Investigating AIDS science:
Is syphilis the missing link?

by Colman Jones
December 2000

In the fall of 1987, while looking through newspaper clippings for stories to feature on a weekly radio show on Toronto community station CKLN, I came across what continues to be the most serious controversy in the field of medical research, namely whether the virus known as HIV (left, apparently) is really the cause of the often deadly acquired immunoeficiency syndrome (AIDS). This question was first raised in the scientific literature by Peter H. Duesberg, a veteran retrovirologist at the Department of Molecular Biology and Virus Laboratory at the University of California at Berkeley, in a paper entitled "Retroviruses as Carcinogens and Pathogens: Expectations and Reality" (published in Cancer Research, March 1, 1987). Duesberg's paper took the already HIV-obsessed AIDS establishment a bit by surprise when it first came out. Two years later came "Human Immunodeficiency virus and acquired immunodeficiency syndrome: Correlation but not causation", published in the Proceedings of the National Academy of Sciences (U.S.A.) in February 1989.

Duesberg's entry into the fray allowed the views of other dissidents to be heard, including those of New York physician Joseph Sonnabend (left), his famous long-term survivor patient Michael Callen, and Michigan State University's Robert Scott Root-Bernstein (right), author of the 1993 encyclopedic Rethinking AIDS: The Tragic Cost of Premature Consensus, probably the best overall scientific critique of the HIV=AIDS hypothesis. The debate also began to erupt in the pages of the New York Native, in a series of articles penned by John Lauritsen (lower right), followed by SPIN Magazine, in a series of hard-hitting columns by the truly heroic Celia Farber (lower left), much of which you can read online, at Robert Laarhoven's Rethinking AIDS website. For example there's "Sins of Omission", her thorough 1989 investigation of the AIDS drug AZT; her ground-breaking 1992 article on the whole HIV debate, "Fatal Distraction"; "Out of Africa", her two-part journey to see if there really was an AIDS epidemic on the dark continent; a report on the various legal actions against Glaxo Wellcome, the manufacturer of AZT, and insightful April 1997 examination of the new craze over AIDS "cocktail" therapy. But perhaps the best thing she's "The End of the End?", an written is "Fear and Loathing in Geneva", a spirited rant about the state of AIDS reportage, published by Impression, a now-defunct online magazine.

All in all, mainstream media coverage of this debate was scarce until about the year 2000, when South African President Thabo Mbeki began publicly raising questions about AIDS science. What early open-minded coverage there was appeared in the Miami Herald with a series of articles by staff writer Elinor Burkett, who later wrote the book 'The Gravest Show on Earth: America in the Age of AIDS' - the odd article in the Wall Street Journal, the San Diego Union-Tribune, the Times of London, and the Montreal Gazette, where award-winning writer Nicholas Regush tackled a number of these questions during his twelve years at the paper, later moving on to ABCNews.com, where he has continued to rattle the AIDS establishment as part of his Second Opinion columns, including "No AZT for My Baby, Please", "Never, Never Land", "The HIV Party Line", "Dare We Rethink AIDS?", and "Is HIV in Our Genes?". Regush now runs his own online newsletter, redflagsweekly.com, whose mission is to probe health and medical scientific issues in a manner that one rarely encounters in mainstream news reports. He has also published a book, "The Virus Within: The Coming Epidemic", which investigates the possible role of the Human Herpes Virus 6 (HHV-6) in a variety of brain and nervous system diseases, including multiple sclerosis, even AIDS. I wrote a somewhat mixed review of the book in the March 18, 2000 edition of Canada's national newspaper, the Globe and Mail.

Of all the mainstream newspapers, the one that probably gave the HIV/AIDS debate more attention than others in its early days has to be the Sunday Times, which for a few years in the early 1990s ran a series of cutting-edge articles by former medicine and science correspondent Neville Hodgkinson, who I first met in Amsterdam in 1992 at that year's big international AIDS conference. After leaving the Times, Neville went on to write the book AIDS: The Failure of Contemporary Science - How a Virus that Never Was Deceived the World (left), which runs some 420 pages, and is one of the best contributions to the AIDS debate in years, truly a 'paradigm-shattering investigation into the origins of the HIV theory', as the inner jacket so aptly puts it, and I strongly recommend it to anyone who's even peripherally concerned about this critical issue. You can try ordering it from your local bookstore: it's published by Fourth Estate, in London, UK, and the ISBN number is 1-85702-337-4. If you cannot get it at your local bookstore, you can probably order it direct from the publisher: their phone number is country code 44 (0)171-727-8993.

Neville was kind enough to personally autograph a copy of the book for me when I went to visit him in 1996 just outside of Oxford, at the Global Retreat Centre in Nuneham Park, run by the Brahma Kumaris. His affiliation with this international spiritual organization has made him the target of a certain amount of criticism, especially from the Sunday Observer, in a scathing article that appeared just after I arrived. The piece, by writer Mick McGovern, amounted to nothing more than a smear campaign against a fellow journalist from a competing newspaper, which also took former Sunday Times editor Andrew Neil to task for his support of Hodgkinson's line of inquiry while at the paper. The Observer article never addresses, however, the scientific points raised in Neville's book, and contents itself with printing false allegations about him and his personal beliefs. You can read some of his AIDS articles here, including "AIDS: Is Anyone Positive?", published in The European, June 22, 1998, and "Some observers are critical of HIV theory and they have a right to be heard", published in The Sunday Independent (Johannesburg) July 9, 2000.

  The Sunday Times, as well as most outlets that have given voice to these ideas, has subsequently retreated back to conventional thinking, leaving practically no regular print outlets for dissident views. For many years, a bimonthly glossy from London called Continuum (subtitled Changing the Way We Think About AIDS), featured articles critiquing AIDS science for the past several years and was really the best regular publication dealing with different views about AIDS. Continuum also offered advice and information, workshops, and a network of support through their board of consultants.

The magazine spotlighted the work of German virologist Stefan Lanka and a team of scientists from Perth, Australia headed by Eleni Papadopulos (right), who question the very existence of HIV as a distinct microbiological entity - unlike Duesberg, who insists that HIV is a real virus, although he's convinced it can't cause AIDS. Talk about debates within debates! To raise the stakes a bit, Continuum actually placed an ad in Britain's Pink Paper in the fall of 1995, offering to pay a £1000 reward (right) to the first person finding one scientific paper which shows real isolation of HIV, an award which has yet to be claimed and has since climbed to many times that amount. The magazine has a basic information web page on the Rethinking AIDS website, and you can also read an interview the magazine conducted with cultural theorist Camille Paglia here, on Chuck Ortleb's and Tom Steele's quirky Refuse and Resist site and another with celebrated linguist Noam Chomsky here. The magazine last appeared in print in 1998 and then surfaced briefly again in February 2001 on the Internet, but the organisation really (left) ceased to exist after Editor-in-Chief Huw Christie returned to Australia in 2000, subsequently passing away on August 17, 2001 .

During my stay in England in October 1996, I visited with Christie at the magazine's offices, and spent time with old friends Joan Shenton, Michael Verney-Elliott and Hector Gildermeister, from the British TV production company Meditel, which has produced a whole series of documentaries questioning conventional AIDS wisdom, including 'AZT: Cause for Concern' (1992) and 'AIDS and Africa' (1993). When I last spoke with them, they were planning a new program for Channel 4's Dispatches series, exploring the issue of false-positive HIV tests, especially among immigrant communities in England. Meditel has played a major role in getting important questions about the direction of AIDS research raised in England, even in the House of Parliament!

I also met with fellow AIDS investigative journalist Jad Adams (upper right), author of the 1988 book 'AIDS: The HIV Myth', and his lovely wife Julie. I later traveled to Bristol to interview Professor Gordon Stewart (lower right), a retired professor from the University of Glasgow, where he was head of the Department of Public Health and Preventive Medicine. He was also a former WHO adviser on AIDS, and has expressed some strong views in the ongoing scientific debates about the syndrome, although my purpose in visiting him was to interview him about his work with Sir Alexander Fleming on penicillin for a documentary on antibiotics I was working on at the time.  

In any event, at about the same time I first heard about Duesberg's contrarian ideas about AIDS in late 1987, I also stumbled across a couple of articles arguing that undiagnosed syphilis may really be at the root of this apparently new form of sexually-acquired immune suppression. At the time, there was very little hope in the way of AIDS treatments, the anti-HIV drug AZT already beginning to show its limitations, so the idea that an anti-syphilis regimen might actually treat - perhaps even cure - AIDS was most enticing indeed.  

The idea that chronic infection with Treponema pallidum, the causative organism of syphilis (left), might be playing an unrecognized role in the disease was first voiced by German anasthesiologists Klaus Dierig and Urban Waldthaler along with Berkeley physiologist Joan McKenna, whose paper, "Unmasking AIDS: Chemical Immunosuppression and Seronegative Syphilis" appeared in 1986 in the journal Medical Hypotheses. She argued that in populations with a high incidence of syphilis and multiple exposures to infectious diseases, be they gay men or Sub-Sharan Africans, there is often abuse of antibiotics, which can mask and distort the expression of syphilis. She theorized that this "chemically immunosuppressed" syphilis is a factor in AIDS, and took part in several town meetings in the late 1980s in the Bay area.

McKenna's early work was later followed up by people like Harris Coulter (right), author of the 1987 book "AIDS and Syphilis: The Hidden Link (left), later revised in 1990 (click here to read a fairly uninspired review from the British Homoeopathic Journal). The book was the first to suggest that AIDS and syphilis are not merely difficult to separate clinically but are actually causally connected. Coulter argued that AIDS is actually a modified form of syphilis, and that HIV is at most a mere co-factor, possibly an innocuous 'passenger'. Coulter, mostly known for his work in the field of homeopathy, interviewed McKenna, as well as the late New York physician Stephen Caiazza (lower left), who treated his AIDS patients with penicillin, suspecting they were dying from syphilis.

In January of 1988, I got on the phone and succeeded in getting Caiazza interviewed on both CKLN and the nightly CBC Radio current affairs show As It Happens. I subsequently interviewed him myself when he came to Toronto to speak to a group of doctors in March, at a big old house in the city's west end (which I later moved into). The meeting was organized by the house's owner John Scythes, who had lost countless friends to AIDS over the years, and was determined to get to the bottom of what's causing them to die.

AIDS doctors in other cities also began to suspect a possible role for the disease in their patients, like Larry Bruni in Washington, D. C., who was interviewed by Denny Smith of AIDS Treatment News, widely respected by the grassroots AIDS community as a critical source of information on AIDS therapies. Bruni, who [has] had a large HIV practice for several years, talks here about treating syphilis in people with AIDS, italics are my own (you can read the full interview here):  

DS: I understand that you favor the empirical use of antibiotics, when a set of symptoms is eluding any particular diagnosis or treatment. Is there a concern that antibiotic drugs could suppress the immune system further?
LB: I haven't really seen any systemic damage from antibiotics. Indeed, my own experience is that a course of antibiotics frequently perks up the immune picture. The first antibiotic I tried on an empirical basis was doxycycline, in 1988, based on Stephen Caiazza's ideas.
DS: Since HIV isn't affected directly by antibiotics, this must be a way of dealing with cofactors in hiding.
LB: It often seems that something else is driving the infection. The notion that latent syphilis may be treated this way is interesting. I can't think of any topic in medical school that professors were more smug about than syphilis treatment. "We know everything there is to know about this disease," they'd say. Reminds me of the character in Voltaire's Candide.
DS: Dr. Pangloss!
LB: Yes, as though we live in the best of all possible worlds, and we know everything we need to know. But meanwhile, one treatment they were using to treat syphilis failed to cross the blood/brain barrier, and those people may be chronically infected with syphilis, including many people with HIV.
DS: So the cerebrospinal fluid could be "reseeding" the body, and doxycycline may be dealing with it?
LB: I've had some excellent results with doxycycline; tetracycline, as well, will cross the blood/brain barrier. I try it in people who have a residual indicator of syphilis in their blood. And now we know that we could be treating mycoplasma infections empirically, too. I have actually seen rises in T- helper cells in some patients during treatment with doxycycline.

Other writers who have researched the syphilis/AIDS connection include Katie Leishman, who wrote an article about this in the January 1988 issue of the Atlantic Monthly, and was later contracted to write a book about this whole mess for the Atlantic Monthly Press, but from what I understand, failed to convince her editors to publish it, in part due to the failure of Dierig and Waldthaler to cure their patients with megadoses of penicillin (in fact, as of 1995, the two doctors were involved in lawsuit against each other!). It was hoped, of course, that massive doses of penicillin would somehow cure AIDS - not so, unfortunately - and this treatment failure led most AIDS dissidents to dismiss the syphilis/AIDS connection sometime around 1991.

Joan McKenna gave a talk at the world's first alternative AIDS conference in Amsterdam in 1992, which was followed by an article in the Sept.-October 1992 issue of Borderlands magazine (vol. 48, no. 5). On her web page, last updated in December 1997, McKenna, now minister of the Vaca Valley Church of Religious Science, writes that her research has continued quietly, outside of the public eye, adding that death threats forced the closure of her institute. As for Caiazza, he passed away in 1990, never publishing any of his results in a peer-reviewed journal, and his patient practice scattered.

Another early advocate of a syphilis/AIDS connection is Robert Ben Mitchell (right), author of the 1989 book "Syphilis as AIDS" as well as the summary "Syphilis as AIDS? - A Call For Research", published in Medical Hypothesis (1993), and included as an appendix in his book "Before I get AIDS: A Past, Present and Future Guide For Those With and Without HIV". Mitchell is so convinced of the connection between syphilis and AIDS, and the fact that no one in the medical establishment is willing to seriously consider this connection, that he has spent 10 years becoming a doctor, and is now an osteopathic physician, fully licensed and practicing general medicine in Florida. He plans to open a clinic treating newly diagnosed AIDS patients on the basis of a T. Pallidum etiology. He wrote myself and John Scythes for advice about how best to go about this, and you can read the initial discussion starting at http://groups.yahoo.com/group/AIDSsyphilis/messages/21, (on the online archives of the AIDSsyphilis mailing list), where we express a certain amount of skepticism that he will be able to get access to patients and build up publishable data from a prospectively-designed syphilis intervention strategy.

Fundamental research questions are the focus of the continuing efforts of Scythes (pictured on the right at the January 2000 Gordon Conference on the Biology of Spirochetes in Ventura, California), who has continued to pursue the question with great vigour, a passion that has taken him around the world several times over, attending major AIDS and STD conferences, where he has published, i.e. co-authored, five reviews of syphilis serology in HIV-infected gay men, three times at the Toronto Hospital, and twice at the Semmelweiss University in Budapest, (that's top Hungarian researcher István Horváth chatting with Scythes on the left at the 1995 ISSTDR meeting in New Orleans). He has become quite the controversial figure in the relatively small international syphilis research community, and he communicates on a regular basis with STD authorities around the world, and has also been invited to speak at major European universities, like the Algemeines Krankenhaus in Vienna and the Academic Medical Centre in Amsterdam.

I first interviewed Scythes in 1989, for my first-ever article in NOW Magazine. I conducted a much more in-depth television interview with him the next year, after receiving a $5,000 grant from a local weekly community television series, the AIDS Cable Show, to produce a half-hour program highlighting the various aspects of the HIV debate, which eventually ballooned into a 4-hour series, entitled "The Cause of AIDS: Fact and Speculation". It was essentially a one-man effort of shooting, lighting, sound, editing, scriptwriting, narration, and music. The shows, produced for the Rogers Cable 10 community channel, will soon be available again online, and for now you can screen the one-hour summary I prepared in 1995, "Lest We Forget: Syphilis in the AIDS Era", first publicly screened November 15, 2000 at the NFB's John Spotton Cinema in Toronto:

Hard copies of the entire series can be still obtained from V-Tape (click here to obtain ordering information). Included are in-depth interviews with some of the key figures in the AIDS dissident movement, as well as footage shot at the world's first "alternative" AIDS conference in Amsterdam, which I videotaped in its entirety, material which also formed the basis for a 3-hour IDEAS on Camera special report, "The Amsterdam Debates About AIDS: Its Causes, Cures and Context", and aired July 4, 11, & 18, 1992 on the CBC's all-news cable channel Newsworld (since renamed CBC News Network.

In the summer of 1991, I put together a radio documentary for CBC Radio's IDEAS, where I had begun working in 1988, doing research, conducting interviews, and reading on-air scripts for the latter half of "The AIDS Campaigns", an 8-part series which looked at how AIDS campaigns - scientific and political - reappraise sex and morality.  This time, I was tackling the very science behind AIDS itself, in a 2-hour program entitled "What Causes AIDS? A Second Look", which included interviews with one of the fathers of retrovirology (the study of retroviruses), Harry Rubin (left), a professor of molecular and cell biology at the University of California at Berkeley and a colleague of Duesberg, as well as with Walter Gilbert (right), professor in molecular biology at Harvard and winner of the 1980 Nobel prize for chemistry. The show won that year's Canadian Science Writers' Association (CSWA) award for Radio over 30 Minutes.

While I continued to research the syphilis/AIDS connection, I also explored a number of other scientific controversies surrounding AIDS, including the astonishing success in reversing the progress of the disease in HIV-positive hemophiliacs by purifying the blood products they receive (see "Coagulation Substitutes and CD4 Decline in Hemophilia" by Naomi Pfeiffer and Greg Haas). These purification processes remove other blood-borne contaminants which may play a role in the downregulation of the immune systems of hemophiliacs with HIV, (even in those without HIV). These contaminants include exposure to foreign cytokines (see below) such as transforming growth factor-beta, which has been shown to be a natural and potent inhibitor of many immunologic responses. This investigation eventually resulted in 1993's "Blood Poisoning - Act II", an IDEAS Special Report, which took an in-depth look at this startling new information and the ramifications for the mid-80s tainted blood scandal and subsequent inquiries and commissions.

There was also "The Strange Case of the Florida Dentist" in 1994, a show examining the story of Kimberly Bergalis (left), the Florida college student whose dentist, David Acer, allegedly infected her and several other of his patients with HIV - or did he? This question also attracted the attention of SPIN Magazine, which commissioned me to write a column about the whole Bergalis affair for its August 1994 issue. I subsequently went on to write other columns about the new findings on high-purity clotting factor and HIV-positive hemophiliacs (October 1994), the failure of experimental HIV vaccines to prevent infection and/or the progress of the disease in those already infected - and how vaccine manufacturers are now pursuing the Third World as a testing ground and market - (January 1995), and new HIV research purportedly demonstrating a high level of virus replication early on the disease, apparently refuting arguments by critics of the HIV theory of AIDS, claiming the virus is too inactive to destroy the immune system (May 1995).

In June of 1995, SPIN commissioned me to write a long article on the possible connection between syphilis and AIDS, and sent me to New Orleans to attend the 1995 International Society for STD Research (ISSTDR) meeting, where I interviewed a dozen of the world's top syphilis experts - even Dr. Joycelyn Elders, former U.S. Surgeon General (right). I then spent a couple of months ironing out a final draft with features editor Alyssa Katz, but at the last minute, publisher Bob Guccione Jr. changed his mind and decided not to publish it, although you can read the unpublished draft here (N.B. Guccione eventually sold SPIN in 1997, and the new editors promptly and permanently removed the monthly AIDS column).

The work I did on the syphilis article was put to good use, however: I still managed to write a feature article for Toronto's news and entertainment weekly NOW Magazine, and I prepared a 2-hour radio documentary series for IDEAS entitled "Déjà Vu: AIDS in Historical Perspective", which I'm proud to say also won the CSWA1996 Science in Society Journalism Award for Radio Items 10 Minutes and Over . You can listen to an MP3 excerpt and/or visit the web site the CBC set up to accompany the series (now archived at the Internet Archive) - there's tons of stuff there, including illustrations from STD campaigns past and present, transcripts from past programs, published scientific abstracts, newsgroup debates on sci.med.aids, other articles I've written, a rather extensive reading list, and links to other sources of information.

Here is a complete list (last updated April 2007) of the articles and documentaries on AIDS science I've worked on to date, listed in chronological order, with links where applicable:

• "The AIDS Campaigns" (Part 5: The Canadian response), IDEAS, June 6, 1988 (co-produced)
• "The AIDS Campaigns" (Part 6: Beyond the scope of medicine), IDEAS, June 7, 1988 (co-produced)
• "The AIDS Campaigns" (Part 7: Prejudice and the media), IDEAS, January 4, 1989
• "The AIDS Campaigns" (Part 8: A death sentence?), IDEAS, January 5, 1989
• "Grassroots data sheds light on AIDS", NOW, June 1, 1989
• "Lost cause: some doubt HIV is the sole cause of AIDS", Xtra!, June 1989
• "Challenging the AIDS establishment over HIV", Rites, July/August 1989
• "New findings defy AIDS research fundamentals", NOW, October 11, 1990
• "Symptoms of AIDS could be syphilis in disguise", NOW, January 3, 1991
• "What Causes AIDS? A Second Look", IDEAS, November 6 & 7, 1991 (Winner of the CSWA 1991 Science Journalism Award for Radio)
• "Poisoned hopes", NOW, April 30, 1992
• "Researchers question role of HIV in causing AIDS", NOW, June 4, 1992
• "Alternative AIDS Research: The Amsterdam Symposium", IDEAS on Camera, CBC Newsworld, July 4, 11 & 18, 1992 (shot location footage and interviews)
• "Mystery AIDS cases point to limits of HIV science" NOW, July 30, 1992
• "AIDS theories questioned", Xtra!, December 11, 1992
• "An epidemic within an epidemic?", Xtra!, January 8, 1993
• "Officials drag heels on new hemophilia treatment", NOW, January 14, 1993
• "Blood Poisoning: Act II", IDEAS, March 18, 1993
• "Drug firm stages hasty AZT defence", NOW, April 8, 1993
• "A Curious Finding Lends Support to the Co-Factor Hypothesis for AIDS", Lexicon (Toronto), August 1993
• "AIDS heretic pioneered grassroots drug research" (Michael Callen obituary), NOW, January 6, 1994
• "Science journal wrestles Times over HIV meaning", NOW, January 20, 1994
• "Did he or didn't he?", NOW, April 14, 1994
• "The Cause of AIDS: Fact and Speculation", Rogers Cable 10, April 1994 (4-hour television documentary series, divided into Parts One (HIV: A Deadly Virus?), Two (Redefining AIDS), Three (Déja Vu: A History of STDs) and Four (Syphilis in the AIDS Era), winner of MacLean-Hunter's 1993 Lizzie Awards in the Current Affairs Category, and runner-up in the 1993 Ontario Cable Television Producers Association Awards)
• "Drug in Denial", NOW, May 26, 1994
• "The Strange Case of the Florida Dentist", IDEAS, June 24, 1994
• "New evidence suggests Florida dentist innocent", Medical Post, July 5, 1994
• "AIDS: Words from the Front"(Kimberly Bergalis), SPIN, August 1994
• "AIDS Vaccine Risky Venture", NOW, September 29, 1994
• "Mysterious HIV eludes vaccine", NOW, September 29, 1994
• "AIDS: Words from the Front" (AIDS co-factors in hemophiliacs), SPIN, October 1994
• "AIDS: Words from the Front" (HIV vaccines in the Third World), SPIN, January 1995
• "Lest We Forget: Syphilis in the AIDS Era", Rogers Cable 10, February 1995 (updated, edited summary of "The Cause of AIDS: Fact and Speculation") - *now viewable online via Google Video*
• "HIV ideologues lock horns over the cause of AIDS", NOW, March 30, 1995
• "How Safe is Safe Sex?", NOW, April 20, 1995
• "AIDS: Words from the Front" (New HIV findings challenge skeptics), SPIN, May 1995
• "Syphilis Sleuth", NOW, September 21, 1995
• "Déjà Vu: AIDS in Historical Perspective"on IDEAS, January 5 & 6, 1996 (CSWA 1996 Science in Society Journalism Award) (MP3 excerpt)
• "AIDS in the 1990s: More Questions than Answers", Science Link (newsletter of the Canadian Science Writers' Association), January, 1996
• "Pox Kills", Angles (Vancouver), February 1996 issue
• "What if HIV Doesn't Exist?", NOW, November 21, 1996
• "Has AIDS been beaten?" , NOW, January 2, 1997
• "Searching for Dr. Ho", NOW, February 6, 1997
• "Spectrum of Cellular Immune Responses to the Human Immunodeficiency Viruses and the Human Treponematoses" (co-authored with John Scythes), accepted for a co plenary presentation in the oral sessions at the VenSouth '97 International Union for Venereal Diseases and Treponematoses (IUVDT) HIV/STD World Congress, Melbourne, Australia, June 1997
• "Clear thinking on AIDS, and about time", Globe and Mail, August 2, 1997
• "Is this AIDS group more harm than good?" , NOW, April 9, 1998
• "AIDS activism doesn't need dissidents like this", NOW, October 22, 1998
• "Sign oath or get out, AIDS activists told" , NOW, December 10, 1998
• "The HIV chimp theory that fell off a tree", NOW, February 4, 1999
• "Implications of the Recent Lyme Culture Technique for the Diagnosis of Syphilis" (co authored with John Scythes), presented at the 12th International Conference on Lyme Disease and Other Spirochetal and Tick-Borne Disorders, New York City, April 9 & 10, 1999
• "Monkey business over HIV's origins", Science Link, May 1999 issue
• "The Bacteria Revolution" on IDEAS, May 28 & June 4, 1999 (available in RealAudio)
• "Bacterial bombshell", NOW, June 3, 1999
• "Fudged facts: AIDS science does a number on Africa", NOW, March 9, 2000
• "AIDS maverick finds new villain", Globe and Mail, March 18, 2000
• "AIDS scientist wants to jail me", NOW, May 4, 2000
• "Insensitive syphilis tests: Implications for HIV/AIDS?" , June 28, 2000 commentary (co-authored with John Scythes) on a poster presentation at the 2000 General Meeting of the American Society for Microbiology
• "Syphilis shocker", NOW, July 27, 2000, with subsequent correspondence, "That syphilis mystery not such a mystery", NOW, August 3, 2000 (scroll to bottom of page)
• "Shots misses", NOW, November 16, 2000
• "Syphilis: the "elephant in the room" of AIDS?" (co-authored with John Scythes), British Medical Journal, April 30, 2002 online Rapid Response to the March 16 BMJ editorial "Shame: the elephant in the room", by Frank Davidoff
• "A New Gold Standard for Syphilis?" (Journal of the European Academy of Dermatology and Venereology, Volume 18, Supplement 1, May 2004, PS 230), April 29, 2004, poster presentation for the European Academy of Dermatology and Venereology Spring Symposium in Budapest, Hungary (co-authored with John Scythes and Robert Notenboom)
• "Can We Reliably Diagnose Syphilis?" (International Journal of STD & AIDS, Volume 17, Supplement 1, 2006, O0001), oral presentation at the 22nd IUSTI-Europe Conference On Sexually Transmitted Infections, Versailles, France, 19-21 October 2006, co-authored with John Scythes
• "Syphilis in the AIDS era: Diagnostic dilemma and therapeutic challenge" (Acta Microbiologica et Immunologica Hungarica, Volume 60, Number 2, June 2013), co-authored with John Scythes

The most recent IDEAS documentary, the 2-part series "The Bacteria Revolution" explored evidence linking specific bacteria with a wide variety of diseases, and examines the implications these discoveries are having on everything from diagnostic practice to theories about the process of evolutionary change. The series first aired May 28 & June 4, 1999, but you can still glance through an extensive illustrated summary and bibliography I prepared.

You can obtain printed transcripts for many of these documentaries, incidentally - for example, you can order "IDEAS About AIDS: A Decade of reporting about the science and politics of an epidemic", an anthology containing 21 programs about AIDS (complete with reading lists and references), by sending a cheque or money order for $25.00 (includes all taxes and shipping) to IDEAS Transcripts, Box 500, Station A, Toronto, Ontario, Canada M5W 1E6. You can also order by credit card by calling 1-(416)-205-6010. For a listing of other programs on AIDS, click here. For more information on ordering transcripts, click here. "The Cause of AIDS: Fact and Speculation" is available in hard-copy videotape from V-Tape, 401 Richmond Street West, Suite 452, Toronto, Ontario, M5V 3A8, CANADA. Phone: (416)-351-1317; Fax: (416) 351-1509. To rent, preview or purchase this series, click here to send e-mail to indicate which parts you're interested in, and whether the request is for Rental or Purchase or Purchase-Preview.

I've been invited to give talks to organizations like the Science Writers' Association, the AIDS Committee of Windsor, the University of Toronto's Sexual Education and Peer Counselling Centre, the National Lesbian & Gay Journalists Association, and I occasionally appear as a guest on other radio and TV programs like the now-defunct CBC Radio program Morningside, CBC Newsworld's Sunday Morning Live, CTV's Canada AM, and local Toronto radio station Talk 640. I've also turned up a number of times over the years on the University of Toronto community radio station CIUT-FM, on a show called Undercurrents (no relation to the CBC-TV show of the same name), as well as the Wednesday morning Caffeine Free show, where I've been given lots of airtime to advance these radical notions to an unsuspecting radio audience. I also helped prepare an official submission to the Krever Commission of Inquiry on the Blood System in Canada, and although Scythes' and my names are listed as contributors in the appendices at the end, the important points we made to the Commission on the impact of switching HIV-positive hemophiliacs on to ultra-pure clotting factor went right past them, I'm afraid.

I've largely stopped trying to hunt down all the new AIDS dissident websites springing up all the time - my last complete list can be found at the Déja Vu: AIDS in Historical Perspective site. Certainly, the most complete WWW resource devoted to alternative AIDS theories has to be Laarhoven's Rethinking AIDS Website, which houses hundreds of pages of information - much of it not published elsewhere - with profiles of key scientists and journalists, book information, over 150 articles and scientific papers. If you're still left wanting more, you can consult a 1992 bibliography I compiled of some of the more definitive alternative AIDS research in print.

The World Wide Web Virtual Library: Sumeria / The Immune System is another comprehensive site, featuring a host of articles about alternative AIDS research (although nothing on the AIDS/syphilis link). HIV=AIDS Controversy houses a good collection of sources assembled by Alan Koontz, including Fred Cline's excellent AIDS Bibliography, while Ben Gardiner's AIDS BBS is the first and oldest AIDS bulletin board. There's Does HIV Cause AIDS?, a comprehensive site set up by the Valley Advocate, a newsweekly based in Hatfield, Mass (click here for a no-frames version); Reappraising AIDS, a journal edited by Paul Philpott. Also worth noting is HEAL Toronto, the local chapter of Health Education AIDS Liaison (HEAL) an international association of AIDS dissidents.

As far as web resources on the syphilis/AIDS connection, here is where you'll find the only other online articles that I've been able to locate, which I found on Ben Gardiner's AIDS BBS, although there's also a brief excerpt of an interview Jon Rappoport conducted with Dr. Caiazza, on March 21, 1988 here. It seems that Déja Vu site is the most comprehensive resource of material on this topic, but if there are other places on the net where people are talking about this stuff, please let me know.

Despite this sizeable body of work questioning the HIV=AIDS paradigm, the ruling orthodoxy remains firmly entrenched. This whole question of the rigidity of scientific paradigms, or thought collectives, has been addressed by many classic philosophers and science historians, from Ludwig Fleck to Thomas Kuhn, and more recently by Laarhoven, who organized the alternative conference in Amsterdam. The careful scientific re-evaluation of this complex syndrome hasn't been helped - in my view - by the particular focus on claims that AIDS is not even an infectious disease at all, but largely one induced by recreational drugs, stuff like cocaine, heroin, poppers (amyl nitrite inhalants), even the main AIDS drug AZT. There's no question these things probably aren't good for people in the long-term, but to suggest that AIDS is solely due to these toxins ignores the many people with AIDS who do not engage in drug use of any kind (not to mention all the heavy drug users who never got AIDS).

After years of reviewing the literature, communicating with experts across the globe, and publishing our views at international HIV/STD meetings (including five international AIDS conferences), Scythes and I have reached a somewhat different conclusion, one we feel is more realistic and practical, although it's fairly complex and requires a pretty grasp of medicine, hence the occasionally technical language that follows in this summation, culled from various posts and letter Scythes and I have co-authored:

In our view, there are different explanations for the expression or appearance of HIV (i.e. a positive antibody test) in each of the AIDS risk groups. Following on this line of thinking, how well an HIV-positive individual does may therefore vary greatly, perhaps depending on how well their co-infections or conditions are identified and resolved.

It is true that, in some contexts, AIDS does not appear to be easily transmitted via sexual means. Recipients of contaminated transfusions (including clotting factor) and allogeneic tissues do not appear to easily transmit AIDS to their spouses or partners. The transmission is at least extremely inefficient, and this curious anomaly has formed the basis for much of the emerging dissident position that AIDS is not infectious.

However, in North America, the main AIDS population has mostly consisted of multi-partner homosexual males (and those who received blood and blood products from them). Duesberg's non-infectious hypothesis (drug abuse/malnutrition) doesn't seem to consistently explain AIDS in these cohorts, where most evidence suggests that the syndrome has an infectious basis. Many who have died were neither drug abusers, nor users of AZT, nor malnourished, but rather appeared to have normal healthy lives until they turned "HIV-positive" (whatever this laboratory marker ultimately turns out to mean), seemingly as a consequence of sexual or blood-borne exposure.

We have developed a position that reconciles, at least in our view, the anomalies between the picture of sexually-acquired AIDS in Western homosexuals and the situation on the African continent, where other endemic chronic diseases may trigger the appearance of HIV antibody and result in a much different clinical picture. We believe that once the immune system is stimulated by a chronic infection that it cannot successfully resolve, HIV tests may become positive. Laboratory evidence suggests latent HIV can reactivate due to the stress associated with unresolved infection(s). Tuberculosis and malaria would be two main candidate diseases in Africa.

But since high levels of tuberculosis, malaria and enteric pathogens did not exist in previously healthy young well-to-do homosexuals in Europe and North America, what might explain why they became susceptible to chronic active HIV infection and died in such high numbers?

Anti-HIV treatments like AZT/HAART, while potentially a co-factor for a certain amount of morbidity and mortality - as admitted to me as far back as 1998 by leading AIDS clinician Michael Saag at the University of Alabama - these drugs are not sufficient to explain AIDS all by themselves, since over a hundred thousand people died of AIDS before any of them came into use. Furthermore, the early epidemiologic work by the CDC, flawed as it was, nonetheless convinced me that something was being spread by sexual contact.

It is our view that silent re-infection with syphilis plagued Western homosexuals during the late 1970s and early 1980s, and is now spreading among heterosexuals around the world, especially in Africa. Existing diagnostic tests woefully lack sensitivity for the detection of chronic infection with T. pallidum (the causative organism of syphilis) - especially in the context of re-infection. This test insensitivity is acknowledged by major authorities in the field as well as a vast body of syphilis literature. Evidence also suggests repeated syphilis exposures may induce AIDS in experimental animal models.

Of course, if you're someone who has been reading up on the regular literature on STDs and their relationship to HIV, you will already know that the presence of STDs increases the risk of HIV transmission about 3- to 5-fold by causing inflammation and lesions of the genital tract, thus creating an accessible place of entry for HIV, or at least so the thinking goes. Scythes agrees that by stopping syphilis and other ulcerative STDs, or at least slowing them down, far fewer people will become HIV-infected and/or develop AIDS - but not just because of fewer opportunities for transmission of the virus: he and I are convinced that syphilis represents far more than simply an ulcerative, or focal activation phenomenon, in HIV acquisition/AIDS - syphilis may also turn out to be an important immunologic co-factor for susceptibility to active viral expression and progression to AIDS.

Of course, some brave researchers do go a step further and suggest the debilitating effects of STDs may accelerate progression of "HIV disease", or conversely that the suppressive effects of HIV on the immune system worsen the symptoms of other STDs and decrease the healing effects of STD therapies. However, the best evidence from the biggest study that was have actually suggests that, oddly enough, the presence of HIV has no bearing on the course of classically- recognized syphilis nor how well someone responds to treatment.

This is strange, considering how critical a vigorous and specific T-cell response is in controlling syphilis in ordinary people, i.e. without HIV. Or is the syphilis we see in people with HIV only the sensitized form, in which people are healthy enough to make the classical reaction? Are we really only seeing the tip of the iceberg of a much larger group of immunologically unresponsive (i.e. desensitized, anergic), "burnt out", chronic syphilitics, whose blood tests are negative and whose immune breakdown is being blamed on HIV?

Of course, you might wonder how syphilis could be involved in AIDS, since penicillin cures syphilis right? So how come it hasn't cured any AIDS patients? While it's true that early syphilis in a naïve population can be successfully diagnosed and cured most of the time within our current paradigm for the management of the disease, what needs to considered is the problem of latent syphilis, when the disease has gone untreated or inadequately treated for some highly variable period of time, a phenomenon which has always plagued people with multiple sexual partners, and which has simply not been investigated in modern times in terms of its immunologic consequences.

There are plenty of reasons to doubt that antibiotics alone will cure a chronic latent syphilitic infection: it's well known that penicillin only affects organisms that are actively proliferating. In the absence of such replication, and a vigorous immune response, this kind of chronic syphilis would be - and always was historically - exceptionally difficult to treat. In the latent stage of syphilis, the bacteria stop dividing and can hide away, remaining in what are called "immunologically privileged sites", out of reach of the body's defenses. The trick seems to be in getting the bugs to divide again, otherwise they don't appear to respond to either antibiotics or the body's own antibodies.

This phenomenon is also seen in another spirochetal infection, Lyme disease (see below), in which the organism can persist and symptoms progress despite very aggressive treatment with antibiotics. If AIDS patients are suffering from a relatively latent chronic syphilis infection, it may in fact be very difficult to treat by current methods, especially in people who've lost effective immune responses against the organism, which the documented loss of syphilis antibody - independent of other antibodies - among HIV-positive individuals suggests.

Historically speaking, a great deal of excess mortality from pneumonias, TB and cancer is strongly associated with a history of syphilis. The older American syphilis literature, both actuarial and medical, strongly indicates that T. pallidum dispatched its victims far more often via other opportunistic infections (i.e. TB reactivation) or cancer, rather than via the classical direct effects of late syphilis, judging from the increased mortality amongst syphilitics, independent of the classical syphilis picture, with causes of death like re-activation tuberculosis, various atypical pneumonias, and rare cancer - sound familiar?

Indeed, a role of latent (i.e. hidden) syphilis in lowering susceptibility to other fatal conditions has been speculated for decades. As top American syphilis author Joseph Earle Moore wrote in 1939, "In spite of 400 years of study, we still do not know the actual importance of syphilis as a cause of death. To what extent does death directly from syphilis masquerade under other diagnoses: or to what extent is syphilis an indirect cause of death from other conditions? Is it justifiable to assume, as did Osler, that syphilis actually ranks first, instead of its apparent tenth, among killing infections?"

There are dozens of such references, all in the regular literature, prior to 1950, and there is every reason to suggest this is still going on today.

Naturally, it's hard for most people to think of AIDS as an old disease - or more correctly, syndrome, as AIDS is defined as 30 different diseases in the presence of HIV. But it is not that unreasonable to suggest that these 30 different diseases have - and always have had over the centuries - a reactivation mechanism in common. To be specific (for you scientific/medical types), this mechanism is a defect in the Gell and Coombs Type IV delayed-type hypersensitivity (DTH) immunologic memory. Throughout all the old editions of Harrisons's Principles of Internal Medicine (or the original Harrison editions), many of the 30 AIDS-defining diseases are described, and what seems clear is that only a small proportion of those actually exposed and infected developed any unmanageable late symptoms.

This is true of all the fungi, herpetic infections, mycobacterial diseases, and so on. In every description, there was always a small percentage of untreatable, disseminated cases, which were confirmed by isolation/culture of the pathogen, and were characterized by negative skin tests and death - all AIDS-defining by today's definitions. It is the immune suppression that ties opportunistic infections together - and always has - but this immune suppression was unmeasurable in the past (i.e. using CD4 counts), except by way of skin tests.

The clinical picture that defined these older AIDS cases was the absence of the DTH skin test reaction in the presence of the pathogen and illness - only a defect in immunologic memory can explain the reactivation of these otherwise harmless (or at least generally manageable) ubiquitous human pathogens, old diseases that have always been with us. The CDC's mistake was to suggest that, because of an explosion of the syndrome among previously healthy gay men, this was an inherently new phenomenon. If the changes in immune system genetics we now refer to as AIDS are indeed old, this would explain the susceptibility to all these diseases reported in the older literature.

Oddly, enough syphilis is the one sexually-transmitted infection that never behaves like an opportunistic infection on the context of AIDS. This is perhaps the most tell-tale sign that something is askew with our current concepts - if HIV causes immune suppression, it should have a big impact on the course of syphilis and how well it responds to treatment - like it does in TB and other similar infections controlled by T-cells - and yet HIV doesn't seem to affect syphilis at all. Based on the known rates of untreated syphilis among gay men, we should be seeing hundreds of thousands of classical presentations of late syphilis in immune-suppressed individuals, and yet we see practically none - at least, in the conventional, sensitized form described in the textbooks - a very puzzling anomaly, given the overwhelming epidemiological association between these two infections, and the critical importance of the cellular immune response (i.e., the response that gets depleted in AIDS) for the effective control of syphilis. Since we already have evidence suggesting that HIV itself may well be opportunistic, one has to ask: which horse is pulling the cart here - HIV or chronic, undiagnosed syphilis?

Much of the concern about the dangers of chronic, undiagnosed syphilis derives from emerging concepts in the study of immuno-regulation, i.e. how the immune system regulates itself in response to various infections. It does this in part through the production of specific and highly interactive chemicals in the blood called cytokines, which are essentially the chemical messengers the body's cells normally produce to turn various immune responses on and off at the right times.

In people with AIDS, these cytokine signals are totally out of whack, and the AIDS researchers who specialize in studying the immune system are starting to suggest that it's this cytokine imbalance that probably leads to the eventual burning out of the critical T-4 cells, which eventually go missing in AIDS patients, not a direct cell-killing effect by HIV.

These newly evolving concepts of immuno-regulation, coupled with the ability of researchers to identify the specific cytokines involved in regulating various immune responses, are now shedding light on why certain bacterial diseases persist in a chronic form - despite an apparently strong immune response at the beginning - while others are successfully resolved.

Scythes is of the view that the persistent immune activation disease associated with the expression of HIV surface genes and protein production - with the resulting positive HIV screening and confirmatory tests - occurs not just due to infection with HIV, but because the immune system has been genetically deviated (or injured) in the stem and precursor populations of cells, for lack of better words. CD4-bearing cells are apoptotic and rapidly turning over, and the signaling is in disarray. The problem seems to stem from the critical early cell-based immune responses - called Th1 - being shut off too soon, with a predominantly antibody response - called Th2 - then taking over. The immune system is somehow tricked into thinking the infection has been beaten, but a few organisms remain, that then slowly multiply and give rise to persistent infection. This phenomenon of premature shutdown is known as immune deviation.

Scythes feels the classical bacterial infections associated with AIDS have been under-rated in terms of the injury they cause to immune system genetics. In the poorer parts of the world, diseases like TB, leishmaniases, trypanosomiases, and all the enteric stress could be enough to allow a retrovirus like HIV to re-activate. The severity of the injury then predicts the individual outcome, as does timely therapy for some of the diseases, before too much damage is done to the immuno-regulatory mechanism.

This signaling injury to the immune system is likely transmissible through blood or blood products by low molecular weight signaling cytokines, quite independently of actual pathogens - viral or bacterial. These molecules are heat-resistant and go through filters, and indeed a non-native product for haemophilia is associated with much slower AIDS progression (Seremetis, S. et al., Lancet (1993) vol. 342, p. 700-703). There are a dozen other references associating clotting factor impurities with AIDS progression in HIV-positive haemophiliacs. For gay men in the industrialized countries, syphilis could easily be involved in initiating this alteration, Scythes suggests, but only in the untreated and re-exposed person (who is therefore not resistant), thereby allowing HIV to be chronically active and persistent in producing its surface (and supposedly AIDS-inducing) proteins.

Papers published during the 1970s and early 1980s in the British Journal of Venereal Diseases described immunological phemonema suggesting that cell-mediated immunity is depressed during secondary syphilis. This immune regulation is also seen during acute responses to other infections, of course, but more recent research suggests a completely different kind of problem in syphilis once people have reached the latent stages, i.e. immuno-regulation against Th1 responses by Th2 cytokines. The Th1/Th2-like switch in syphilitic infection: is it detrimental?, courtesy of Medline, is a really important paper by the late immunologist Tom Fitzgerald, comparing the complex immune regulation operating in the chronic stages of syphilis with that seen in other chronic bacterial diseases. Polish researcher Jadwiga Podwinska, who works at the Laboratory of Medical Microbiology in the Department of Immunology of Infectious Diseases at the Institute of Immunology and Experimental Therapy in Wraclaw, Poland, has also published on the dominance of the Th2 cytokine profile in many human subjects with latent syphilis.

Admittedly, this work is controversial, because other researchers in the field have not found evidence for Th2 predominance, but it's not clear whether patients with latent syphilis have been adequately studied. Syphilis is rarely inactive and the word "latent" is a misnomer, at least in how we seem to understand it from standard medical teaching. Latent means "hidden" in Latin, not "inactive". From the immunologic standpoint, latent syphilis is chronic active syphilis, and is both more dangerous for immune system genetics and harder to treat than the outward classical symptoms of late syphilis. Judging from the work of Podwinska and Fitzgerald, a Th2 cytokine pattern begins to predominate in most persons once syphilis goes into latency like this, injuring the immune system's capacity to resist further infection.

Furthermore, no amount of treatment reverses the situation - a scenario supported by all of the published animal and deliberate human inoculation experiments, which indicate clearly that syphilitic infection, if allowed to persist long enough, shuts down the immune system's responses against it, so that the disease quietly redisseminates in the body, which is then unable to mount a vigorous immune response in the event of re-exposure. As the famous American syphilologist E.W. Thomas wrote in 1949, "Within 2 years after infection, untreated syphilis produces immune changes in the host which, with rare exceptions, are permanent and make it impossible for tissues to react to subsequent infection with development of early syphilitic lesions."

Subsequent re-exposure without this Th1-driven immunologic memory probably leads to the silent re-dissemination of treponemes all over the body. Early syphilis is probably amenable to treatment because this switch has not yet fully occurred, but Podwinska's findings cast doubt on the diagnosis and treatment of later, or latent disease, including re-infections.

What's clear from all this is that the widely used non-treponemal screen tests - which pick up a poorly understood non-specific reaction involving antibodies directed against the body's own connective tissue - are insensitive in populations at risk for multiple exposures to T. pallidum - in other words they're simply not adequate to tell when someone has become re-infected.

A thorough review of the classical literature makes clear that re-exposure to syphilis will often go undetected by the regular symptoms and/or blood tests unless the first infection is promptly and thoroughly adequately treated, so as to allow a proper protective immune response by the body the second time around. This simply did not happen among the high-risk multipartner gay cohorts in the 1970s and early 1980s -- hundreds of thousands of men in North America and Europe who became multiply re-infected with syphilis, but went either untreated or were inadequately treated, as confirmed by numerous references.

To put it simply, the tests for syphilis - especially among people with HIV antibodies - have huge problems. The Wassermann-type non-specific screen tests (i.e. VDRL/RPR) seem reliable in the naïve populations, i.e. not previously exposed, but often fail to detect re-infection/relapse.

Of course, the big problem in clarifying the role of syphilis in AIDS is that there is no gold standard for the detection of syphilis - the spirochete T. pallidum is very difficult to culture. Paradoxically, it may be a finding in the field of another disease caused by spirochetes - Lyme disease - that holds the key to getting syphilis researchers interested in improving the methods for detecting the disease in AIDS patients.

Both the detection and the treatment of Lyme, one of several diseases spread by insects called deer ticks, are surrounded by controversy. As Dr. Kenneth Liegner from the New York Medical Center in Armonk, New York, pointed out to me, many academicians have staked their reputations on the view that Lyme disease is easily diagnosed and cured. However Liegner is convinced, based on many years of clinical experience, that many patients are difficult to diagnose and there may be no way of curing this infection with currently available methods. Professor James N. Miller (right), an expert in both Lyme disease and syphilis at the Department of Microbiology and Immunology, UCLA School of Medicine, agrees that there's not a clear consensus with respect to how to diagnose Lyme disease, adding the blood tests for Lyme have problems in terms of their specificity, sensitivity and reproducibility.

In a controversial paper entitled "A Proposal for the Reliable Culture of Borrelia burgdorferi from Patients with Chronic Lyme Disease, Even from Those Previously Aggressively Treated", published in the November/December 1998 issue of the medical journal Infection (vol. 26, p. 364-367), a group of American researchers describe a complex technique with which they claim to be able to culture previously undetectable Lyme bacteria from the blood of patients with chronic disease.

I've not been able to quiz Phillips in detail about this work, but I did speak to one of his co-authors, Dr. Hamid Moayad, a neurologist from Fort Worth, Texas, who says this new culturing technique, if it becomes widely accepted, "would actually be the gold standard for diagnosis of Lyme disease, because if you are able to culture the bacteria, then no one can doubt the diagnosis any more, especially in the chronic late stages, which the controversy is about". This article, he says, "proves without a shadow of a doubt that it is a chronic infection - chronic Lyme means chronic infection."

Moayad first heard from Phillips in 1997, through their joint association with Lida Holmes Mattman, a Wayne State University microbiologist well-known for her work on stealth pathogens, and who now runs a private lab in a suburb of Detroit. Mattman says the Infection paper developed because Moayad and Phillips both had many Lyme patients, and supplied her with blood samples, out of which she allegedly grew the Lyme bacterium in laboratory cultures, where it could be studied indefinitely.

The material used to grow the Lyme bacterium - the culture medium - has to be ingeniously designed, and includes sugar, starch and a variety of laboratory chemicals (along with Detroit tap water). Using this special culture medium, Mattman claims to be able to grow the Lyme bacterium from the blood of patients with suspected chronic Lyme disease - patients who had been missed by the standard tests.

But many of the experts I have talked to can't understand how the Lyme bacteria could still persist in the blood of patients who have been aggressively treated with antibiotics for months, even years. The answer may lie in a very important idea that surrounds the work of Phillips and colleagues: disease-causing bacteria may be able to transform themselves into something that's resistant to standard treatment and invisible to the body's immune system.

Mattman has spent many decades studying all different forms that bacteria can take, publishing a textbook entitled Cell-Wall Deficient Forms, published by CRC Press LLC. Mattman says the first course on microbiology teaches everyone that bacteria have only a few shapes - balls, either in ones, twos or in chains (streptococci); rods or sticks (the well-known E. coli bacteria), and snakes (spirochetes and other spiral-shaped organisms).

Spirochetal L-forms in MS patient (Photo: Lida Holmes Mattman)

One of those is the Lyme-causing spirochete - Borrelia burgdorferi - which Mattman, Phillips, and Moayad (not to mention a number of European researchers) say can take on a form different than the usual coiled spiral shape characteristic of the spirochete family to which it belongs. Indeed, there's a lot of evidence, especially from the older syphilis literature, that suggests spirochetes can form what are called "cysts", containing tiny granules that may form the basis for new "daughter" spirochetes.

The precedent for much of this thinking came from work in other pathogenic spirochetal diseases like leptospiroses and the human treponematoses (the venereal treponematosis being syphilis). In the 1950s, the electron microscopists in several American research centers, as well as in Russia and in Budapest, demonstrated what they thought was unequivocal cell-wall deficient survival mechanisms for T. pallidum to explain the latency and many of the relapsing phenomenona in clinical syphilis.

  Today, support for this concept comes from none other than the discoverer of the B. burgdorferi himself, Willy Burgdorfer, a microbiologist with the U.S. National Institutes of Health (NIH), and editor-in-chief of the Journal of Spirochetal & Tick-Borne Diseases.

Burgdorfer gave the keynote address at the 12th International Conference on Lyme Disease and Other Spirochetal and Tick-Borne Disorders - The Complexity of Vector-borne Spirochetes (Borrelia spp) - which explored the idea of spirochete cysts "hiding" in the human body.

Stock Strain of Borrelia Burgdorferi (B31) has pleomorphic colonies (click on image for full-size view) (Photo: Lida Holmes Mattman)

Burgdorfer noted this was once called "granulation theory" and was considered as the organism's mode of reproduction. He's not sure whether the cyst forms represent a true propagative mechanism, but he is confident they represent a complex defense mechanism of the organism in a human host.

Asked what implications this way of looking at spirochetes has for the diagnosis of Lyme disease, Burgdorfer told me, "It's probably the answer for the difficulties we have in diagnosing Lyme and other spirochetal diseases, in that we can demonstrate these cysts by microscopy, and once they are in the tissues of the patient, we can no longer detect them. It is quite possible that this material that we cannot see by microscopy is responsible for producing prolonged and chronic disease."

Indeed, many Lyme disease physicians have dismissed their patients' neurologic symptoms, and will now have to reconsider that indeed neuroborreliosis is untreatable with antibiotics, and indeed the very antibiotics - the beta-lactams - probably induce the cell-wall deficient form, referred to as an L-form/cyst/mycoplasma-like form.

I was curious as to whether Burgdorfer had seen the Phillips paper, which purports to have reliably identified this same "cyst" - or "bleb" material, as it's called - from the blood of late-stage Lyme patients.

Borrelia burgdorferi spherical bodies induced by penicillin after 48h of incubation (MKP-medium, 33ºC): two spherical bodies adhering with a slight connection in the coil of a Borrelia organism. From "Formation and Cultivation of Borrelia burgdorferi Spheroplast-L-Form Variants." Infection 24(3):218-225, 1996.

He hadn't seen it, but when shown a copy, responded immediately: "This is exactly what I'm talking about".

He pointed to the electron microscope photographs included in the paper (left). "Here you see blebs, and these are shed by the mother spirochetes, and they are thought the germinative units out of which the daughter spirochetes develop. I personally believe that the significance of these blebs as the agent responsible for prolonged and chronic disease is very important, and it may be the answer to the diagnosis of these chronic diseases such as Lyme disease - because that's what we are looking for: something that produces diseases long after the initial treatment, and then relapse occurs after several months - or years - and the question is: where did this relapse come from? Well, it may come from these surviving crystals or bleb material that is in the tissue, and it stays there until the antibiotic or immune pressure is gone, and then when the conditions are right for its further development, they develop into typical spirochetes again."

A view of Spirochaeta pallida under the electron microscope showing continuous envelope or membrane; also end-knob. (from Wile, U.J. Picard, R.G. and Kearny, E.B.. The Morphology of Spirochaeta Pallida in the Electron Microscope. J.A.M.A. 119 (1942), p. 880

It is very difficult, he said, to see these blebs or these morphologically atypical spirochetes microscopically in tissues. "You don't see a typical long spirochete - all you see is granules, and atypical material, and to demonstrate that this is actively living material is very difficult."

Spirochaeta pallida as seen with the electron microscope, with two lateral protrusions, one of which is shown very clearly to be made up of small spherical bodies. Meierowsky's observation that a stalk often carries more often than one minute bud led him to conclude that the buds have the property of dividing. (Strain P126B (88a) X 14,000.) (from Morton, H. E. and Anderson, T. F. Some Morphologic Features of the Nichols Strain of Treponema Pallidum as Revealed by the Electron Microscope. Am. J. Syph., Gonor., and Ven. Dis. 26 (1942), p. 565)

In his talk, Burgdorfer reminded the audience that the notion of a spirochetal life cycle was first proposed in the syphilis literature long ago, which described how Treponema pallidum is not only present as a classical, beautiful spirochetal structure but it may also adopt "cyst-like" forms. Liegner notes "one couldn't even recognize these as having anything to do with syphilis or spirochetes unless one had made a very detailed study of the nature of the syphilis organism in tissues under various conditions."

Miller, who has worked for nearly half a century with the spirochetes of both Lyme and syphilis, says "There's never been any definitive proof that the so-called cyst-like forms of T. pallidum occur in vivo, either in an animal or human." He admits that when the fluid from lymph nodes of syphilitic rabbits - in which he could not find any organisms - were injected into rabbits who had never been exposed to the disease, the newly-infected animals developed the disease, complete with classic spirochete organisms. But he can't say whether there were cyst-like forms present in the lymph nodes of the original rabbits, or simply very few spirochetes that he could not detect.

To Scythes and I, this work is very important for understanding how latent syphilis can survive in a host with the treponemes being so sparse. We feel this potentially revolutionary technique for culturing previously undetected spirochetes in the blood of patients suffering from chronic Lyme disease could serve as an important precedent for the detection of undiagnosed chronic syphilis among AIDS patients, which is why we wrote and presented a poster at the same Lyme conference to that effect, entitled "Implications of the Recent Lyme Culture Technique for the Diagnosis of Syphilis"- click on the image of me above to read the full paper, which includes a dozen illustrations and 61 references, or click here to read the press release we prepared.

We were honoured when Burgdorfer himself wandered up to our poster, recognizing many of our illustrations. I asked him if everything that he's said about Borrelia would apply to Treponema as well.

"Of course", he says. "As far the ability of T. pallidum to undergo development into cyst forms, that has already been proven."

Plate 14 (from DeLamater, E. D. et al. Studies on the Life Cycle of Spirochetes. III. The Life Cycle of the Nichols Pathogenic Treponema Pallidum in the Rabbit Testis As Seen by Phase Contrast Microscopy. J. Exp. Med. 92 (1950), p. 246) (click on image for detailed explanation)

"And of course, in the old literature, these formations of the spirochetes were considered to be a degeneration process due to the fact that spirochetes cannot survive under these conditions and therefore they will eventually die and no longer develop. But in those days all the investigators had was the ordinary microscope to investigate what the spirochetes looked like. And then once the spirochete developed into these cyst forms, they were no longer detectable by the ordinary microscope. So, for them, that was the end of the spirochetes and they called it degeneration."

"Yet there was that other group of scientists who said, 'No, all these are are a phase in the complex development from a mother spirochete to a daughter spirochete'. Still today, both theories have a lot of supporters. A lot of scientists say it has nothing to do with the further development, it has nothing to do with the immune process, and these are organisms that degenerate and are no longer able and capable of reverting to actively developing daughter spirochetes. Yet there is now mounting evidence of this complex development, and the ability of the organism to withstand unfavourable conditions."

A few days after the Lyme conference, I went to visit biologist Lynn Margulis (right) at the University of Massachusetts at Amherst. She is famous as one of the leading proponents of the Gaia Hypothesis - the idea that the earth as a whole acts like a gigantic living organism. Her concepts of symbiosis - the natural co-existence and co-development of different organisms - have transformed the study of evolution.

Part of Dr. Margulis' work involves looking at microscopic spirochetes found in the natural environment. Margulis says that free living spirochetes set a precedent, in the sense that they can survive dessication. She has gone into their natural habitat and removed muds for as long a period as a few years - muds which look to the naked eye to be dry.

"We put that mud material back into supportive media for spirochetes and we see spirochetes come out - the spirochete form; which suggests that spirochetes are hiding in a form that's not the swimming spirochete. Now, if we take those spirochetes that look fine and healthy, and we put them into any kind of media that is threatening to them, they immediately round up, they pull in their bodies. And this is active: this is not a falling apart, like when you hit them with alcohol or something like that. It's not a lysis, it's not a falling apart, it's not immediate death like you could easily cause immediate death by lots of negative conditions, like too much acid and so on. It's not the extreme that you see in immediate death but quite the contrary: you see active cells ballooning out their membranes, actively pulling in their bodies."

A videotape of spirochetes called Spirosymplokos (found in the hindguts of desert termites) shows the vigorous recoiling of the organisms into little balls, a remarkable behaviour to watch in real time as Margulis explains what we're seeing.

"Making these membraneous structures, that is making these non-spirochetal type morphologies, is a normal part of the life history of spirochete bacteria. It's likely that organisms like Borrelia and Treponema that have been found in human tissue can burrow into tissue and make the same kind of resistant bodies, and wait and come out when conditions are suitable twenty years later. I mean, I've got a couple of years in mud, why not in human bodies?"

Of course, T. pallidum may not persist in all - or even any - AIDS cases, since such an injury to immune system genetics could easily proceed independently of its triggers, a scenario for which there are many precedents in auto-immune diseases (although we still need to explain our results showing the selective and rapid disappearance of treponemal antibody in people who then uniformly go on to develop AIDS).

Even the U.S. Centers for Disease Control (CDC) stated for years that serologic tests for syphilis "fail to assist in the diagnosis of congenital syphilis, reinfections with T. pallidum, neurosyphilis, and infections with other pathogenic treponemes" and that "the role of current syphilis diagnostic tests in the diagnosis of syphilis among HIV-infected persons has been questioned" in its online fact sheet.

But in the summer of 2000, the CDC reversed its stand, and on July 10 - co-incidentally following the extended online debate about syphilis serology Scythes and I had with key AIDS dissidents (a debate which was sent to many CDC scientists) - the agency actually altered their online fact sheet on syphilis in order to remove any doubts whatsoever about the reliability of serologic tests for syphilis. This deletion of major concerns over the diagnosis of a deadly disease is simply bizarre, and the revised version's new assertion - namely that the levels of the non-specific antibodies picked up by screen tests usually rise when reinfection occurs - flies in the face of 100 years of published evidence suggesting these tests are quite unreliable beyond the initial primary infection.

We cited a small part of this evidence in an August 7, 2000 communication to Dr. Vickie Pope of the CDC's Bacterial STD Branch (right) and several dozen other HIV and STD researchers. Pope shot back with a four-sentence reply that simply did not address any of the specific concerns we raised, followed by an irritating one-line message from Professor Daniel Musher (left), a leading American syphilis authority at the Veteran Affairs Hospital in Houston, Texas, simply agreeing with Pope's canned response.

This was particularly vexing, given that in 1990, Musher and colleagues tested 36 HIV-positive men for syphilis, looking for a specific class of antibody known as IgM (the presence of IgM antibody against T. pallidum is usually used to help determine whether newborn babies have an active syphilis infection or have just inherited antibodies from their mother). 19 out of the 36 men showed this kind of antibody, suggesting an unresolved syphilis infection. Interestingly, only half of them had ever received a diagnosis of syphilis in the past. This led Musher et al. to conclude in the Annals of Internal Medicine:

"A substantial proportion of HIV-infected men may have unrecognized, latent, inadequately treated syphilis. These findings support more aggressive treatment of T. pallidum infection in this patient population." (Musher D.M., Hamill RJ, Baughn RE. "Effect of human immunodeficiency virus (HIV) infection on the course of syphilis and on the response to treatment." Annals of Internal Medicine, vol. 113 (1990), p. 872-881)

But when I up caught with Musher in September 2000, at the Interscience Conference on Anti-Microbial Agents and Chemotherapy (ICAAC) in Toronto, his doubts appeared to have disappeared. In fact, he actually denied ever writing the above words when I quoted them to him - a denial he would have to retract when I brought him the actual paper the following day. You can listen to the interview/argument I had with him in Real Audio. It's clear that Musher had little interest in the questions being raised over the reliability of currently-used serologic tests for syphilis, and simply no interest at all in whether syphilis plays a role in AIDS.

Interestingly enough, the concerns about syphilis as a possible co-factor in AIDS were taken more seriously by Dr. Pope's predecessor at the CDC, namely Sandra Larsen, formerly Chief of Treponemal Research at the federal agency. In an abstract presented at an STD conference in 1991, Larsen wrote that "the clinical manifestations of syphilis, which have taken various forms over the centuries, have now been transformed to mimic the appearance of the opportunistic infections and cancers that may accompany HIV infection, as well as the clinical symptoms of AIDS itself."

In a 1995 taped telephone interview, Larsen acknowledged that Scythes and I had indeed raised fundamental questions about a possible syphilis/HIV interaction that urgently need answering. "We're trying our best to address some of the questions you have raised," Larsen told me. "I think we're just not at a point where we can say anything with certainty. We have a limited budget, and a limited number of people, and we're shrinking daily."

She was surprisingly candid with me: "I really do think you're asking a lot of very hard questions. We're looking at what we can look at now. A lot of it, in the universities, the funding for syphilis has just been not there - it's just been hard to get funding. People feel that syphilis can be controlled with penicillin. I mean, you have to be realistic: syphilis is not in the populations that are the favored populations."

To me, Larsen's last astute comments sums up the whole problem with AIDS research - the people affected by this awful condition - be they gay men, IV drug users, or Africans - are simply not important enough to society as a whole to apply a top-notch, all-encompassing scientific effort to this problem. As a result, we're left with smug, third-rate HIV scientists like Robert Gallo (left) and the particularly arrogant Mark Wainberg (right) running the show. These people were propelled into power in April 1984 by a desperate coalition, consisting of a Reagan administration seeking re-election, drug companies anxious to develop new treatments and vaccines, and thousands of screaming patients desperate for an answer - any answer.

This mammoth HIV research effort is now gobbling up (and wasting, in my view) billions upon billions of dollars of taxpayers money, with no hope of a truly effective long-term treatment or vaccine anywhere on the horizon - and all this without any convincing animal models to demonstrate that the virus can actually do anything to us (SIV in chimps does not behave anything like HIV is said to in humans), nor any proven biological mechanism by which it supposedly does it what we are told it does. The complete failure of the vaccine effort, after nearly two decades of intensive research, should be particularly perplexing to anyone who knows how little DNA material HIV actually consists of, and a bit about the history of vaccines in general, which amply demonstrates that, if HIV was really all there was to AIDS, we should have had an effective vaccine years ago.

Meanwhile, those who know better - the more intelligent, historically-minded STD experts (you know who you are) - just stand by silently and watch all this unfold from their comfy university positions without a raising a voice in protest - unless, of course, they get cornered on the phone, or in person at a conference, by an impatient investigative journalist who's actually read the classical syphilis literature, and understands what terms like "symptomless re-exposure" and "lack of anamnestic response" actually mean in the context of the modern AIDS epidemic.

One day I will publish a list of startling concessions I have extracted from leading American syphilis researchers on these important questions. These scientific admissions will no doubt be of great interest to the many inquiries that will be called in the (distant?) future to investigate how the venerable institutions of Science and Medicine could have got both AIDS and syphilis dreadfully wrong, and why no one basically did anything about it for 20 years (and counting) - despite millions upon millions of deaths, and clearly unsatisfying results from the scientists upon who we depend. But then again, the dead people are not among the favored populations, remember?

To be fair, concerns about syphilis as a possible co-factor in AIDS - or at least an open-mindedness about it - are shared by some syphilis experts in America, including the above-mentioned Sandra Larsen, Noel Rose at Johns Hopkins University, as well as Konrad & Victoria Wicher at the New York State Health Department. Support has also been forthcoming from Austria's highest-placed physician, Anton Luger, and his colleague Bruno Schmidt (left); István Horváth and Nagy Karoly in Budapest; Poland's Jadwiga Podwinska (right); Konstantin Borisenko from Moscow (sadly deceased); Robert Notenboom, former chief serologist, Laboratory Services Branch, Ontario Ministry of Health, and Douglas MacFadden, associate professor of medicine at the University of Toronto.

In fact, none other than the discoverer of HIV itself, Professor Luc Montagnier, has communicated - in private correspondence - an ongoing interest in Scythes' work. In a March 17, 2000 interview in the magazine Frontiers, Montagnier re-iterated his decade-old concern that something more than HIV is involved in AIDS: "We must know whether a virus acts alone or with an accomplice as we try to stop its spread. I have found that HIV on its own does not always cause disease.. Of course, we don't know yet if there is one or many co-factors. I think it is possible another virus could be the culprit; we seek the answer to that."

Of course, Scythes has communicated his concerns - on repeated occasions - to the key American syphilis researchers best in a position to make a fuss about all this, like Justin Radolf (left), formerly of the University of Texas Southwestern Medical Centre, now director of the Center for Microbial Pathogenesis, and a Professor of Microbiology at the University of Connecticut Health Center, and Sheila Lukehart (right), who works at the Department of Pathobiology at the School of Public Health and Community Medicine, University of Washington in Seattle - both of whom Scythes met with again at the Gordon Conference on the Biology of Spirochetes in January 2000 - as well as posting his concerns several times to the Spirochete Research Discussion Group, an electronic mailing list which over a hundred international spirochete researchers subscribe to, but there have been no substantive responses.

Scythes has also written to the Task Force for the Urgent Response to the Epidemics of Sexually Transmitted Diseases in Eastern Europe and Central Asia, based at the WHO Regional Office for Europe, in Copenhagen, to try to interest them in improving syphilis diagnosis to hopefully thereby slow down the rates of new HIV infections in the region. We remain concerned that some variation of these approaches could shed some light on the direction that Eastern European health officials might take, from a practical and affordable public health point of view, to slow the emerging HIV crisis in that part of the world.

Scythes and I have had some online discussions with various people, like New York University epidemiologist Robert Holzman, Australian HIV researcher Leonard Pattenden, Seattle syphilis researcher and Lukehart colleague Wesley Van Voorhis, and Russian AIDS dissident Vladimir Koliadin, but nothing concrete has ever emerged from these discussions in terms of bringing about the necessary research.

We have also directed our attention to South African president Thabo Mbeki, who has infuriated activists, doctors and especially pharmaceutical companies by refusing to offer drugs like AZT to the country's HIV-positive women and by consulting with AIDS dissidents, including David Rasnick, Ph.D. who designs protease inhibitors, the class of substances touted as the latest anti-AIDS miracle drug. In the spring of 2000, Mbeki set up a controversial expert advisory panel, consisting of about 30 persons from Europe, America and Africa, a panel designed, according to an invitation sent out by the South African government to a number of scientists, to "reach consensus on the appropriate ways forward for South Africa in dealing with HIV/AIDS", whose task was/is to review, among other things, "evidence for the viral aetiology of HIV and other concerns regarding the pathogenesis and diagnosis of HIV/AIDS in Africa."

As syphilis may represent a key co-factor in the progression of this syndrome, Scythes and I accordingly wrote to him and his health minister on March 10, 2000, not only to lend our wholehearted support to his timely initiative, but also to voice our hopes that the panel will include a re-investigation of the sensitivity of syphilis serology and the treatment of syphilis in Africa in its attempt to better understand the possible infectious component in AIDS. We added that we would be honoured to participate in the panel's efforts.

Alas, Mbeki didn't take us up on our offer, and the panel had its first meeting on May 6 & 7, 2000 in Pretoria, after which a minority group of dissident scientists issued a brief report and recommendations, stressing lifestyle, drugs and malnutrition as key components of AIDS in Africa - a report to which we responded with our own public point-by point statement, urging the panel not to rule out infectious co-factors in AIDS. Our bold response generated a number of subsequent e-mail exchanges with both orthodox and dissident panel members, and you can read all the back-and-forth communications on an Irish website entitled AidsMyth Dissident News.

You may have noticed that in my speech at the Opening Session of the XIII International AIDS Conference earlier this month, I mentioned the incidence of STDs as one of the conditions that contribute to Africa's health crisis and referred to teenage pregnancies.

I believe that STDs are very relevant to the collapse of immune systems among many Africans, including our own people, and therefore the acquired immune deficiency syndrome.

There are many scientists who have been conducting research into this matter for some time.

One of these, John B. Scythes of Canada has written to the WHO as follows:

"Latent syphilis is chronic active syphilis from the immunological standpoint, and is both more dangerous for immune system genetics and harder to treat than exanthematous late syphilis. Judging from the word of Poland's Jadwiga Podwinska and the late Tom Fitzgerald from Minnesota, a Th2 cytokine pattern begins to predominate in most persons with latent syphilis, and standard treatment does not reverse this phenomenon. Subsequent re-exposure without TH1-driven immunologic anamnesis would lead to the silent re-dissemination of treponemes."

I hope that the international scientific panel on AIDS that we have convened will address the important issue of STD's.

...

Shortly after our exchange with the dissidents on Mbeki's panel, an important scientific presentation was made by officials Neal denHollander and colleagues at the Public Health Laboratory of Ontario, entitled "Treponemal Based Screening for Syphilis—Detecting Latent Cases", at the American Society of Microbiology 2000 Annual Meeting, held May 21-25, 2000, in Los Angeles, California. They found that the use of treponemal antigen-based screening for syphilis - in the form of a new test called the Trep-Chek - identified almost 5% of randomly selected specimens from a downtown Toronto STD clinic as potentially syphilitic, but negative in the standard screening tests, raising serious questions about the reliability of existing tests. I wrote an article about these results, "Syphilis shocker" in the July 27, 2000 edition of NOW Magazine, which was met with a dismissive letter in the following week's issue, "That syphilis mystery not such a mystery", (scroll to bottom of page) by Robert Trow, of Toronto's Hassle Free Clinic (from which most of the samples in the study were taken). 

Whether syphilis ultimately proves to play a role in AIDS or not, there remain pressing unanswered questions that urgently need research funding, with several possible research directions for investigating the possible role of occult syphilis in HIV disease. For example:

• The Phillips/Mattman Lyme culture technique needs to be applied to the T. pallidum/HIV synergy question. As our Lyme paper states, there is a well-published position in the syphilis field, especially from the 1950s and 1960s, during the early period of electron microscopy, that T. pallidum might also have a similar latency mechanism. If this were true for syphilis, then it could imply that antibody techniques and PCR for T. pallidum are insensitive for the late stages of syphilis, as they seem to be for the late stages of Lyme, in light of the genetic homology of these organisms. We think it is incumbent on the American syphilis research community to try this technique on the blood and lymphatics of treponemal antibody-negative and history-negative gay men with AIDS. T. pallidum survives on artificial media only for a few days, so it may be more difficult to coax the L-forms back into virulent T. pallida, but the mere isolation of a spirochete, whether pathogenic or not, would be quite hard to explain and could suggest further genetic probing.
• Another area of possible investigation would be to see how improved antibody tests may play a role in better syphilis diagnosis. To this end, Scythes has tried to interest the Toronto Hospital's Immunodeficiency Clinic in continuing the work he started in the late 1980s with MacFadden, the medical director of the hospital's Western Division HIV Clinic until 1994, alas to no avail. Scythes has suggested using, for perhaps a year, a recombinant antigen-based syphilis antibody detection system, which could be used alongside existing techniques among a gay male population at risk for HIV and syphilis, such as those seeking the services of the Hassle Free Clinic or a downtown physician specializing in HIV/STD care. Ontario's former chief serologist Notenboom, now at Phoenix Bio-Tech Corp in Mississauga, Ontario, has been developing these newer tests and there is a building literature on the improved sensitivity offered by such a system (see Erbelding, E.J. et al., Journal of Infectious Diseases, November 1997, vol. 176(5), pp. 1397-1400, or "Syphilis Serology May Be Misleading in Some HIV-Infected Individuals", Reuters Health Information Services, November 3, 1997).

  The recombinant system compares favourably with existing techniques from the cost point of view. While doctors we know in Vienna and Budapest are now running these new tests on their patients, the HIV and STD interaction pattern in those cities is relatively established, with only a few new syphilis cases each year in each clinic. A project like this needs to be done in an area where syphilis is epidemic, i.e. where there is an emerging, rather than established, pattern of HIV/STD interaction, and needs to be continued for a 5-year period on all follow-up visits, with special emphasis on the response to these antigens in persons with HIV.

  In 1996, Scythes and I submitted a grant application to George Soros' Open Society Institute (OSI), wanting to use funding offered by the philanthropic Hungarian billionaire to to investigate the possible role of latent syphilis in an HIV-infected cohort at the Semmelweis outpatient Dermatology clinic (OBNI) in Budapest, with the permission of the clinic. The grant application was also rejected - rather surprising, given that this novel research would be conducted on Soros' own home turf. We have also written to Luc Montagnier to see whether he might lend his support to the development of better syphilis screening protocols, using recombinant antigen-based assays, in the regions of Africa where there are new "HIV" cases emerging, both at steady/endemic and epidemic rates.

• There's also the possibility of reviving a classical blastogenesis technique, which is a way of quantifying cellular or tissue immunologic memory. This memory could be measured by in vivo skin testing, but generally this is considered too risky, except in certain well-tried areas, such as TB recall or allergy management. Therefore, in vitro stimulation of the PBMC became a standard procedure for many years in assessing the prevalence of exposure to infectious diseases, and has been used as well in the HIV field to show prior exposure to the virus, even in people who make no antibody to it.

  Back in 1993, MacFadden, his clinical associate Richard Fralick, post-doc fellow David Phipps and Scythes became intrigued by the idea of trying in vitro detection of Th1/CD4 DTH priming, using sonicated T. pallidum antigen on the PBMCs of HIV-infected persons. They wanted to attempt to quantify a response which would suggest that these people had been exposed to syphilis but no longer reacted appropriately at the antibody level. Was there a peripheral inhibitory effect in the serum which made the antibody tests go negative? This was a very important question, because they had seen so many problems with treponemal tests associated almost exclusively with HIV infection. Other centers, both in North America and Europe, likewise found these anomalies, but the Toronto team went further and found a correlation with a selective loss of treponemal antibody and subsequent severe immune suppression.

  In the fall of 1994, Fralick and Phipps applied for a research grant from the Canadian Foundation for AIDS Research (CANFAR), for $10,000 to stimulate the mononuclear buffy cell layer in 90 HIV+ men without AIDS, with CD4 cell counts of 300 or less, and measure priming in vitro by thymidine uptake and IL-2 production. The idea was to get the primed cells away from the serum factors (cytokines), so they can show a past syphilis history and ongoing interactions. The grant, which had lots of written support from GPs in this area, was turned down as "low priority research" by CANFAR reviewers, whose terse one-page dismissal suggested a lack of familiarity with many of the above concerns.

• Animal re-inoculation experiments, conducted in the first half of this century, should also be repeated in the AIDS era with modern immunologic tools and proper follow-up, with a view to possibly producing an AIDS model secondary to repeated challenges with T. pallidum in the mouse, rabbit or preferably chimpanzee, as their genetic make-up is the closest to humans. Monoclonal antibodies to count CD4 and CD8 cell numbers and ratios are available for rabbits, mice and chimpanzees - all developed for an AIDS animal model secondary to HIV infection. Of course, HIV does not induce AIDS in any animal model to date, save a chimp or two, and it's not clear whether other factors associated with the stress of captivity may have been involved. Repeated syphilis exposure in these models - not yet tried - may well lead to immune deviation against the CD4 TH1 DTH, which is the classical AIDS immunology.

  HIV has failed, at any dose, to do any harm in our closest phenotypic relatives, and syphilis was always dangerous for primates in experimental systems. Alan Chesney from Johns Hopkins stated in the 1920s and 1930s that primates often used to die prematurely of other infections (not the direct effects of syphilis, in other words) if re-inoculated with syphilitic tissues from other animals with early disease (Chesney, Alan. Immunity in Syphilis. Baltimore: Williams and Wilkins Co., 1927), but they were discarded, as this possible 1920s AIDS model was not understood as relevant to the welfare of humankind. In the 1960s, Dr. Chandler of the CDC found quite by accident that four gang-housed owl monkeys developed fatal PCP after one of them had been inoculated with T. pallidum (Arch. Path. Lab Med. (March 1976) vol. 100, p. 163).

  Animal syphilis frankly has more potential for characterizing AIDS than any model with HIV. It may be possible to generate an AIDS animal model very easily if the animals are infected with syphilis three months apart, and if HIV is included in the experiment, chronic syphilis may allow the HIV infection to become activated, as several papers suggest (Theus SA et al. "Treponema pallidum, lipoproteins, and synthetic lipoprotein analogues induce human immunodeficiency virus type 1 gene expression in monocytes via NF-kappaB activation." J. Infect. Dis. 177: 941-50 (1998); Tseng, C. K. et al. "Syphilis superinfection activates expression of human immunodeficiency virus I in latently infected rabbits." Am. J. Path., vol. 138 (1991), p. 1149-64).

• On the treatment front, there remains the intriguing possibility that AIDS might be treated by an expanded placental stem cell infusion. Back in 1993, an unsuccessful attempt was made to xenograft baboon T-cells, or their precursors, into an AIDS patient, the thinking being that baboon T-cells would be resistant to HIV. But most HIV-negative, healthy humans seem to be capable of resisting HIV (Immunology Today, vol. 14, no. 3 (1993), pp. 107-111; Immunology Today, vol. 17, no. 1 (1996), p. 21-24). As the degree of required HLA compatibility becomes better understood from all the work in the globinopathies and lymphomas/leukaemias, stem cell infusions from a suitable donor - or maybe eventually from expanded pluripotent stem cells in vitro - may help to revert the chronic active HIV expression (seen in AIDS) back into the HIV-resistant (surface antigen/Western blot negative) immune profile discussed by the immunologists Mario Clerici and George Shearer in the papers cited above, similar to the profile of HBV antibody responses as immunity develops in most healthy persons.

  The larger question is: as transplantation techniques and availability seem to be making large strides, would an affordable placental stem cell transplant possibly result in the patient becoming HIV-negative, at least in the conventional HIV screening tests? They would likely remain ab-positive to core antigens, and as well retain a strong cellular response to surface proteins, a response that has already been qualified and quantified by classical blastogenesis, anti-idiotype antibody and interleukin detections. This latter profile describes thousands of persons who remain persistently HIV-negative despite documented and often repeated exposure to strains of HIV identical to those found in persons with full-blown AIDS, i.e. in HIV-discordant couples. This resistant profile is also seen in other diseases.

  At least 5 possible scenarios can be imagined as a consequence of a reconstituted immune system in an HIV-case, perhaps in some combination: 1) cure of HIV disease 2) HIV reinfection of the new lineages 3) re-awakened early (and treatable) syphilis 4) no change in immune status due to untreatable chronic syphilis 5) transplantation problems (graft rejection or GVHD). Yes, lympho-poetic replacement is a dangerous thing to do, but AIDS is dangerous too. Are we just going to keep devising more and more expensive anti-HIV drugs and vaccines of borderline efficacy, or are we going to try something new?

So there it is - a compelling alternative paradigm rooted in historical, microbiological and immunological precedents, plenty of sensible research directions, and yet next to no interest - at least on the part of the American and Canadian syphilis research communities; the massively-entrenched heavily-funded HIV/AIDS infrastructure of government and corporate scientists (obviously); well-meaning HIV primary care doctors; otherwise noisy and demanding AIDS activists; normally critical investigative media outlets (with the thankful exception of CBC Radio's IDEAS and Toronto's NOW Magazine); even most of the other AIDS dissidents - including those right here in Toronto - and I have ten years worth of personal correspondence with all those constituencies to prove it! I also have thoughtful conversations with, and letters from, intelligent people - many of whom have no personal stake in the AIDS debate - who agree there are good questions here, while other - in some cases influential - people who took a strong interest in these arguments have passed away, alas, including such people as the tireless activist and patient Michael Callen, British film-maker Stuart Marshall, and writer James Jerome - may their brave souls rest in peace.

John Scythes and I can only hope that some day a more refined historical perspective may eventually prevail over the current - and in our view misguided - direction of AIDS research. If you're a journalist and interested in doing a story about this, write to me at <webmail@colman.net>- it's time someone else sunk their teeth into this. If you're more a scientist/doctor-type and want to have a more technical discussion about research possibilities, you should drop a note to Scythes at <jscythes@infinity.net>as well.

I have also set up a special electronic mailing list to discuss all this evidence suggesting that chronic latent syphilis is a major co-factor in HIV activation and disease progression in sexually-acquired AIDS. To subscribe, go to http://health.groups.yahoo.com/group/AIDSsyphilis/join. Before posting to the list, it would be a good idea to familiarize yourself with what little has already been posted to the list - at the publicly available online archives at http://health.groups.yahoo.com/group/AIDSsyphilis/messages - as well as the considerable material already posted online, both linked from this page and as found at the extensive web site to accompany the "Deja Vu: AIDS in Historical Perspective" series - at http://www.cbc.ca/ideas/features/Aids/ - a site which features audio excerpts from the program, as well as links to published abstracts and other miscellaneous communications.

The list welcomes messages from anyone interested in furthering research on the possible AIDS/syphilis connection, by posting personal observations, news items, new (and old) scientific papers and abstracts, conference announcements, web links, etc., etc. Contributions from medical professionals, especially those studying the immunopathogenesis of chronic bacterial infections - how nasty bugs affect your immune system, basically - are most welcome. Any lab scientists with access to the appropriate facilities to conduct the research described above are especially welcome to get in touch. The list is moderated, but only messages that are either inflammatory or clearly at odds with the intent of the list will be subject to screening. The hope is that this online medium will serve as an important conduit for resolving fundamental questions about one of the deadliest infections known to humanity, and its relationship to the latest pandemic facing the planet.  

-Colman Jones, December 2000
webmail@colman.net