independent risk factor for KS (Beral et al., 1992).

Anilingus is also the most important factor for the transmission of

intestinal parasites among adults in this country. It is certain,

given the high prevalence of parasites in the homosexual risk group,

that these HIV-negative patients with KS and reporting frequent oral-

anal contact were heavily parasitized.

Thus, KS and lymphomas both may be present in HIV negative gay men

immunosuppressed by parasites. Those more severely immunocompromised

by the CD4 depleting effects of HIV may have more aggressive tumors.

This appears to be the case as KS in HIV(-) patients runs a more

indolent course than in HIV(+) patients.

Parasites Explain the High Incidence of AIDS in Women in the Tropical

Areas Compared to Developed Countries

Parasitic infection may be a primary contributing factor to AIDS in

Africa where men and women alike are at risk (Quinn et al. 1987).

Parasites are also endemic in Belle Glade, Florida ( and Buster,

1983), Ethiopia (Bentwich et al., 1995), and among the indigenous

peoples of Papua New Guinea (Dwyer et al., 1997) and the Caribbean -

all risk groups for AIDS. Activation of T cells, macrophages and

other APC is necessary for HIV replication. This fact alone, may

explain why lymphotropic and monocyte-tropic viruses originated in

parasite endemic regions where suitable hosts reside. Indeed, HTLV-1,

HIV-1, HIV2, and EBV - all lymphotropic viruses - are all found in

close geographical relationship with parasite endemic regions (Tajima

et al., 1981, 1985; Merino et al.; Pearce, 1989; Burkitt, 1969).

Women, especially in the devloping countries of the world, are also

prone to harbor chronic vaginal infections such as trichomoniasis, or

have other predisposing vaginal factors for HIV.(van de Wijgert, et

al., 1996).

In 1982, the CDC and Several Clinical Researchers Recommended That

Physicians Treat " Non-pathogenic " Amebae in Gay Men

In 1982, the CDC issued a recommendation that asymptomatic intestinal

parasitic infections in persons " for whom anal-oral contact is a

sexual practice should be treated in accordance with recommendations

for symptomatic individuals " (CDC, 1982). With few exceptions, this

recommendation has not been followed.

Unfortunately, most physicians caring for homosexual patients are

unaware of the potential adverse consequences of chronic parasitism

on the course of HIV infection and their patients are often not being

provided with the option of treating these chronic infections. Since

the infections are often aysmptomatic in terms of gastrontestinal

criteria, infections often continue undiagnosed and untreated for

months and longer.

Safe Sex Guidelines Are Not Focused on Preventing Fecal Contamination

Although sexual behaviors in other areas have changed in response to

safer sex campaigns, the practice of rimming (anilingus) has not

diminished in recent years (Elford et al., 1992) nor is it adequately

addressed in safer sex guidelines. Although some safe sex guidelines

generally caution against oral-anal contact, the need to avoid fecal

contamination during foreplay and when removing condoms is not

emphasized.

Present-day gay erotic videos faithfully show condom use and

avoidance of semen ingestion, but rimming is frequently featured. Men

viewing these socially conscious videos may regard all activities

portrayed as " safe. "

Unfortunately, most gays are totally ignorant that they may be

infected with parasites or that many AIDS researchers consider them

possible cofactors for AIDS. The estimated 1/2 to 1 million HIV(+)

gay men in this country who are also infected with parasites, and

their physicians, ought to be informed that many leading researchers

consider parasite treatment a prudent course of action. Most

importantly, from a public health standpoint, studies of the possible

exacerbating role of parasites in AIDS need to be conducted.

Groups Without Activating Cofactors Appear to Have a Slower

Progression to AIDS

Approximately 20% of wives or sex partners of HIV(+) hemophiliacs or

HIV(+) transfusion recipients in this country have seroconverted to

HIV (Kim et al., 1988; Chorba et al., 1993; man et al., 1988),

but the incidence of AIDS in these " at risk " individuals is

remarkably low. This is in spite the probability that a sizeable

fraction of them may be misclassified and are actually a part of

other risk groups.

Low HIV infection and AIDS progression rates have been reported by

others for heterosexual partners of hemophiliacs (Kamradt, 1990). If

HIV alone were sufficient to cause disease, it is likely that a much

higher percentage of sexual partners of hemophiliacs should have

gotten AIDS by now.

Their progression rate may be low because they are one of a few

groups with HIV-1 but without chronic immune activation.

The Parasite Cofactor Theory has Support from Many Top AIDS

Researchers and has Appeared in Mainstream Journals Including

Science, Nature, The New England Journal of Medicine, The Lancet,

Immunology Today, and JAMA

The idea that parasites are possible cofactors for AIDS has been

expressed by many researchers in reputable journals (Fauci 1988,

1993 ; Lange et al., 1983; Bentwich et al., 1995; Quinn et al. 1987;

Stanley et al., 1996 ; Rene et al., 1984; Bergstrøm et al., 1986;

Pearce, 1983, 1984, 1986; Pearce and Abrams 1984, 1987; Krogstadt et

al., 1986; , 1990; Archer and Glinsman 1985, Piot et al., 1988).

However, neither the majority of gay men nor their physicians are

aware of the possible consequences of enteric infections. Most are

not even aware there is an epidemic of parasitic infections in gay

men! As reviewed here, there is much circumstantial and some direct

evidence to suggest that parasites are an important if not obligatory

factor in AIDS.

The diagnosis of parasites in asymptomatic or mildly symptomatic gay

men is rarely sought and, when parasites are disclosed, treatment for

non-pathological amebae is seldom offered. Indeed, some have argued

that because these parasites do not invade the bowel wall, they do

not need to be treated (Allason- E et al., 1986).

This argument has held sway among many public health officials and

clinicians for several years but it has been countered by

epidemiologists, immunologists, and retrovirologists. Parasites are

likely to continue to be transmitted as an STD among individuals at

risk for HIV until and unless studies show a direct and definitive

role for non-opportunistic parasites in AIDS or KS (if any).

Chronic Non-Opportunistic Parasitism as a Co-Factor for AIDS © 1997

Bowman Pearce rpearce@...

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