77 replies to this topic

[bobdrake12]

BobDrake, are you a computer?

Limitless,

While AI is a worthwhile gift, it should never be exploited by interfering with the "essence of being" in others.

bob

[Limitless]

I know Bob, I know, I know. I was joking with the computer reference. I guess I'm just bored. [sleep]

[Lazarus Long]

Bob,

I meant to get back to you sooner on this but I have had numerous comp problems and my new beast won't be in ver stables for another week. But while I have my old pony up again I wanted to thank you for your kind words before and say that personally I admit to feeling quixotic about having been able to provide a more accurate understanding of what occurred to your brother.

"Knowing the truth", will never remove the sorrow and pain of your personal but perhaps united with truth we can prevent such miscalculations for future generations. Your personal loss can never be recompensed in any way but if we can prevent the deaths of so many from been for "nothing". If we can seek justice not as revenge but as the amelioration of unjust conditions, then the loss of your brother may not been in vain, a statistic, and another personal tragedy lost in the maze of history.

The personal invective, zealous harangue, and ad homimen attacks of the last attempt to address this crucial issue are something I trust will not occur between us. I know you to be too focused on truth from your repeated demonstrations of rational behavior. I know us to be "brothers in arms" in this battle. Yes at times we will spar and practice our craft against each other, testing our mettle and honing our blades and skills but I know us to be on the same side of this issue and many others. I sincerely hope nothing I have ever said has ever been cause for personal offense and if it was I apologize.

Together let us try to set a standard for investigation so high that only those prepared to meet it are allowed to joust upon this field. Let all who read this understand that challenge, we do not battle each other but are together in a struggle against corruption, ignorance, and injustice.

I sense our mutual focus is clear and through our eyes and honorable actions, perhaps the haze and obscurity of this insane diatribe and demagoguery may be dissipated in favor of recognizable common cause.

[bobdrake12]

I sincerely hope nothing I have ever said has ever been cause for personal offense and if it was I apologize.

Lazarus Long,

I have been enjoying ND's winning streak to even think about personal offenses. )

What I do like to do at times is to take the "other side" in a discussion to learn more about the subject. Thus, my discussions are often made in a stone cold, factual manner even though on paper they may not appear to be made that way.

Yes, I do believe that AIDS is at least impacted (probably significantly) by the HIV virus. What I found odd was that so far I could find no significant scientific evidence presented that was convincing to strongly back up my basic belief. That one hurt because I may need to adjust my paradigm. [ph34r]

Since I represent the minority view on challenging that the HIV virus causes AIDS, I will continue to take that stand although I really don't believe that point of view at this time. :D

I trust that that this all makes perfectly good sense to you.

BTW, ND has a huge game against FSU this week. I have no idea which team is going to win that one. [?]

Common sense is what is learned prior to the age of 16. Thus, that paradigm at times should be challenged.

Perhaps, the way to view things is that we live in a type 0 civilization. If we lived a 1000 years ago, we could readily see the mistaken paradigms that were considered as fact. Perhaps, that condition might be the same if we came to this planet from a 1000 years into the future.

Best regards,

bob

[Lazarus Long]

Against the Odds, Firm Works on AIDS Vaccine
Sat Nov 16, 8:07 AM ET

By Maggie Fox, Health and Science Correspondent

WASHINGTON (Reuters) - Dr. Donald Francis is feeling combative these days.

His company, VaxGen, is about to find out whether what could prove to be the first-ever AIDS (news]News - web sites) vaccine actually works. Results from the trial, which started in June 1998, will be unveiled and analyzed early next year.

Hardly anyone thinks it will work.

AIDS vaccine experts have been cautioning for years that no one has come up with the right formula for fighting the AIDS virus, which has killed 25 million people around the world and which infects 40 million more.

At best, doctors now hope that one or more of the vaccines may simply help people to live a little longer with the virus, or perhaps to reduce the ease with which it is transmitted from person to person.

But Francis, a career vaccine specialist who helped wipe out smallpox in India and Bangladesh in the 1970s when he worked for the U.S. Centers for Disease Control and Prevention (news - web sites), has little patience with sniping from academic researchers.

VaxGen, he said, is testing a real vaccine on real people while university-based researchers do theoretical tests involving animals.

"The crime is not to lead the country. Put your money where your mouth is and go test it, for God's sake," Francis said in an interview. Having just turned 60, he feels he has earned the right to speak bluntly.


FIRST EFFORT

VaxGen's AIDSVAX vaccine is based on some of the earliest knowledge of HIV (news - web sites), the virus that causes AIDS. It is the only HIV vaccine currently in Phase III clinical trials -- the last step before a vaccine or drug maker can seek approval from the U.S. Food and Drug Administration (News - web sites).


About 30 other vaccines are in earlier stages of human testing.

Many vaccines use a live but weakened virus, or a "killed" virus, to stimulate the body's immune response. But this is considered to be to dangerous a thing to do with HIV, a retrovirus that integrates its genetic material right into the human immune system cells it infects.

AIDSVAX uses two proteins, based on the gp-120 protein found on the outside "envelope" of the virus. The hope is the body's immune system can become sensitized to anything carrying gp-120 and will mount a response to the virus.

VaxGen has immunized two-thirds of the 5,400 volunteers in its first Phase III trial -- 5,000 homosexual or bisexual men and 400 women considered to be at high risk of getting HIV.

They have been watched since 1998 to see who becomes infected with HIV. No one knows who got the real vaccine and who got a placebo shot, but this information will be "unblinded" early next year.

The hope is, clearly, that fewer vaccinated people will have developed HIV than those who got dummy jabs.

Francis said trials in chimpanzees showed it worked well.

He dismisses some of the newer vaccine approaches as "fad science" and doesn't buy the argument that HIV is a unique virus that will require a whole new vaccine approach.

"I'm confident from the chimpanzees that the vaccine will be efficacious. The question is, how efficacious," he said.

"If it's straightforward nothing, it's easy." But if the results show at least some protection, then the race will be on to find what the correlates of protection are -- something that can be measured in the blood that will show a patient is protected from the virus.

A correlate would be a big shortcut to what VaxGen has just had to do -- vaccinate thousands of people considered to be at high risk of getting infected, and then waiting several years to see how many become infected.

"Everybody who gets the vaccine has a good antibody response," Francis said. He hopes measurements of antibody levels will work as a correlate to show whether the vaccine is working.

Even if just 20 percent of those vaccinated are immune to becoming infected by HIV, Francis believes this could have an impact on the AIDS epidemic.

The volunteers who do become HIV infected and who got the vaccine will be followed for two years to see if the vaccine at least makes the virus grow more slowly in the body.

DIFFERENT VERSIONS OF VIRUS

HIV comes in various versions called A, B, C, D and E. Subtype B is found mostly in Europe, the Americas and Japan, while A, C, D and E are spreading in Africa and Asia.

This first version of AIDSVAX, tested in the United States, Canada and the Netherlands, works against the B subtype. A B/E subtype vaccine is being tested in Thailand in trials that will finish at the end of next year.

A big question, Francis said, is whether the vaccine will work across these subtypes, or whether a specific vaccine will have to be built for each subtype.

Because the HIV epidemic is worse in Africa than anywhere else, the hope is for a vaccine that will work in Africa. Francis said it is easy to get funding for a vaccine that can be sold in the United States and Europe. VaxGen's investors have been enthusiastic for this approach.

As for an African vaccine, "There's not support for it," Francis said. "We've been limping along with it, much to our dissatisfaction." Francis has asked the government and private groups like the Bill and Melinda Gates Foundation (news - web sites) for funding.

If it does work, then the real labor starts. VaxGen is a spinoff from biotech giant Genentech, which was originally going to gear up to make the vaccine if it worked. But Francis said Genentech is now too busy with its own products, which include the cancer drugs Herceptin and Rituxan.

"We are going to have to build a facility," Francis said.

They have made a deal with a group of South Korean investors and formed a joint venture called Celltrion, which has started work on facilities to make vaccines and other products in South San Francisco and in Inchon, South Korea (news - [url="http://rd.yahoo.com/dailynews/nm/sc_nm/inlinks/*http://rd.yahoo.com/DailyNews/manual/*http://search.yahoo.com/bin/search?cs=nw&p=South%20Korea"]web sites).

[Lazarus Long]

And for another side to the story:
LL

Dr. Clark Solves HIV/AIDS Mystery - Now there is an answer to HIV/AIDS. Read Dr. Clark's ...

Welcome to Dr. Hulda Clark's HIV/AIDS Page



Dear Visitor

You came here to find out more about Dr. Hulda Clark's approach to HIV and AIDS. Dr. Clark is the Researcher who claims: "AIDS can now be cured!"

I can imagine that the first things you are interested to know is

Who is Dr. Hulda Clark?
What are her findings about HIV and AIDS?
How have those findings been corroborated?
Who is Dr. Hulda Clark?

Dr. Hulda Clark is a researcher in the field of Alternative Medicine. You can find her CV here:
http://www.drclark.n...ilities/drc.htm

She has published five books, one of them on HIV/AIDS, which you can find here:
http://www.drclark.com

Dr. Hulda Clark has a clinic in Tijuana, Mexico, called Century Nutrition, where she treats mostly terminal cancer and AIDS patients. Many report miracle successes. Centruy Nutrition can be contacted at
P 01152-6646-828215
F 01152-6646-834454.

You can find more information on all aspects of Dr. Hulda Clark here:
http://www.drclark.net.
On this page you will also find a search engine where you can search our site for any other topic of interest to you.

Please also go to the home page http://www.drclark.net to sign up for the free e-zine and the free CD ROM.

What are Dr. Hulda Clark's findings about HIV and AIDS?

Excerpts from Dr. Hulda Clark's book "The Cure for HIV and AIDS" are found here:
http://www.drclark.n...v/hiv_frame.htm.

To understand her therapy, you will also find a lot of information and excerpts from her books here in the Info Section: http://www.drclark.net/info/info.htm, including a list of professionals who are working with her protocol.

Dr. Clark's work is based on bio-feedback testing (the Syncrometer™), with which she determines the ACTUAL CAUSES of HIV/AIDS and other health conditions. Knowing the cause will open the door to prevention and treatment. For this purpose Dr. Hulda Clark uses a large number of approaches in natural medicine, but ALL TARGETED AT THE EXACT CAUSE of the conditions.

If you are an AIDS dissident, you already know HIV is not the answer to AIDS. The view that the HIV virus "causes" AIDS is simplistic. If that was so then the patients taking the highly effective drugs against HIV should all be cured of AIDS. Would it not be logic that eliminating the cause would be a cure? But they are not cured. For more information on AIDS dissidents, refer to http://www.duesberg.com. However, Dr. Clark even though explaining HIV is not the cause of AIDS, does explain why there is a correlation between AIDS and HIV and how it comes about.

Dr. Clark shows that it is mainly toxins depressing production of white blood cells in the bone marrow and thymus gland, or directly killing white blood cells, that are responsible for AIDS. With her approach, so she claimes, she has been curing even most advanced AIDS patients.

For details about Dr. Clark's findings, consult her book "The Cure for HIV/AIDS". However be advised that this book was last updated in 1998 and a lot more work has been done in this field which will shortly be published in an updated version of the book. If you are in a hurry to get better, do not wait for the updated version. It might still be two months or more down the road. Rather, also get "The Cure for All Advanced Cancers", which has important chapters on immunity that you will need.

How have those findings been corroborated?

The best proof for Dr. Hulda Clark's theories is the fact that she has been able to recover even most advanced AIDS patients at her clinic. In 2000 she accepted a number of advanced AIDS patients in the course of a study which proved highly successful. Also, Dr. Clark has achieved a number of close to 20 CONSECUTIVE HIV cases that became HIV negative as confirmed by the lab with the state of the art PCR test -- with the exception of a couple of cases whose count was significantly lower but not negative yet. Some of these cases are described in the book "The Cure for HIV and AIDS".

Furthermore, Dr. Michael Biamonte, naturopath in Manhattan (139 Fulton St. #507 New York, NY. 10038, +1-212-587 2330) has published a study in 1998 using Dr. Clark's protocol with a number of patients. Although he did not fully follow the protocol, but additionally used colloidal silver and diet changes, 30 people became HIV negative as per PCR testing within 8-12 months.

Another small test has been done with three HIV positive individuals in Africa. After one months on only Dr. Hulda Clark's zapper and colloidal silver, the viral titer had dropped by half on average, it was significantly lower for all three individuals.

Finally, you may be interested in reading a well written paper, a comparison between AIDS and other diseases caused mainly by benzene toxicity (as claims Dr. Hulda Clark), put together by Dr. Stephen C. Byrnes here: http://www.sumeria.n...ds/lubejob.html

A final word

Having said all this, and considering that Dr. Clark's approach is low cost and safe, I find it warrants the use of this wonderful approach. But do not mistake Dr. Hulda Clark's claim that she has found the cause and cure of AIDS to mean that it is as simple as taking a pill. Dr. Clark's approach includes many steps, from a dental clean-up to diet changes to healthy living to herbs, electric stimulation and others. For advanced patients, it is a lot of work, and the success will depend on how carefully the program can be followed.

However, be aware that the person writing this (David P. Amrein) is not a medical doctor. Do not consider any of this medical advice. It is information which I feel anyone should have access to, but you will have to make your own evaluation of these facts. Please read our disclaimer here: http://www.drclark.n...disclaimer2.htm


--------------------------------------------------------------------------------

info@drclark.net
Last changes: 21 January 2002
©1999-2002 by Dr. Clark Research Association and David P. Amrein

[Lazarus Long]

This site deserves attention as well:

LL

http://www.ihv.org/





Our Mission
The Institute of Human Virology was established to create and develop a world-class center of excellence focusing on chronic viral diseases and virally linked cancers. The IHV is dedicated to the discovery, research, treatment and prevention of these diseases and cancers. Its unique structure seeks to connect cohesive, multidisciplinary research and clinical programs so that new treatments are streamlined from discovery to patient. The IHV serves patients locally and the scientific community globally.


Kidney Transplants Available To HIV-Positive Patients
more http://www.ihv.org/n...transplant.html

The Common Flu - or Bioterrorism?
more http://www.ihv.org/news/bioterror.html

Promising Multi-Strain HIV Vaccine Candidate
more http://www.ihv.org/n...ain_vaccine.htm


AIDS at 20: A Look Back, A Look Ahead with World-Renowned Scientist Dr. Robert Gallo more

Five-year Highlights more

IHV is a Center of UMBI (University of Maryland Biotechnology Institute

University of Maryland Medical School

University of Maryland Medical Center

[bobdrake12]

But do not mistake Dr. Hulda Clark's claim that she has found the cause and cure of AIDS to mean that it is as simple as taking a pill. Dr. Clark's approach includes many steps, from a dental clean-up to diet changes to healthy living to herbs, electric stimulation and others. For advanced patients, it is a lot of work, and the success will depend on how carefully the program can be followed.

Lazarus Long,

Thanks for the information.

bob

[Lazarus Long]

I think because of recent news and a subtle overlap of issues this article is appropriate:

Lessons for battle
Mon Mar 3,12:00 AM ET
Article & Links
BY JOANNIE FISCHER

As soon as news broke last week that the first AIDS vaccine to be widely tested in humans failed to prevent infection--except perhaps in a small group of racial minorities--there was lots of debate about whether to call the experiment a total flop or a partial success. Some AIDS experts hailed the vaccine as history's first case of human protection from the human immunodeficiency virus, which causes AIDS. Others dismissed the seemingly positive results as a statistical fluke. Investors fled VaxGen, the firm that developed the vaccine, called AIDSVAX. Some even accused the company of giving false hope to African-Americans by suggesting the vaccine might help them.

Lost in all the clamor is the fact that, regardless of the vaccine's commercial success or failure, the study yielded a wealth of vital information. The new data will guide AIDS research for years and, possibly, hasten an end to the plague that has claimed more than 20 million lives and takes an additional 8,000 each day.

Old and new. The gold mine of data exists in the form of billions of microscopic particles stored in 70,000 vials of blood serum from more than 5,000 study subjects. Those particles tell the story of how the rapidly mutating virus and the human body are now doing battle, and they may point to better ways to attack HIV (news - web sites).

Hundreds of study subjects contracted HIV, and their blood samples provide the first national catalog of the virus strains that are most successful at infecting the body. "HIV first enters the body as a swarm of many different forms of the virus," says Phillip Berman, the vaccine's inventor. "But one form outperforms all the others to invade the body's cells." The collection of recent infections may prove especially valuable because, until now, most samples of HIV used to design vaccines have come from those who are suffering from full-blown AIDS. But by the time AIDS is diagnosed, the virus may have mutated so many times that it bears little resemblance to the one that originally infected the patient. This could help explain why this and other vaccine candidates have not been more successful. Knowing the precise genetic makeup of the most invasive HIV would allow all vaccine researchers to design better weapons against it.

Having a collection of very recent HIV infections will also serve purposes unrelated to vaccine development, says Michael Para, an AIDS researcher at Ohio State College of Medicine. For example, by testing the new virus samples for resistance to various drugs, practitioners can get a better sense of how to treat new AIDS patients. That's important because the virus shows resistance to one or more drugs in 80 percent of AIDS patients. And because the study collected frequent blood samples from volunteers, scientists can go back to blood samples that were negative for HIV, taken just before infection was revealed, to see if more-sensitive tests can detect HIV earlier.

The National Institutes of Health is funding further study of the blood samples to see if people with certain genetic profiles may be more susceptible to the disease. By studying what are known as HLA antigens--a group of immune cells that differ with each individual's DNA--researchers can start to develop a picture of who may or may not respond to certain AIDS prevention measures or treatments. "The results may be similar to what we've found with hepatitis B vaccine," says Para. "No matter how many times you inoculated certain people, they were not protected from the disease, and they tended to share the same HLA profile." Those HLA profiles tend to correspond with certain racial and ethnic groups, which may explain why some groups fend off certain diseases better than others do.

Levels of safety. But the ultimate prize for AIDS researchers would be data known as the "correlates of immunity." This would be a simple way to show when someone is sufficiently protected from the disease. If the results showing a drastic decrease of infection in vaccinated African-Americans hold true, they may point toward this holy grail. Some 300 blacks were enrolled in the study; roughly 100 received a placebo, and about 200 received the vaccine. In the placebo group, nine people became infected with HIV. If the vaccine had no effect, the corresponding number should have been 18 infections in the vaccine group. Instead, the number was four, a 78 percent reduction in infection.

The numbers are "statistically significant"--that is, there is a less than 2 percent chance that they are a fluke. The number of infections is so small that VaxGen researchers are loath to make any bold claims right now. Yet there are some intriguing clues that the results may be useful in identifying some correlates of immunity. For example, the nonwhites who were vaccinated appear to have a higher level of certain antibodies (the body's defenses against HIV) than unvaccinated subjects. If those results bear out, it may be possible to quantify the antibody levels needed for protection.

Another intriguing finding is that the nonwhites who were not vaccinated tended to be infected with a particular form of the virus (the common "MN" variation that the vaccine was designed to fight). By contrast, those who were vaccinated but infected tended to be infected by different types of the virus, suggesting that the vaccine successfully shielded them from the MN variety. And initial data also suggest that the vaccinated people who were infected may have a stronger immune response to the virus. "If AIDS researchers find reliable ways to measure protection from HIV," says Don Francis, president of VaxGen, "then future vaccines could be tested using a sample of 20 or 50 instead of 5,000."

No matter what the final analysis yields, the study provides a major contribution to AIDS research simply by showing that a large-scale trial is possible, says Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (news - web sites). For two decades, researchers have debated whether it would be possible to recruit and retain enough people at high risk for HIV to get meaningful results. But this study is being universally praised as a flawless human vaccine trial. "It is a model for all future trials," says Fauci. "It's ridiculous that after 20 years of this epidemic, one pissant little company had to yell and scream to get the funds to test one single vaccine," says Francis, who failed to get federal funding and turned to private sources. "Now we've taken away all the excuses for not testing AIDS vaccines in humans." AIDSVAX may be a far cry from an effective vaccine, but experts say the study will go down in history as paving the way toward ultimate success.

[Lazarus Long]

I wrote the follownig to Mr. kissinger in a PM and after rflection I think it is appropriate to include in the discussion too.

My gut is leaning to the polio vaccine corruption as to why AIDS spread so fast. Ignorance was the enemy and true conspitator not the direct efforts of bioweapons projects of that period.

I am privvy to some info on this for reasons of proximity to research that went on then and from later study.

My father, as a pathologist worked for the Pentagon and was involved in the analysis of weapons efficacy during the Korean War and afterward worked as a freelance forensic pathologist for the Medical Examiner of the City of New York.

I may be a rogue but I recieved a royal education.

He did a necropsy on one case of a highly sexually active male adolescent in the late 1950's that died from complete immune system collapse and they couldn't determine the actual cause. The tissue samples from that case were subsequently analyzed during the mid 90's and tested positive for HIV.

So we shuold ask a different question perhaps: How did HIV get into the population here that early?

Also I can think of more than a few additional questions this "odd fact' implies.

But I will also say that there is a second piece of evidence that works against the conspiracy theorists, even though they DID work their nefarious games on IRT Subway Riders and Rhodesian Blacks, the fact is that they simply didn't yet have the theory and tools to make a single stranded DNA Virus do anything, they didn't yet understand that such things could even exist.

In reference to your rhetorical question about AIDS please understand that their are all kinds of diseases, which are not significantly pathogenic in one species that:

A: Are extremely damaging to a second species, incubate, or operate through and intermediary host species, Influenza being one of the most common examples.

B: Are not particularly virulent in the primary species but once exposed to a second species then mutate and acquire dangerous new virulent characteristics.

AIDS has a cousin we see in common feline distemper, it isn't even very different than Chicken Pox which as it turns out is a single stranded RNA virus. But when an examination of the monkey population is done we find the virus is prevalent in the natural world, what it doesn't explain is the cross species transmission.

Getting bit while hunting the animals, or butchering them is sufficient for a single infection but because of the unique transmission characteristics of AIDS. To serious epidemiologists it still doesn't adequately explain the vast number of infections globally, or the rate of infection that has blossomed out of Africa.

Something had to infect a vast population simultaneously, and that is why serious students of this keep coming back to the Polio Vaccine Program of UN WHO during the late 1950's.

They used captured native monkeys to incubate BOTH the Salk Vaccine which utilizes the "killed virus" as the means of transferring immunity to polio and the Sabbine vaccine which used attenuated " Live Virus".

The problem is that if HIV was present in some of these subject monkies then the methods used for making either polio vaccine at that time may not have "killed" the AIDS virus and instead turned the program to save millions of people into a kind of unguided stealth weapon that infected thousands of people with a sleeping killer.

http://www.chronicil...e/bensweet.html
If you read the article carefully it s NOT talking about AIDS but a very similar odd cancer that operates by parallel means of transmission to how AIDS does. Also understand please it isn't JUST Green Monkies.

http://www.whale.to/v/aids2.html

ABCNEWS.com : Test: No Proof of Polio in AIDS Origins - ... found no evidence to support the theory that an early version of the polio vaccine tested in the 1950s inadvertently triggered the AIDS epidemic, scientists ...
http://abcnews.go.co...ds_origins.html

Polio vaccines and the origin of AIDS - Key writings about the theory that AIDS developed from contaminated polio vaccines used in Africa in the late 1950s. Polio vaccines ...
http://www.uow.edu.a...documents/AIDS/

AIDS & polio vaccine connection - ... All these variables lead Oleske and other scientists to wonder if the polio/AIDS hypothesis can ever be proved, or disproved, or whether this view will linger ...
http://www.vaccinati...SPolioVax30.htm

I hope you enjoy your homework on this and that this letter, which I started as just a personal note to you, is sufficient after careful reading to be the start of a CIRA thread on the subject of AIDS. Please feel free to copy/paste it but the point is that there are still a lot of unanswered questions and hysterical speculation.

They WERE playing with Biological WMD's during this period (1950's through late 1980's) and so some people will never absolve them of at least complicity in the matter as some of these biological weapons were actually used in Africa like we see with the Mini Smallpox epidemic in Rhodesia that White separatists unleased on the black population and killed over 9000 people. But guilt by association is not sufficient to indict.

I hope this is helpful.

[Dmitri]

Interesting thread, I wanted to bump it and see if people here still have doubts about HIV causing AIDS.

I found the following article: I wanted to know why these scientists claim HIV fulfills koch's postulates while those who oppose the HIV theory claim it does not?


http://www.niaid.nih...ets/evidhiv.htm


HIV fulfills Koch's postulates as the cause of AIDS. Among many criteria used over the years to prove the link between putative pathogenic (disease-causing) agents and disease, perhaps the most-cited are Koch's postulates, developed in the late 19th century. Koch's postulates have been variously interpreted by many scientists, and modifications have been suggested to accommodate new technologies, particularly with regard to viruses (Harden. Pubbl Stn Zool Napoli [II] 1992;14:249; O'Brien, Goedert. Curr Opin Immunol 1996;8:613). However, the basic tenets remain the same, and for more than a century Koch's postulates, as listed below, have served as the litmus test for determining the cause of any epidemic disease:

• Epidemiological association: the suspected cause must be strongly associated with the disease.
• Isolation: the suspected pathogen can be isolated - and propagated - outside the host.
• Transmission pathogenesis: transfer of the suspected pathogen to an uninfected host, man or animal, produces the disease in that host.

With regard to postulate #1, numerous studies from around the world show that virtually all AIDS patients are HIV-seropositive; that is they carry antibodies that indicate HIV infection. With regard to postulate #2, modern culture techniques have allowed the isolation of HIV in virtually all AIDS patients, as well as in almost all HIV-seropositive individuals with both early- and late-stage disease. In addition, the polymerase chain (PCR) and other sophisticated molecular techniques have enabled researchers to document the presence of HIV genes in virtually all patients with AIDS, as well as in individuals in earlier stages of HIV disease.

Postulate #3 has been fulfilled in tragic incidents involving three laboratory workers with no other risk factors who have developed AIDS or severe immunosuppression after accidental exposure to concentrated, cloned HIV in the laboratory. In all three cases, HIV was isolated from the infected individual, sequenced and shown to be the infecting strain of virus. In another tragic incident, transmission of HIV from a Florida dentist to six patients has been documented by genetic analyses of virus isolated from both the dentist and the patients. The dentist and three of the patients developed AIDS and died, and at least one of the other patients has developed AIDS. Five of the patients had no HIV risk factors other than multiple visits to the dentist for invasive procedures (O'Brien, Goedert. Curr Opin Immunol 1996;8:613; O'Brien, 1997; Ciesielski et al. Ann Intern Med 1994;121:886).

In addition, through December 1999, the CDC had received reports of 56 health care workers in the United States with documented, occupationally acquired HIV infection, of whom 25 have developed AIDS in the absence of other risk factors. The development of AIDS following known HIV seroconversion also has been repeatedly observed in pediatric and adult blood transfusion cases, in mother-to-child transmission, and in studies of hemophilia, injection-drug use and sexual transmission in which seroconversion can be documented using serial blood samples (CDC. HIV AIDS Surveillance Report 1999;11[2]:1; AIDS Knowledge Base, 1999). For example, in a 10-year study in the Netherlands, researchers followed 11 children who had become infected with HIV as neonates by small aliquots of plasma from a single HIV-infected donor. During the 10-year period, eight of the children died of AIDS. Of the remaining three children, all showed a progressive decline in cellular immunity, and two of the three had symptoms probably related to HIV infection (van den Berg et al. Acta Paediatr 1994;83:17).

Koch's postulates also have been fulfilled in animal models of human AIDS. Chimpanzees experimentally infected with HIV have developed severe immunosuppression and AIDS. In severe combined immunodeficiency (SCID) mice given a human immune system, HIV produces similar patterns of cell killing and pathogenesis as seen in people. HIV-2, a less virulent variant of HIV which causes AIDS in people, also causes an AIDS-like syndrome in baboons. More than a dozen strains of simian immunodeficiency virus (SIV), a close cousin of HIV, cause AIDS in Asian macaques. In addition, chimeric viruses known as SHIVs, which contain an SIV backbone with various HIV genes in place of the corresponding SIV genes, cause AIDS in macaques. Further strengthening the association of these viruses with AIDS, researchers have shown that SIV/SHIVs isolated from animals with AIDS cause AIDS when transmitted to uninfected animals (O'Neil et al. J Infect Dis 2000;182:1051; Aldrovandi et al. Nature 1993;363:732; Liska et al. AIDS Res Hum Retroviruses 1999;15:445; Locher et al. Arch Pathol Lab Med 1998;22:523; Hirsch et al. Virus Res 1994;32:183; Joag et al. J Virol 1996;70:3189).

AIDS and HIV infection are invariably linked in time, place and population group.

Historically, the occurence of AIDS in human populations around the world has closely followed the appearance of HIV. In the United States, the first cases of AIDS were reported in 1981 among homosexual men in New York and California, and retrospective examination of frozen blood samples from a U.S. cohort of gay men showed the presence of HIV antibodies as early as 1978, but not before then. Subsequently, in every region, country and city where AIDS has appeared, evidence of HIV infection has preceded AIDS by just a few years (CDC. MMWR 1981;30:250; CDC. MMWR 1981;30:305; Jaffe et al. Ann Intern Med 1985;103:210; U.S. Census Bureau; UNAIDS).

Many studies agree that only a single factor, HIV, predicts whether a person will develop AIDS.

Other viral infections, bacterial infections, sexual behavior patterns and drug abuse patterns do not predict who develops AIDS. Individuals from diverse backgrounds, including heterosexual men and women, homosexual men and women, hemophiliacs, sexual partners of hemophiliacs and transfusion recipients, injection-drug users and infants have all developed AIDS, with the only common denominator being their infection with HIV (NIAID, 1995).

In cohort studies, severe immunosuppression and AIDS-defining illnesses occur almost exclusively in individuals who are HIV-infected.

For example, analysis of data from more than 8,000 participants in the Multicenter AIDS Cohort Study (MACS) and the Women's Interagency HIV Study (WIHS) demonstrated that participants who were HIV-seropositive were 1,100 times more likely to develop an AIDS-associated illness than those who were HIV-seronegative. These overwhelming odds provide a clarity of association that is unusual in medical research.

In a Canadian cohort, investigators followed 715 homosexual men for a median of 8.6 years. Every case of AIDS in this cohort occurred in individuals who were HIV-seropositive. No AIDS-defining illnesses occurred in men who remained negative for HIV antibodies, despite the fact that these individuals had appreciable patterns of illicit drug use and receptive anal intercourse (Schechter et al. Lancet 1993;341:658).

Before the appearance of HIV, AIDS-related diseases such as PCP, KS and MAC were rare in developed countries; today, they are common in HIV-infected individuals.

Prior to the appearance of HIV, AIDS-related conditions such as Pneumocystis carinii pneumonia (PCP), Kaposi's sarcoma (KS) and disseminated infection with the Mycobacterium avium complex (MAC) were extraordinarily rare in the United States. In a 1967 survey, only 107 cases of PCP in the United States had been described in the medical literature, virtually all among individuals with underlying immunosuppressive conditions. Before the AIDS epidemic, the annual incidence of Kaposi's sarcoma in the United States was only 0.2 to 0.6 cases per million population, and only 32 individuals with disseminated MAC disease had been described in the medical literature (Safai. Ann NY Acad Sci 1984;437:373; Le Clair. Am Rev Respir Dis 1969;99:542; Masur. JAMA 1982;248:3013).

By the end of 1999, CDC had received reports of 166,368 HIV-infected patients in the United States with definitive diagnoses of PCP, 46,684 with definitive diagnoses of KS, and 41,873 with definitive diagnoses of disseminated MAC (personal communication).

In developing countries, patterns of both rare and endemic diseases have changed dramatically as HIV has spread, with a far greater toll now being exacted among the young and middle-aged, including well-educated members of the middle class.

In developing countries, the emergence of the HIV epidemic has dramatically changed patterns of disease in affected communities. As in developed countries, previously rare, "opportunistic" diseases such as PCP and certain forms of meningitis have become more commonplace. In addition, as HIV seroprevalence rates have risen, there have been significant increases in the burden of endemic conditions such as tuberculosis (TB), particularly among young people. For example, as HIV seroprevalence increased sharply in Blantyre, Malawi from 1986 to 1995, tuberculosis admissions at the city's main hospital rose more than 400 percent, with the largest increase in cases among children and young adults. In the rural Hlabisa District of South Africa, admissions to tuberculosis wards increased 360 percent from 1992 to 1998, concomitant with a steep rise in HIV seroprevalence. High rates of mortality due to endemic conditions such as TB, diarrheal diseases and wasting syndromes, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people in many developing countries (UNAIDS, 2000; Harries et al. Int J Tuberc Lung Dis 1997;1:346; Floyd et al. JAMA 1999;282:1087).

In studies conducted in both developing and developed countries, death rates are markedly higher among HIV-seropositive individuals than among HIV-seronegative individuals.

For example, Nunn and colleagues (BMJ 1997;315:767) assessed the impact of HIV infection over five years in a rural population in the Masaka District of Uganda. Among 8,833 individuals of all ages who had an unambiguous result on testing for HIV-antibodies (either 2 or 3 different test kits were used for blood samples from each individual), HIV-seropositive people were 16 times more likely to die over five years than HIV-seronegative people (see table). Among individuals ages 25 to 34, HIV-seropositive people were 27 times more likely to die than HIV-seronegative people.



In another study in Uganda, 19,983 adults in the rural Rakai District were followed for 10 to 30 months (Sewankambo et al. AIDS 2000;14:2391). In this cohort, HIV-seropositive people were 20 times more likely to die than HIV-seronegative people during 31,432 person-years of observation. Similar findings have emerged from other studies (Boerma et al. AIDS 1998;12(suppl 1):S3); for example,

• in Tanzania, HIV-seropositive people were 12.9 time more likely to die over two years than HIV-seronegative people (Borgdorff et al. Genitourin Med 1995;71:212)
• in Malawi, mortality over three years among children who survived the first year of life was 9.5 times higher among HIV-seropositive children than among HIV-seronegative children (Taha et al. Pediatr Infect Dis J 1999;18:689)
• in Rwanda, mortality was 21 times higher for HIV-seropositive children than for HIV-seronegative children after five years (Spira et al. Pediatrics 1999;14:e56). Among the mothers of these children, mortality was 9 times higher among HIV-seropositive women than among HIV-seronegative women in four years of follow-up (Leroy et al. J Acquir Immune Defic Syndr Hum Retrovirol 1995;9:415).
• in Cote d'Ivoire, HIV-seropositive individuals with pulmonary tuberculosis (TB) were 17 times more likely to die within six months than HIV-seronegative individuals with pulmonary TB (Ackah et al. Lancet 1995; 345:607).
• in the former Zaire (now the Democratic Republic of Congo), HIV-infected infants were 11 times more likely to die from diarrhea than uninfected infants (Thea et al. NEJM 1993;329:1696).
• in South Africa, the death rate for children hospitalized with severe lower respiratory tract infections was 6.5 times higher for HIV-infected infants than for uninfected children (Madhi et al. Clin Infect Dis 2000;31:170).

Kilmarx and colleagues (Lancet 2000; 356:770) recently reported data on HIV infection and mortality in a cohort of female commercial sex workers in Chiang Rai, Thailand. Among 500 women enrolled in the study between 1991 and 1994, the mortality rate through October 1998 among women who were HIV-infected at enrollment (59 deaths among 160 HIV-infected women) was 52.7 times higher than among women who remained uninfected with HIV (2 deaths among 306 uninfected women). The mortality rate among women who became infected during the study (7 deaths among 34 seroconverting women) was 22.5 higher than among persistently uninfected women. Among the HIV-infected women, only 3 of whom received antiretroviral medications, all reported causes of death were associated with immunosuppression, whereas the reported causes of death of the two uninfected women were postpartum amniotic embolism and gunshot wound.

Excess mortality among HIV-seropositive people also has been repeatedly observed in studies in developed countries, perhaps most dramatically among hemophiliacs. For example, Darby et al. (Nature 1995;377:79) studied 6,278 hemophiliacs living in the United Kingdom during the period 1977-91. Among 2,448 individuals with severe hemophilia, the annual death rate was stable at 8 per 1,000 during 1977-84. While death rates remained stable at 8 per 1,000 from 1985-1992 among HIV-seronegative persons with severe hemophilia, deaths rose steeply among those who had become HIV-seropositive following HIV-tainted transfusions during 1979-1986, reaching 81 per 1,000 in 1991-92. Among 3,830 individuals with mild or moderate hemophilia, the pattern was similar, with an initial death rate of 4 per 1,000 in 1977-84 that remained stable among HIV-seronegative individuals but rose to 85 per 1,000 in 1991-92 among seropositive individuals.

Similar data have emerged from the Multicenter Hemophilia Cohort Study. Among 1,028 hemophiliacs followed for a median of 10.3 years, HIV-infected individuals (n=321) were 11 times more likely to die than HIV-negative subjects (n=707), with the dose of Factor VIII having no effect on survival in either group (Goedert. Lancet 1995;346:1425).

In the Multicenter AIDS Cohort Study (MACS), a 16-year study of 5,622 homosexual and bisexual men, 1,668 of 2,761 HIV-seropositive men have died (60 percent), 1,547 after a diagnosis of AIDS. In contrast, among 2,861 HIV-seronegative participants, only 66 men (2.3 percent) have died (A. Munoz, MACS, personal communication).

HIV can be detected in virtually everyone with AIDS.

Recently developed sensitive testing methods, including the polymerase chain reaction (PCR) and improved culture techniques, have enabled researchers to find HIV in patients with AIDS with few exceptions. HIV has been repeatedly isolated from the blood, semen and vaginal secretions of patients with AIDS, findings consistent with the epidemiologic data demonstrating AIDS transmission via sexual activity and contact with infected blood (Hammer et al. J Clin Microbiol 1993;31:2557; Jackson et al. J Clin Microbiol 1990;28:16).

Numerous studies of HIV-infected people have shown that high levels of infectious HIV, viral antigens, and HIV nucleic acids (DNA and RNA) in the body predict immune system deterioration and an increased risk for developing AIDS. Conversely, patients with low levels of virus have a much lower risk of developing AIDS.

For example, in an anlysis of 1,604 HIV-infected men in the Multicenter AIDS Cohort Study (MACS), the risk of a patient developing AIDS with six years was strongly associated with levels of HIV RNA in the plasma as measured by a sensitive test known as the branched-DNA signal-amplification assay (bDNA):

Plasma RNA concentration
(copies/mL of blood) Proportion of patients
developing AIDS within six years <500
501 - 3,000
3,001 - 10,000
10,001 - 30,000
>30,000 5.4%
16.6%
31.7%
55.2%
80.0%

(Source: Mellors et al. Ann Intern Med 1997;126:946)

Similar associations between increasing HIV RNA levels and a greater risk of disease progression have been observed in HIV-infected children in both developed and developing countries (Palumbo et al. JAMA 1998;279:756; Taha et al. AIDS 2000;14:453).

In the very small proportion of untreated HIV-infected individuals whose disease progresses very slowly, the amount of HIV in the blood and lymph nodes is significantly lower than in HIV-infected people whose disease progression is more typical (Pantaleo et al. NEJM 1995;332:209; Cao et al. NEJM 1995;332:201; Barker et al. Blood 1998;92:3105).

The availability of potent combinations of drugs that specifically block HIV replication has dramatically improved the prognosis for HIV-infected individuals. Such an effect would not be seen if HIV did not have a central role in causing AIDS.

Clinical trials have shown that potent three-drug combinations of anti-HIV drugs, known as highly active antiretroviral therapy (HAART), can significantly reduce the incidence of AIDS and death among HIV-infected individuals as compared to previously available HIV treatment regimens (Hammer et al. NEJM 1997;337:725; Cameron et al. Lancet 1998;351:543).

Use of these potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, among both adults and children (Figure 1; CDC. HIV AIDS Surveillance Report 1999;11[2]:1; Palella et al. NEJM 1998;338:853; Mocroft et al. Lancet 1998;352:1725; Mocroft et al. Lancet 2000;356:291; Vittinghoff et al. J Infect Dis 1999;179:717; Detels et al. JAMA 1998;280:1497; de Martino et al. JAMA 2000;284:190; CASCADE Collaboration. Lancet 2000;355:1158; Hogg et al. CMAJ 1999;160:659; Schwarcz et al. Am J Epidemiol 2000;152:178; Kaplan et al. Clin Infect Dis 2000;30:S5; McNaghten et al. AIDS 1999;13:1687;).

For example, in a prospective study of more than 7,300 HIV-infected patients in 52 European outpatient clinics, the incidence of new AIDS-defining illnesses declined from 30.7 per 100 patient-years of observation in 1994 (before the availability of HAART) to 2.5 per 100 patient years in 1998, when the majority of patients received HAART (Mocroft et al. Lancet 2000;356:291).

Among HIV-infected patients who receive anti-HIV therapy, those whose viral loads are driven to low levels are much less likely to develop AIDS or die than patients who do not respond to therapy. Such an effect would not be seen if HIV did not have a central role in causing AIDS.

Clinical trials in both HIV-infected children and adults have demonstrated a link between a good virologic response to therapy (i.e. much less virus in the body) and a reduced risk of developing AIDS or dying (Montaner et al. AIDS 1998;12:F23; Palumbo et al. JAMA 1998;279:756; O'Brien et al. NEJM 1996;334:426; Katzenstein et al. NEJM 1996;335:1091; Marschner et al. J Infect Dis 1998;177:40; Hammer et al. NEJM 1997;337:725; Cameron et al. Lancet 1998;351:543).

This effect has also been seen in routine clinical practice. For example, in an analysis of 2,674 HIV-infected patients who started highly active antiretroviral therapy (HAART) in 1995-1998, 6.6 percent of patients who achieved and maintained undetectable viral loads (<400 copies/mL of blood) developed AIDS or died within 30 months, compared with 20.1 percent of patients who never achieved undetectable concentrations (Ledergerber et al. Lancet 1999;353:863).



Nearly everyone with AIDS has antibodies to HIV. A survey of 230,179 AIDS patients in the United States revealed only 299 HIV-seronegative individuals. An evaluation of 172 of these 299 patients found 131 actually to be seropositive; an additional 34 died before their serostatus could be confirmed (Smith et al. N Engl J Med 1993;328:373).

Numerous serosurveys show that AIDS is common in populations where many individuals have HIV antibodies. Conversely, in populations with low seroprevalence of HIV antibodies, AIDS is extremely rare.

For example, in the southern African country of Zimbabwe (population 11.4 million), more than 25 percent of adults ages 15 to 49 are estimated to be HIV antibody-positive, based on numerous studies. As of November 1999, more than 74,000 cases of AIDS in Zimbabwe had been reported to the World Health Organization (WHO). In contrast, Madagascar, an island country off the southeast coast of Africa (population 15.1 million) with a very low HIV seroprevalence rate, reported only 37 cases of AIDS to WHO through November 1999. Yet, other sexually transmitted diseases, notably syphilis, are common in Madagascar, suggesting that conditions are ripe for the spread of HIV and AIDS if the virus becomes entrenched in that country (U.S. Census Bureau; UNAIDS, 2000; WHO. Wkly Epidemiol Rec 1999;74:1; Behets et al. Lancet 1996;347:831).

The specific immunologic profile that typifies AIDS - a persistently low CD4+ T-cell count - is extraordinarily rare in the absence of HIV infection or other known cause of immunosuppression.

For example, in the NIAID-supported Multicenter AIDS Cohort Study (MACS), 22,643 CD4+ T-cell determinations in 2,713 HIV-seronegative homosexual and bisexual men revealed only one individual with a CD4+ T-cell count persistently lower than 300 cells/mm³ of blood, and this individual was receiving immunosuppressive therapy. Similar results have been reported from other studies (Vermund et al. NEJM 1993;328:442; NIAID, 1995).

Newborn infants have no behavioral risk factors for AIDS, yet many children born to HIV-infected mothers have developed AIDS and died.

Only newborns who become HIV-infected before or during birth, during breastfeeding, or (rarely) following exposure to HIV-tainted blood or blood products after birth, go on to develop the profound immunosuppression that leads to AIDS. Babies who are not HIV-infected do not develop AIDS. In the United States, 8,718 cases of AIDS among children younger than age 13 had been reported to the CDC as of December 31, 1999. Cumulative U.S. AIDS deaths among individuals younger than age 15 numbered 5,044 through December 31, 1999. Globally, UNAIDS estimates that 480,000 child deaths due to AIDS occurred in 1999 alone (CDC. HIV/AIDS Surveillance Report 1999;11[2]:1; UNAIDS. AIDS epidemic update: June 2000).

Because many HIV-infected mothers abuse recreational drugs, some have argued that maternal drug use itself causes pediatric AIDS. However, studies have consistently shown that babies who are not HIV-infected do not develop AIDS, regardless of their mothers' drug use (European Collaborative Study. Lancet 1991;337:253; European Collaborative Study. Pediatr Infect Dis J 1997;16:1151; Abrams et al. Pediatrics 1995;96:451).

For example, a majority of the HIV-infected, pregnant women enrolled in the European Collaborative Study are current or former injection drug users. In this ongoing study, mothers and their babies are followed from birth in 10 centers in Europe. In a paper in Lancet, study investigators reported that none of 343 HIV-seronegative children born to HIV-seropositive mothers had developed AIDS or persistent immune deficiency. In contrast, among 64 seropositive children, 30 percent presented with AIDS within 6 months of age or with oral candidiasis followed rapidly by the onset of AIDS. By their first birthday, 17 percent died of HIV-related diseases (European Collaborative Study. Lancet 1991;337:253).



In a study in New York, investigators followed 84 HIV-infected and 248 HIV-uninfected infants, all born to HIV-seropositive mothers. The mothers of the two groups of infants were equally likely to be injection drug users (47 percent vs. 50 percent), and had similar rates of alcohol, tobacco, cocaine, heroin and methadone use. Of the 84 HIV-infected children, 22 died during a median follow-up period of 27.6 months, including 20 infants who died before their second birthday. Twenty-one of these deaths were classified as AIDS-related. Among the 248 uninfected children, only one death (due to child abuse) was reported during a median follow-up period of 26.1 months (Abrams et al. Pediatrics 1995;96:451). The HIV-infected twin develops AIDS while the uninfected twin does not.

Because twins share an in utero environment and genetic relationships, similarities and differences between them can provide important insight into infectious diseases, including AIDS (Goedert. Acta Paediatr Supp 1997;421:56). Researchers have documented cases of HIV-infected mothers who have given birth to twins, one of whom is HIV-infected and the other not. The HIV-infected children developed AIDS, while the other children remained clinically and immunologically normal (Park et al. J Clin Microbiol 1987;25:1119; Menez-Bautista et al. Am J Dis Child 1986;140:678; Thomas et al. Pediatrics 1990;86:774; Young et al. Pediatr Infect Dis J 1990;9:454; Barlow and Mok. Arch Dis Child 1993;68:507; Guerrero Vazquez et al. An Esp Pediatr 1993;39:445).



Studies of transfusion-acquired AIDS cases have repeatedly led to the discovery of HIV in the patient as well as in the blood donor. Numerous studies have shown an almost perfect correlation between the occurrence of AIDS in a blood recipient and donor, and evidence of homologous HIV strains in both the recipient and the donor (NIAID, 1995).

HIV is similar in genetic structure and morphology to other lentiviruses that often cause immunodeficiency in their animal hosts in addition to slow, progressive wasting disorders, neurodegeneration and death.

Like HIV in humans, animal viruses such as feline immunodeficiency virus (FIV) in cats, visna virus in sheep and simian immunodeficiency virus (SIV) in monkeys primarily infect cells of the immune system such as T cells and macrophages. For example, visna virus infects macrophages and causes a slowly progressive neurologic disease (Haase. Nature 1986;322:130).

HIV causes the death and dysfunction of CD4+ T lymphocytes in vitro and in vivo.

CD4+ T cell dysfunction and depletion are hallmarks of HIV disease. The recognition that HIV infects and destroys CD4+ T cells in vitro strongly suggests a direct link between HIV infection, CD4+ T cell depletion, and development of AIDS. A variety of mechanisms, both directly and indirectly related to HIV infection of CD4+ T cells, are likely responsible for the defects in CD4+ T cell function observed in HIV-infected people. Not only can HIV enter and kill CD4+ T cells directly, but several HIV gene products may interfere with the function of uninfected cells (NIAID, 1995; Pantaleo et al. NEJM 1993;328:327).

<H4 align=center>ANSWERING THE SKEPTICS:
RESPONSES TO ARGUMENTS THAT HIV DOES NOT CAUSE AIDS</H4>MYTH: HIV antibody testing is unreliable. FACT: Diagnosis of infection using antibody testing is one of the best-established concepts in medicine. HIV antibody tests exceed the performance of most other infectious disease tests in both sensitivity (the ability of the screening test to give a positive finding when the person tested truly has the disease ) and specificity (the ability of the test to give a negative finding when the subjects tested are free of the disease under study). Current HIV antibody tests have sensitivity and specificity in excess of 98% and are therefore extremely reliable WHO, 1998; Sloand et al. JAMA 1991;266:2861).

Progress in testing methodology has also enabled detection of viral genetic material, antigens and the virus itself in body fluids and cells. While not widely used for routine testing due to high cost and requirements in laboratory equipment, these direct testing techniques have confirmed the validity of the antibody tests (Jackson et al. J Clin Microbiol 1990;28:16; Busch et al. NEJM 1991;325:1; Silvester et al. J Acquir Immune Defic Syndr Hum Retrovirol 1995;8:411; Urassa et al. J Clin Virol 1999;14:25; Nkengasong et al. AIDS 1999;13:109; Samdal et al. Clin Diagn Virol 1996;7:55.

MYTH: There is no AIDS in Africa. AIDS is nothing more than a new name for old diseases.

FACT: The diseases that have come to be associated with AIDS in Africa - such as wasting syndrome, diarrheal diseases and TB - have long been severe burdens there. However, high rates of mortality from these diseases, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people, including well-educated members of the middle class (UNAIDS, 2000).

For example, in a study in Cote d'Ivoire, HIV-seropositive individuals with pulmonary tuberculosis (TB) were 17 times more likely to die within six months than HIV-seronegative individuals with pulmonary TB (Ackah et al. Lancet 1995; 345:607). In Malawi, mortality over three years among children who had received recommended childhood immunizations and who survived the first year of life was 9.5 times higher among HIV-seropositive children than among HIV-seronegative children. The leading causes of death were wasting and respiratory conditions (Taha et al. Pediatr Infect Dis J 1999;18:689). Elsewhere in Africa, findings are similar.

MYTH: HIV cannot be the cause of AIDS because researchers are unable to explain precisely how HIV destroys the immune system.

FACT: A great deal is known about the pathogenesis of HIV disease, even though important details remain to be elucidated. However, a complete understanding of the pathogenesis of a disease is not a prerequisite to knowing its cause. Most infectious agents have been associated with the disease they cause long before their pathogenic mechanisms have been discovered. Because research in pathogenesis is difficult when precise animal models are unavailable, the disease-causing mechanisms in many diseases, including tuberculosis and hepatitis B, are poorly understood. The critics' reasoning would lead to the conclusion that M. tuberculosis is not the cause of tuberculosis or that hepatitis B virus is not a cause of liver disease (Evans. Yale J Biol Med 1982;55:193).

MYTH: AZT and other antiretroviral drugs, not HIV, cause AIDS.

FACT: The vast majority of people with AIDS never received antiretroviral drugs, including those in developed countries prior to the licensure of AZT in 1987, and people in developing countries today where very few individuals have access to these medications (UNAIDS, 2000).

As with medications for any serious diseases, antiretroviral drugs can have toxic side effects. However, there is no evidence that antiretroviral drugs cause the severe immunosuppression that typifies AIDS, and abundant evidence that antiretroviral therapy, when used according to established guidelines, can improve the length and quality of life of HIV-infected individuals.

In the 1980s, clinical trials enrolling patients with AIDS found that AZT given as single-drug therapy conferred a modest (and short-lived) survival advantage compared to placebo. Among HIV-infected patients who had not yet developed AIDS, placebo-controlled trials found that AZT given as single-drug therapy delayed, for a year or two, the onset of AIDS-related illnesses. Significantly, long-term follow-up of these trials did not show a prolonged benefit of AZT, but also never indicated that the drug increased disease progression or mortality. The lack of excess AIDS cases and death in the AZT arms of these placebo-controlled trials effectively counters the argument that AZT causes AIDS (NIAID, 1995).

Subsequent clinical trials found that patients receiving two-drug combinations had up to 50 percent increases in time to progression to AIDS and in survival when compared to people receiving single-drug therapy. In more recent years, three-drug combination therapies have produced another 50 percent to 80 percent improvements in progression to AIDS and in survival when compared to two-drug regimens in clinical trials. Use of potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, an effect which clearly would not be seen if antiretroviral drugs caused AIDS (Figure 1; CDC. HIV AIDS Surveillance Report 1999;11[2]:1; Palella et al. NEJM 1998;338:853; Mocroft et al. Lancet 1998;352:1725; Mocroft et al. Lancet 2000;356:291; Vittinghoff et al. J Infect Dis 1999;179:717; Detels et al. JAMA 1998;280:1497; de Martino et al. JAMA 2000;284:190; CASCADE Collaboration. Lancet 2000;355:1158; Hogg et al. CMAJ 1999;160:659; Schwarcz et al. Am J Epidemiol 2000;152:178; Kaplan et al. Clin Infect Dis 2000;30:S5; McNaghten et al. AIDS 1999;13:1687).



MYTH: Behavioral factors such as recreational drug use and multiple sexual partners account for AIDS. FACT: The proposed behavioral causes of AIDS, such as multiple sexual partners and long-term recreational drug use, have existed for many years. The epidemic of AIDS, characterized by the occurrence of formerly rare opportunistic infections such as Pneumocystis carinii pneumonia (PCP) did not occur in the United States until a previously unknown human retrovirus - HIV - spread through certain communities (NIAID, 1995a; NIAID, 1995b).

Compelling evidence against the hypothesis that behavioral factors cause AIDS comes from recent studies that have followed cohorts of homosexual men for long periods of time and found that only HIV-seropositive men develop AIDS.

For example, in a prospectively studied cohort in Vancouver, 715 homosexual men were followed for a median of 8.6 years. Among 365 HIV-positive individuals, 136 developed AIDS. No AIDS-defining illnesses occurred among 350 seronegative men despite the fact that these men reported appreciable use of inhalable nitrites ("poppers") and other recreational drugs, and frequent receptive anal intercourse (Schechter et al. Lancet 1993;341:658).

Other studies show that among homosexual men and injection-drug users, the specific immune deficit that leads to AIDS - a progressive and sustained loss of CD4+ T cells - is extremely rare in the absence of other immunosuppressive conditions. For example, in the Multicenter AIDS Cohort Study, more than 22,000 T-cell determinations in 2,713 HIV-seronegative homosexual men revealed only one individual with a CD4+ T-cell count persistently lower than 300 cells/mm³ of blood, and this individual was receiving immunosuppressive therapy (Vermund et al. NEJM 1993;328:442).

In a survey of 229 HIV-seronegative injection-drug users in New York City, mean CD4+ T-cell counts of the group were consistently more than 1000 cells/mm³ of blood. Only two individuals had two CD4+ T-cell measurements of less than 300/mm³ of blood, one of whom died with cardiac disease and non-Hodgkin's lymphoma listed as the cause of death (Des Jarlais et al. J Acquir Immune Defic Syndr 1993;6:820).

MYTH: AIDS among transfusion recipients is due to underlying diseases that necessitated the transfusion, rather than to HIV.

FACT: This notion is contradicted by a report by the Transfusion Safety Study Group (TSSG), which compared HIV-negative and HIV-positive blood recipients who had been given transfusions for similar diseases. Approximately 3 years after the transfusion, the mean CD4+ T-cell count in 64 HIV-negative recipients was 850/mm³ of blood, while 111 HIV-seropositive individuals had average CD4+ T-cell counts of 375/mm³ of blood. By 1993, there were 37 cases of AIDS in the HIV-infected group, but not a single AIDS-defining illness in the HIV-seronegative transfusion recipients (Donegan et al. Ann Intern Med 1990;113:733; Cohen. Science 1994;266:1645).



MYTH: High usage of clotting factor concentrate, not HIV, leads to CD4+ T-cell depletion and AIDS in hemophiliacs. FACT: This view is contradicted by many studies. For example, among HIV-seronegative patients with hemophilia A enrolled in the Transfusion Safety Study, no significant differences in CD4+ T-cell counts were noted between 79 patients with no or minimal factor treatment and 52 with the largest amount of lifetime treatments. Patients in both groups had CD4+ T cell-counts within the normal range (Hasset et al. Blood 1993;82:1351). In another report from the Transfusion Safety Study, no instances of AIDS-defining illnesses were seen among 402 HIV-seronegative hemophiliacs who had received factor therapy (Aledort et al. NEJM 1993;328:1128).

In a cohort in the United Kingdom, researchers matched 17 HIV-seropositive hemophiliacs with 17 HIV-seronegative hemophiliacs with regard to clotting factor concentrate usage over a ten-year period. During this time, 16 AIDS-defining clinical events occurred in 9 patients, all of whom were HIV-seropositive. No AIDS-defining illnesses occurred among the HIV-negative patients. In each pair, the mean CD4+ T cell count during follow-up was, on average, 500 cells/mm³ lower in the HIV-seropositive patient (Sabin et al. BMJ 1996;312:207).

Among HIV-infected hemophiliacs, Transfusion Safety Study investigators found that neither the purity nor the amount of Factor VIII therapy had a deleterious effect on CD4+ T cell counts (Gjerset et al., Blood 1994;84:1666). Similarly, the Multicenter Hemophilia Cohort Study found no association between the cumulative dose of plasma concentrate and incidence of AIDS among HIV-infected hemophiliacs (Goedert et al. NEJM 1989;321:1141.).

MYTH: The distribution of AIDS cases casts doubt on HIV as the cause. Viruses are not gender-specific, yet only a small proportion of AIDS cases are among women.

FACT: The distribution of AIDS cases, whether in the United States or elsewhere in the world, invariably mirrors the prevalence of HIV in a population. In the United States, HIV first appeared in populations of homosexual men and injection-drug users, a majority of whom are male. Because HIV is spread primarily through sex or by the exchange of HIV-contaminated needles during injection-drug use, it is not surprising that a majority of U.S. AIDS cases have occurred in men (U.S. Census Bureau, 1999; UNAIDS, 2000).

Increasingly, however, women in the United States are becoming HIV-infected, usually through the exchange of HIV-contaminated needles or sex with an HIV-infected male. The CDC estimates that 30 percent of new HIV infections in the United States in 1998 were in women. As the number of HIV-infected women has risen, so too has the number of female AIDS patients in the United States. Approximately 23 percent of U.S. adult/adolescent AIDS cases reported to the CDC in 1998 were among women. In 1998, AIDS was the fifth leading cause of death among women aged 25 to 44 in the United States, and the third leading cause of death among African-American women in that age group.

In Africa, HIV was first recognized in sexually active heterosexuals, and AIDS cases in Africa have occurred at least as frequently in women as in men. Overall, the worldwide distribution of HIV infection and AIDS between men and women is approximately 1 to 1 (U.S. Census Bureau, 1999; UNAIDS, 2000).

MYTH: HIV cannot be the cause of AIDS because the body develops a vigorous antibody response to the virus.

FACT: This reasoning ignores numerous examples of viruses other than HIV that can be pathogenic after evidence of immunity appears. Measles virus may persist for years in brain cells, eventually causing a chronic neurologic disease despite the presence of antibodies. Viruses such as cytomegalovirus, herpes simplex and varicella zoster may be activated after years of latency even in the presence of abundant antibodies. In animals, viral relatives of HIV with long and variable latency periods, such as visna virus in sheep, cause central nervous system damage even after the production of antibodies (NIAID, 1995).

Also, HIV is well recognized as being able to mutate to avoid the ongoing immune response of the host (Levy. Microbiol Rev 1993;57:183).

MYTH: Only a small number of CD4+ T cells are infected by HIV, not enough to damage the immune system.

FACT: New techniques such as the polymerase chain reaction (PCR) have enabled scientists to demonstrate that a much larger proportion of CD4+ T cells are infected than previously realized, particularly in lymphoid tissues. Macrophages and other cell types are also infected with HIV and serve as reservoirs for the virus. Although the fraction of CD4+ T cells that is infected with HIV at any given time is never extremely high (only a small subset of activated cells serve as ideal targets of infection), several groups have shown that rapid cycles of death of infected cells and infection of new target cells occur throughout the course of disease (Richman J Clin Invest 2000;105:565).

MYTH: HIV is not the cause of AIDS because many individuals with HIV have not developed AIDS.

FACT: HIV disease has a prolonged and variable course. The median period of time between infection with HIV and the onset of clinically apparent disease is approximately 10 years in industrialized countries, according to prospective studies of homosexual men in which dates of seroconversion are known. Similar estimates of asymptomatic periods have been made for HIV-infected blood-transfusion recipients, injection-drug users and adult hemophiliacs (Alcabes et al. Epidemiol Rev 1993;15:303).

As with many diseases, a number of factors can influence the course of HIV disease. Factors such as age or genetic differences between individuals, the level of virulence of the individual strain of virus, as well as exogenous influences such as co-infection with other microbes may determine the rate and severity of HIV disease expression. Similarly, some people infected with hepatitis B, for example, show no symptoms or only jaundice and clear their infection, while others suffer disease ranging from chronic liver inflammation to cirrhosis and hepatocellular carcinoma. Co-factors probably also determine why some smokers develop lung cancer while others do not (Evans. Yale J Biol Med 1982;55:193; Levy. Microbiol Rev 1993;57:183; Fauci. Nature 1996;384:529).

MYTH: Some people have many symptoms associated with AIDS but do not have HIV infection.

FACT: Most AIDS symptoms result from the development of opportunistic infections and cancers associated with severe immunosuppression secondary to HIV.

However, immunosuppression has many other potential causes. Individuals who take glucocorticoids and/or immunosuppressive drugs to prevent transplant rejection or for autoimmune diseases can have increased susceptibility to unusual infections, as do individuals with certain genetic conditions, severe malnutrition and certain kinds of cancers. There is no evidence suggesting that the numbers of such cases have risen, while abundant epidemiologic evidence shows a staggering rise in cases of immunosuppression among individuals who share one characteristic: HIV infection (NIAID, 1995; UNAIDS, 2000).

MYTH: The spectrum of AIDS-related infections seen in different populations proves that AIDS is actually many diseases not caused by HIV.

FACT: The diseases associated with AIDS, such as PCP and Mycobacterium avium complex (MAC), are not caused by HIV but rather result from the immunosuppression caused by HIV disease. As the immune system of an HIV-infected individual weakens, he or she becomes susceptible to the particular viral, fungal and bacterial infections common in the community. For example, HIV-infected people in certain midwestern and mid-Atlantic regions are much more likely than people in New York City to develop histoplasmosis, which is caused by a fungus. A person in Africa is exposed to different pathogens than is an individual in an American city. Children may be exposed to different infectious agents than adults (USPHS/IDSA, 2001).

More information on this issue is available on the NIAID Focus On the HIV-AIDS Connection web page.

Edited by Dmitri, 25 October 2008 - 12:57 AM.

[GoodFellas]

Soo are there ANY supps one could take to reduce the risk of getting AIDS/HIV?

[Dmitri]

Soo are there ANY supps one could take to reduce the risk of getting AIDS/HIV?

Well, it's a virus so I wouldn't think there are any. However, on the regimen section there's a member here who has HIV, he's taking a lot of supplements that have raised his T-Cell count without the help of drugs.

[bgwithadd]

Oh, how I wish they never split up HIV from AIDS. Anyone pointing this out should be anally electrocuted. Everyone knows this. Also, there are other diseases that cause the same symptoms but they are not called AIDS for god's sake.

Anyone who thinks HIV has nothing to do with aids is also a complete crackpot. You could as easily say hepatitus has nothing to do with its symptoms and blame it on OTC nasal spray but it's a ridiculous joke.

[Mind]

Hey bgwithadd, I'll see your crackpot and raise you 3 nutcases.

Reading this thread again so many years later is revealing. I had quite the anti-establishment vigor 5-10 years ago and probably still have more than most. I know that in most people's eyes, in reflection, I look like a crackpot, however, I am able to put in context, being the person who wrote the posts. I read Duesberg's tome ("Inventing the AIDS Virus") back in 1996, perhaps 1997, before I had access to scientists or any journals what-so-ever. In this vacuum, his theory made a lot of sense and it was backed by legitimate evidence (if you are not familiar, Duesberg claims that HIV is a mostly harmless passenger virus and that AIDS is caused primarily by lifestyle factors). At the time Duesberg was promoting his theory, mainstream AIDS theory was in constant fluid transition, the definition was changing, treatments were just coming on to the scene, etc... You really shouldn't judge Duesberg without reading the book and putting it into the proper time context of the mid 80s through the mid 90s. He does a great job chronicling the history of virology and spotlighting how many times the mainstream had it wrong, constantly blaming viruses for diseases caused by nutritional and/or lifestyle factors. It would be funny if it wasn't so tragic. It is a history that almost know one knows. All most people know are the success stories.

He then moves on to AIDS and meticulously documents his arguments with numerous studies. In retrospect, it might be the case that he "cherry picked" the data to support his conclusions - but there was plenty of data none-the-less. He didn't make it up whole-cloth. His references are from the first decade or so of AIDS research when many new things were being discovered and new diagnostic technologies were coming on to the scene. It was not as if mainstream researchers got it correct right out of the starting gate. People who grew up in the 80s probably remember the wild predictions about how AIDS was going to kill 30 million U.S. residents in the U.S. by 1989 and how Africa and India were going to be completely decimated (significant population declines). The theory of how HIV affected the immune system was constantly changed and refined. Duesberg hit the scene at the right time to seep into the cracks of the theory and the gaps in the data.

Over the years, the epidemiological data has solidified, but interestingly, the basic theory is yet the scene of contentious debate, as I learned at UABBA last summer. In that context "rethinking AIDS", rather than being a flashpoint for ideological entrenchment, is a good moniker for continued scientific inquiry. Better understanding and well-supported theory will lead to better treatments.

[kilgoretrout]

Good lord reading over this old thread is a nightmare.

In case there is anyone, or you know anyone, who still engages in this denialism ----

When I finally got a job with health coverage in early 2006, after a long period of being laid off, I had been infected for 15 years and saw my t-cells go from normal to about 50, which is a real danger point where you get all sorts of deadly things that can kill you real fast, like the PCP that killed my lover of 20 years in 3 weeks after he first fell sick with it 8 years ago, despite all the antibiotics they could pump into him. That was his t-cell count when it killed him. I had been getting some inexplicable headaches... who knows what they were, possibly the beginnings of some infection not yet detectable. Fortunately I started therapy on Atripla (one pill once a day, quite low in toxicities and side effects... 3 years running now). My viral load went from off the chart (literally millions) to uindetectable... my t-cells are now 700 and climbing. The horrible multiple wart growths that had started to multiply very rapidly and spread to a nasty ugly degree on one hand... finally after about 6 months on Atripla my T-Cells had recovered enough to where immune system could handle it, and over a period of about 2 months, suddenly, and with no external "wart" treatments, my rejuveneated immune system gobbled them up completely, just like that. All my blood and metabolic parameters are looking great, no problems with The Pill whatsoever.

Denial killed my lover. Science saved me. Don't be a statistic... wishful thinking will not get you anywhere... get tested, get under the care of an experienced specialist if positive, and get on therapy when he thinks it is warranted by the CDC guidelines, which are constantly evolving as they accumulate knowledge. It is only a matter of time... it is a very very slippery and sneaky virus that attacks us at our Achilles Heal, so it is like battling shadows, but before too much longer there will be not only a vaccine but also therapies to better and better treat those already infected, possibly even to the point of persistent undetectable virus.

Don't be an idiot and let HIV destroy you... medical science CAN save your life.

Edited by kilgoretrout, 26 June 2009 - 02:53 AM.

[OneScrewLoose]

My acupuncturist is an AIDS denialist, which makes me really sad cause he is generally a really level-headed guy. This is thanks in part to Gary Null's little radio show...

[tlm884]

Use a condom and don't share needles?