Patricia Nell Warren

HIV's Politically Invisible Cousins: HTLV-1 and -2

Filed By Patricia Nell Warren | September 19, 2009 2:00 PM | comments

Filed in: Living
Tags: discovery of HIV, drug abuse, emerging infectious diseases, HIV co-infection, HIV/AIDS, Luc Montagnier, retroviruses, Robert Gallo

To explore the reasons why these formidable relatives of HIV have such a scanty public profile in the U.S., we need to take a detective's look back over some AIDS history.

In 1983, French researcher Luc Montagnier and a colleague discovered a virus that they called lymphodenopathy-associated virus, or LAV. Then in 1984, U.S. researcher Robert Gallo announced that he had discovered something similar that he called human T-lymphotrophic virus type 3. Subsequently HTLV-3 was renamed the human immunodeficiency virus (HIV). Gallo and Montagnier both claimed credit for discovering HIV. After years of French-American legal strife over the credit, most authorities agreed that Montagnier and his colleague had discovered the HIV virus first -- and the Frenchmen were given the Nobel Prize.

But this thumbnail history leaves us with questions. Before HTLV-3, came HTLV-1 and -2. What diseases do they cause? What have so few Americans heard of them...and what happened to obscure them in public-health policy?

Answers to these questions reveal a story that raises some serious questions about government policy on infectious disease.

The story starts in the 1970s, when Gallo's lab had been pursuing the conviction that viruses cause human cancers, especially leukemias and lymphomas, which are blood cancers originating in the bone marrow or lymphatic tissues. Scientists already knew that a specific genus, the retroviruses, caused leukemias in some animals -- notably primates and domestic cats. Retroviruses are a unique family because their mode of invading cells and reproducing -- the way in which they process their RNA into DNA of the host cell -- is different from that of most other viruses.

A Tangled Web of Discoveries

In 1978, Gallo's people found the first-in-history human retrovirus in a human patient with lymphoma. By 1981 Gallo had named it HTLV-1, but he couldn't prove that the retrovirus actually caused lymphoma. That breakthrough was made by Japanese researchers, who nailed HTLV-1 as the cause of adult T-cell leukemia, which was first noted in Japan and was becoming endemic there. HTLV-1 was later linked to both lymphoma and leukemia, as well as certain crippling disorders of the central nervous system, and possibly multiple sclerosis.

In 1982 Gallo discovered a related retrovirus that he named HTLV-2. Eventually a few studies linked it to a specific disorder -- hairy-cell leukemia. Meanwhile, in 1986 a second sub-type of HIV was identified in West Africa. So far, that region is mainly where the variant is found. The NIH refers to this one as both HIV-2 and HTLV-4.

Scientists have noted differences -- and also similarities -- between HTLV-1/2 and HTLV-3/4. Authors George W. Lowis, Edwin Van Teulingen and William Sheremata discuss these in their article "AIDS in Developing Countries: A Comparative Epidemiologic Analysis." According to them, HTLV-III and IV "were renamed human immunodeficiency virus (HIV) since they differ significantly in their structure and in the pathology of the diseases they cause. ...Despite these important differences, the four members of the HTLV family have sole common epidemiologic features in that: (a) they are exogenous human infecting viruses and (b) their transmission occurs by whole blood or its derivatives and through sexual intercourse." HIV-2/HTLV-4 is an oddball member of the family, because it shares two proteins with HTLV-1 and -2.

Science did note that HTLV-1 progresses to full-blown disease much more slowly than HIV does. Sometimes 10 or 20 years can go by before T-cell leukemia or lymphoma actually develops --and it does this in perhaps 1 out of every 20 carriers. But healthy carriers are able to transmit the HTLV viruses to others, by the same routes as HIV is said to be transmitted, including blood transfusion. By 1983, the CDC even knew that a certain percentage of HIV-positive persons were co-infected with HTLV-1 and -2.

Today, HTLV-1 is described as endemic in Japan, parts of Africa, the Caribbean and South America. But according to Journal of Clinical Virology, "HTLV-2 has a worldwide distribution and is epidemic among injection drug users." This means that many drug-users can be co-infected with HTLV-2. In the U.S., statistics on the incidence of both viruses are hard to find. Yet with all the immigration both legal and illegal that is streaming into the U.S., and the drug-using risk groups being so numerous in our crowded prisons, where infectious organisms are spreading like wildfire, it's possible that there are way more HTLV-1 and HTLV-2 carriers than our government knows.

Yet a decision was evidently made, at the highest levels of government, to soft-pedal the public positioning on HTLV-1 and -2. I've been wondering why.

The Question of Treatments

The search for HIV treatments has constituted high drama for the medical and media worlds. AZT had been developed in 1964 as a type of chemotherapy for cancer, but was shelved because of its high toxicity. But when AIDS came along and there was an outcry for treatment, AZT was hauled off the shelf and fast-tracked to market by the FDA. Next came a whole spate of different groups of new drugs, many of which are also problematical as to side effects. A parallel effort has been the work by various researchers to develop an AIDS vaccine.

But what of treatment for the diseases caused by these two HTLV viruses?

According to the Johns Hopkins HIV Guide, which has a section on the two HTLV viruses, there is "no evidence for benefit of antiviral therapy" for those who have asymptomatic infections. Says the Guide: "HTLV genome [is] integrated into host DNA; therefore, eradication [is] probably not possible." This is radically different advice than given to HIV+ people who are still asymptomatic, for whom early treatment -- HAART -- has been advised.

For those who do develop disease, treatment for adult T-cell leukemia and lymphoma is iffy. These are aggressive and fast-moving malignant disorders -- most patients survive less than a year. Researchers do report some cases of patients who successfully undergo standard chemotherapy and bone-marrow transplants, and who were able to go on living in complete recession.

But the outlook for treating hairy-cell leukemia is apparently more optimistic. New England Journal of Medicine has reported "lasting remissions in hairy-cell leukemia induced by a single infusion of 2-chlorodeoxyadenosine." This infusion is intravenous, and lasts one week. The drug, approved by FDA in 1993 under the brand name Leustatin, was developed by Ortho Biotech.

Leustatin is also being used for treating other leukemias and MS. However, with its cost running at perhaps $800 a month, this is not likely a drug that will handily be available for at-risk demographics in the U.S. (since injection drug-users are often low-income or homeless people). Nor would it be easily affordable in developing parts of the world, where a poor family might earn way less than $800 a year.

Hard-to-Find Information

Though many scientists agree that serious diseases are caused by HTLV-1 and -2, you have to look hard to find mention of them at the CDC website. Even T-cell leukemia and lymphoma are not listed in the CDC's prominent alphabetical index of infectious diseases, though they are caused by infectious organisms.

Instead, T-cell lymphoma/leukemia and these two viruses are buried in CDC's "search results." But if you look there, you do find a healthy literature on both viruses. There's a 2006 article by Siobhán M. O'Connor, Christopher E. Taylor, and James M. Hughes, who tell us, "Evidence now confirms that noncommunicable chronic diseases can stem from infectious agents." The authors mention "three very different outcomes of human T-cell lymphotropic virus type 1 (HTLV-1) infection: acute T-leukemia/lymphoma, tropical spastic paraparesis/HTLV-1-associated myelopathy, and chronic arthropathy."

Tropical spastic paraparesis/HAM is one of the neurological disorders associated with -1 -- it results in progressive crippling weakness of the lower limbs.

Also buried there is an article stating, "HTLV-1 infection in the United States appears to be rare. Although little serologic data exist, prevalence of infection is thought to be highest among blacks living in the Southeast." Yet the article goes on to say, " A prevalence rate of 30% has been found among black intravenous drug abusers in New Jersey, and a rate of 49% has been found in a similar group in New Orleans (8). It is possible that prevalence of infection is increasing in this risk group." Forty-nine and 30 percent are pretty hefty percentages for a virus that is supposedly "rare."

Another CDC abstract says, "Researchers found that 6.7 percent of 1,305 prostitutes surveyed in eight cities between 1986 and 1988 were infected with HTLV-1 or HTLV-2, a related virus. Public health authorities are increasingly concerned with the prevalence of HTLV-1, which is probably transmitted to prostitutes via sex with IV drug users."

Elsewhere, the American Cancer Society sheds a bit more light -- but not much. For 2007 in the U.S., they reported 19,730 lymphoma deaths in 2006, along with 21,790 deaths from leukemia. But all the different forms of leukemia and lymphoma are lumped together, making it difficult to get a profile on the numbers of HTLV-1 caused deaths. The ACS explains that often it is difficult to get exact information on a cancer casualty's cause of death.

But if we posit that the 1 in 20 figure is correct, and that 10,000 of those 21,790 annual deaths are due to the adult T-cell variety, that means that possibly 200,000 Americans would be HTLV-1 positives.

Motive for a Blood Test

Alarming risk-group statistics like these may have motivated the U.S. to quietly develop an antibody test for both viruses. In 1988, just as quietly, the government began screening its blood supply for HTLV-1 and -2. The government also barred organ donations by people infected with the two HTLVs. So we have to wonder -- why the apparent choice of a low profile on viruses that the U.S. considers enough of a threat to screen blood for? Especially in the case of HTLV-2, whose link to disease is questioned by some?

The government's official position was that both viruses were "rare" in the U.S. Yet just a year later, in 1989, the New York Times published a story about some new surveys that were termed "frightening" by David Golde, who worked with Gallo on discovering HTLV-2 in 1982. The story was headlined VIRUS THAT MAY CAUSE LEUKEMIA IS SPREADING AMONG DRUG ADDICTS.

In the article, the Times said: "The virus, HTLV-II, ... has been found in about 20 percent of a group of drug addicts in New Orleans, from 4 percent to 10 percent of a group of drug users in New York, and 20 percent of a group of New York drug addicts who were also suffering from AIDS. A preliminary survey of blood donors in the San Francisco area found that the virus, though very rare, was more widespread than the AIDS virus. Another survey found HTLV-II more prevalent in blood donors in Los Angeles and New Orleans than the results reported from San Francisco."

This Times story about a "rare" virus infecting hundreds of addicts and blood donors, produced only a ripple -- compared to the tidal wave of national panic that had been set off by the Times's now-famous 1981 story headlined RARE CANCER SEEN IN 41 HOMOSEXUALS.

Global Threat?

Today the U.S.'s low profile on HTLV-1 and -2 extends to its global views. The National Institute of Allergy and Infectious Diseases (NIAID) maintains a detailed list of emerging and re-emerging diseases that have global implications for us because of immigration, trade, tourism and terrorism. NIAID's list can be found online -- but it doesn't mention either HTLV-1 or -2.

Outside of the U.S., however, HTLV-1 and 2 are taken more seriously. They have gotten a high profile on the World Health Organization's global list of dozens of emerging infectious diseases that have been recognized since 1973, when the list was first developed. The global list has lengthened to 36, with SARS and swine flu being recent additions. The two "cousin retroviruses" were right there on the WHO list in company with pathogens that cause scary things like Ebola, Lassa fever and hemorrhagic fever. As I write this, the list is headlined in the UN Chronicle

According to Blood Magazine, "Currently, the estimated number of people infected with HTLV-I worldwide is between 15 and 25 million."

Fifteen to 25 million is a lot of people who are capable of transmitting the virus to others -- and those others then have no idea that they might be among those 1-in-20s who will develop a devastating, possibly fatal illness. So...since there is global cause for concern, why didn't the U.S. public get told more about HTLV-1 and -2 over the years?

A Look at Co-Infected PWAs

Did the government soft-pedal HTLV-1 and -2 because it was reacting rapidly to the panic caused by the emergence of AIDS? Because it didn't want to rock the boat by mentioning other retroviruses that are related to HIV?

Eventually the CDC did publish guidelines for the HTLVs, in which the government's schizoid position on the HTLVs is visible. The guidelines are very emphatic that blood donors who test positive for either retrovirus "should be told that [it] is not the AIDS virus, that it does not cause AIDS, and that AIDS is caused by a different virus called HIV." Nevertheless CDC recommendations for HTLVs are almost as stringent as those for HIV -- positives should use condoms, refrain from donating semen and breastfeeding, etc. So the agency is clearly anxious that these retroviruses not be transmitted. Yet the guidelines insist that no link between HTLV-2 and any infectious disease has been proven. So...if there is no proof, why the need for a CDC dictum on HTLV-2?

Today it's still hard to find official estimates of how many Americans are carriers of the HTLVs, or co-infected with HIV.

It's true that CDC, NIAID and NIH have talked a great deal about "co-factors" in AIDS -- especially those that are caused by unrelated organisms, such as tuberculosis, syphilis, Kaposi's sarcoma -- pathogens whose activity in the body could make the HIV+ person more vulnerable to the development of full-blown AIDS. But co-factors that are caused by retroviruses related to HIV might have been a different matter. Was the government concerned that the public would become confused about which organism was actually killing people?

Through the late 1980s and into the '90s, quite a few researchers looked at HIV+ persons who were co-infected with either or both of the HTLV viruses, trying to get a bead on exactly how the HTLVs might impact the history of HIV in each body. But different studies didn't always agree.

Italian researchers, in particular, did some significant study on this question. According to a 1991 article by Italian researchers on the NIH website, HTLV-1 "is known to accelerate progression of the HIV infection to AIDS." In a small Italian study published in Infection in 1995, the researchers claimed that they could find no influence of HTLV-2 on the natural history of HIV infection. But in another Italian study published in 1999, involving 1152 HIV-positive patients who were screened for HTLV-2 infection, patients "had an increased risk of developing peripheral neuropathy .... These results support the hypothesis that HTLV-2 plays a role in the development of neurologic abnormalities in HIV-1-infected patients."

Today the nagging questions of what these two viruses can do to a human system already infected with HIV are still not answered. Johns Hopkins finds "[the] effect of HTLV-I/II on HIV disease progression controversial, with different studies reaching opposite conclusions."

Emerging Patient Activism

As with AIDS, the HTLVs have their patient activists. But HTLV activism has been way slower to develop, given the low profile put on these two retroviruses.

A pioneer in this area is Richard Engnath, an older man who lives in New York State. In 2004, Richard tells me, he thought he was developing AIDS, but his HIV test was negative. Persistence of painful neurological symptoms led his doctor to do further study and testing, and Engnath came up positive on the HTLV-1 test. His doctor thinks that Engnath might be in the early stages of tropical spastic paraparesis/HAM. Engnath is an example of a case cropping up well outside the Southeastern area where U.S. infectious-disease authorities believed the HTLV-1 virus to be concentrated.

When Engnath started looking for information about his disease, he was shocked all over again. Though there were standard tests (ELISA, Western blot) for the infection he had, there was no specific patient-support organization for him to go to. Even the Leukemia & Lymphoma Society doesn't discuss the virally caused T-cell disorders, preferring to concentrate on the B-cell disorders that may have environmental, genetic or other causes. Outraged at the scarcity of information, Engnath started his own NGO and toiled to create printed materials and a poster about HTLV-1 and -2 at his own cost. Slowly but surely, in his home state, he's getting the attention of health-conscious politicians like New York's Congressman Maurice Hinchey.

Engnath's sense of shock is echoed by that of Robert Parete, chairman of the Health Services Committee for the Ulster County legislature in New York State. After he saw Engnath's documentation in summer 2009, Parete put out a memo to the local healthcare facilities, telling them about "a growing epidemic that almost all Committee Members were largely or entirely unaware of." Parete expressed his shock that all 50 state departments of health had known about the HTLVs since the mid-1980s but had never developed an information campaign. He urged them to display Engnath's poster as a measure of education/prevention.

Today the Web offers some informational resources for the HTLVs -- they even include Wikipedia articles -- but there is definitely room for improvement. Meanwhile, Engnath continues his patient activism to help publicize HTLV-1 and -2, and to encourage people to protect themselves and have themselves tested if they want to know their status. For more information, write or phone to:

HTLV National Registry
Richard R. Engnath, Founder
199 Wall Street
Kingston, NY 12401-4517

A last-but-not least-question: Even if the U.S. government were to decide to put a higher priority on HTLV research and prevention, how will its agencies get rolling on this issue in a time of economic crisis, when they are slashing HIV funding right and left? This is a question that might be tough to answer.

Further reading:

Note: For many years, I have written a monthly column on AIDS politics and public-health politics for A & U Magazine. An archive of my columns can be found at the A & U website. A shorter version of this article was published in my "Left Field" column in A & U's August 2009 issue.

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You wrote beginning with the seventh paragraph" "In 1798, Gallo's people found the first-in-history human retrovirus in a human patient with lymphoma."

I'm sure this should be: "In 1978, ...."

Hard-to-Find Information
Though many scientists agree that serious diseases are caused by HTLV- and 2, you have to look hard to find mention of them at the CDC website.

s/b "... HTLV-1 and HTLV-2, ...."

Very interesting article. Not sure of its full implications, but it is still interesting and puzzling how and why we are only spoon-fed certain information by our own government.

Thanks, Patricia. As usual, your comments are edgy and pointed. (Not to complain or anything, but they’re a refreshing change from the interminable ‘explanations’ of why Frank and Obama are not really as bad as they are.)

I think that a consensus of the research points to the approach we'll have to take to fight these diseases, which has to be internationalist at its core. Ignoring their origins and refusing to treat everyone is a recipe for disaster. Or, more precisely, for a greater disaster. We need global socialized medicine.

In early August this year French scientists reported that “a new strain of HIV… crossed from gorillas to humans, with a 62-year-old French woman from Cameroon so far the only person known to be infected… it closely resembles strains of simian immunodeficiency (SIV) recently discovered in western gorillas living in the wild” Simian Immunodeficiency Viruses (SIV) are retroviruses found so far in over 40 African primates.

Viruses from two primates, SIVsm from Sooty Mangabeys and SIVcpz in chimpanzees crossed species barriers into humans causing the first two recognized strains, HIV-2 and HIV-1. (The species barrier is breached when when chimpanzees and other primates are butchered for meat and earlier when chimps eat dwarf chimpanzees, or Bonobos, the closest existing genetic relative of humans. Vegetarian anyone?)

Just a few days before in late July a report in AVERT, the Journal of Averting HIV and AIDS, explained the likely origin of the epidemic, which is believed to have begun in the early 20th century when Europeans began herding Africans in labor camps to extract raw materials for export. It was first proposed in 2000 by Jim Moore, an American specialist in primate behaviour, who published his findings in the journal AIDS Research and Human Retroviruses.

In areas such as French Equatorial Africa and the Belgian Congo, colonial rule was particularly harsh and many Africans were forced into labour camps where sanitation was poor, food was scarce and physical demands were extreme…. SIV could easily have infiltrated the labour force and taken advantage of their weakened immune systems to become HIV. A stray and perhaps sick chimpanzee with SIV would have made a welcome extra source of food for the workers.”
“Moore also believes that many of the labourers would have been inoculated with unsterile needles against diseases such as smallpox (to keep them alive and working), and that many of the camps actively employed prostitutes to keep the workers happy…”

The genetic history of HTLV-1 and HTLV-2 suggest a likely origin in the devastation caused by colonialism in the Americas.

The debate over the lack of socialized medicine in the US has to include information about the spread and development of diseases caused by global warming, population shifts and dwindling resources. HIV strains, HTLV-1 and HTLV-2, Dengue and Yellow fevers, MDR TB and hemorrhagic fevers like Hanta and Ebola are severe dangers to public health. All of them have occurred in the US, including Ebola and some, like Hanta, are endemic.

Insurance companies will fight paying for them instead of fighting them, HMO’s will medically people who become infected and drug companies will scramble to develop expensive palliatives instead of cures. Not only is Obama’s denial of medical services for imported and immigrant workers proof of the Democrats basically racist approach it’s a suicidal policy.

Ebola -


Yellow Fever -

Dengue Fever -

Robert Ganshorn Robert Ganshorn | September 20, 2009 8:20 AM

With as disgusting as French Equatorial Africa and the Belgian Congo were I have to doubt this conclusion for a couple of reasons.

Firstly "Bush Meat" (No former politicians were killed in the rendering of this comment) is a common source of protein in all parts of Africa where such is available. Also to say that "he believes" is no more than gossip.

Secondly had there been a transfer of this virus that long ago we would all be dead already.

Otherwise, I certainly agree that world wide medical prevention and protection are overdue. It makes too much sense and would piss off all the best bigoted people. I, over and again, in our own national health care debate remind conservatives that it is their children, grand children, best friends who could die if we do not isolate and care for an illegal resident of this country.

In other words, do what is decent, out of conscience or fear.

The possible origins of HIV and the two HTLVs are an important subject, and quite a few researchers have worked on this. Some point to the inheritable resistance-to-HIV factor as a hint that HIV has been around for many centuries. The fairly high incidence of the CCR5-delta32 mutant gene in Europe, and its demonstrated link to the inherited resistance factor for bubonic plague, suggests that HIV has been around for as long as plague has been around.

People who have two copies of CCR5-delta32 (one from each parent) are virtually immune to HIV infection. Those who inherit only one copy can be infected with HIV but they won't ever develop full-blown AIDS -- thus accounting for the long-time healthy non-progressors who are out there.

Because of the existence of CCR5-delta32, I have always been suspicious of the theory that "HIV started in African primates and jumped to humans sometime in the 1900s" -- especially since the incidence of CCR5-delta32 is generally much lower throughout Africa. The principles of population genetics tell us that the incidence of a given gene is highest in that region of the globe where the mutation first appeared, because it has had longer to spread through the population.

Similarly some researchers posit that HTLV-1 has been around for quite a while as well.

Meanwhile, I agree with Bill that action on these other HTLV viruses is probably going to come on the international level. International efforts to deal with epidemic disease certainly might be moving in the direction of "global socialized medicine" -- in fact, we are already making a big step in that direction with WHO's actions on swine flu and the U.S. government's efforts to "harmonize" with WHO, including marketing of a controversial vaccine that is going to have the country in an uproar shortly.

The one major question facing global healthcare is the same one facing U.S. healthcare -- what it's going to cost to do it, since the global economic meltdown is already impacting any international efforts to deal with health crises.

I'll be writing more on HTLV-1 and -2, and will cover these and other questions in more detail.

I'd like to see you write about CCR5-delta32 as well, Patricia.

Years ago, I had to give blood for a study about people who had been exposed repeatedly to HIV but never were infected. I never heard anything back, of course, since these things take years, but I was always curious what the results were and what they found.

Hello, I'm currently a grad student and I do research related to HTLV-1. I read your article and I think it's very interesting. I just had a question to ask of you because I've been trying to find update demographic information about the disease. I'm interested in knowing the statistics from your HTLV-1 registry. I'm giving a presentation to my peers and want them to understand how this infection might relate to them. Do you mind sharing that information?

I'm an academic physician and a specialist in hematopathology and can tell you that your article has many factual mistakes steaming from poor understanding of the disease process. I practice in the deep southeast where the HLTV-1/2 related diseases should be common according to your speculation and I can tell you that I see less than 1 case per year per 1,000,000 or so (I have a broad referral consultation practice). My peers on both coasts, mid west, and north often don't see a case in their whole carriers. So much for your speculations and conspiracy theories.

My report was based on CDC materials, so it's hardly "speculative." In spite of whatever the reported infection rates on these diseases may be, the CDC is concerned enough about the viruses that cause them that, starting in 1988, they added HRLV-1 and -2 to the required list for screening for the U.S. blood supply.

ccr5 delta 32 | January 11, 2010 9:12 PM

I have an interest in the ccr5 delta 32 mutation. I have watched the PBS Series Secrets of the Dead, "Case File: Mystery of the Black Death" a couple different times. I think most questions about the mutation are answered by the film. I am pasting the information about the film here. Also that there has been a drug developed and brought to market that mimics the benefits of the mutation. This is long, but it does support the "theory" that the mutation saved the bubonic plague servivors and does indeed block replication of the hiv virus. I've been told that the dvd can be rented from NetFlix. Here it is:

Case File: Mystery of the Black Death


No one knows exactly why, but in the late 1320s or early 1330s, bubonic plague broke
out in China's Gobi desert. Spread by flea-infested rats, it didn't take long for
the disease to reach Europe. In October of 1347, a Genoese ship fleet returning from
the Black Sea -- a key trade link with China -- landed in Messina, Sicily. Most of
those on board were already dead, and the ships were ordered out of harbor. But it
was too late. The town was soon overcome with pestilence, and from there, the
disease quickly spread north along trade routes -- through Italy and across the
European continent. By the following spring, it had reached as far north as England,
and within five years, it had killed 25 million people -- one-third of the European

The bubonic plague is caused by a bacterium called Yersinia pestis and is
characterized by chills, fever, vomiting, diarrhea, and the formation of black
boils in the armpits, neck, and groin. Though the disease was originally called the
"Great Mortality" and the "Great Pestilence," the name "Black Death" was eventually
adopted because of these black boils, which derive their color from dried blood
under the skin caused by internal bleeding. In certain cases the bacterium spreads
to the victims' lungs, causing them to fill with frothy, bloody liquid. This
derivation of the disease is called pneumonic plague, and can quickly spread from
person to person through the air. It is almost always lethal.

The plague first spread to Britain in 1348, travelling from Bristol to Oxford and
London in several days. More than three hundred years later, in 1665, perhaps the
worst of the English epidemics broke out in London. That summer, the nobility and
clergy fled the city, as some 7,000 people died each week. As many as 100,000
lives were lost before winter killed the fleas and the epidemic tapered off.
Contemporary medicine could provide no explanation for the sickness, and most
doctors were afraid to offer treatment. In an attempt to keep from being infected,
the few physicians who did risk exposure wore leather masks with glass eyes and
a long beak filled with herbs and spices that were thought to ward off the illness.
Even one person in a household showing plague-like symptoms was enough to mandate
a 40-day quarantine for the whole home -- a virtual death sentence for everyone
living in it.

In September 1665, George Viccars, a tailor in the small, central-England village
of Eyam, received a parcel of cloth ridden with plague-infected fleas from London.
Four days later, Viccars died. By the end of the month, five more villagers had
succumbed to the plague. The panicked town turned to their rector, William
Mompesson, who persuaded them to quarantine the entire village to prevent the
bacterium from spreading throughout the region. It seemed like suicide. A year
later, the first outsiders ventured into Eyam, expecting a ghost town. Yet,
miraculously, half the town had survived. How did so many villagers live through
the most devastating disease known to man?

Local Eyam lore tells befuddling stories of plague survivors who had close contact
with the bacterium but never caught the disease. Elizabeth Hancock buried six
children and her husband in a week, but never became ill. The village gravedigger
handled hundreds of plague-ravaged corpses, but survived as well. Could these
people have somehow been immune to the Black Death?

Dr. Stephen O'Brien of the National Institutes of Health in Washington D.C.
suggests they were. His work with HIV and the mutated form of the gene CCR5,
called "delta 32," led him to Eyam. In 1996, research showed that delta 32
prevents HIV from entering human cells and infecting the body. O'Brien thought
this principle could be applied to the plague bacteria, which affects the body
in a similar manner. To determine whether the Eyam plague survivors may have
carried delta 32, O'Brien tested the DNA of their modern-day descendents. What
he found out was startling. ...

Clues and Evidence

For a disease-causing microorganism to infect the human body there must be a
gateway or portal through which it enters into human cells. The plague bacterium
works this way, hijacking the white blood cells sent to eliminate it. Traveling
inside the white blood cells to the lymph nodes, the bacteria break out and
attack the focal point of the human immune system. Dr. Stephen O'Brien felt that
the mutated CCR5 gene, delta 32, may have prevented the plague from being able to
enter its host's white blood cells.

Eyam provided O'Brien an ideal opportunity to test this theory. Specifically,
Eyam was an isolated population known to have survived a plague epidemic. Everyone
in the town would have been exposed to the bacterium, so it's likely that any
life-saving genetic trait would have been possessed by each of these survivors.
"Like a Xerox machine," says O'Brien, "their gene frequencies have been replicated
for several generations without a lot of infusion from outside," thus providing a
viable pool of survivor-descendents who would have inherited such a trait.

Knowing who died and who lived through the early years of the plague is somewhat
problematic. Deaths among the general English population were not recorded in the
14th Century -- the height of the Plague -- and most communities did not begin
recording parish registers until around 1538. Fortunately, Eyam began keeping a
parish register in 1630. Thus historian John Clifford began by examining the
register, noting everyone who was alive in 1665, the year the plague came to Eyam.
He searched for evidence of life through the year 1725 -- marriages, baptisms,
burials that took place years after the plague had left the village. Deleting the
names of those lost during the plague period, he was able to determine who the
survivors were.

DNA samples could only be collected from direct descendents of the plague survivors.
DNA is the principal component of chromosomes, which carry the genes that transmit
hereditary characteristics. We inherit our DNA from our parents, thus Eyam resident
Joan Plant, for instance, may have inherited the delta 32 mutation from one of her
ancient relatives. Plant can trace her mother's lineage back ten generations to the
Blackwell siblings, Francis and Margaret, who both lived through the plague to the
turn of the 18th century. The next step was to harvest a DNA sample from Joan and
the other descendants. DNA is found in the nuclei of cells. The amount is constant
in all typical cells, regardless of the size or function of that cell. One of the
easiest methods of obtaining a DNA tissue sample is to take a cheek, or buccal, swab.

After three weeks of testing at University College in London, delta 32 had been
found in 14% of the samples. This is a genetically significant percentage, yet what,
really, did it mean? Could the villagers have inherited delta 32 from elsewhere,
residents who had moved to the community in the 350 years since the plague? Was
this really a higher percentage than anywhere else? To find out, O'Brien assembled
an international team of scientists to test for the presence of delta 32 around the
world. "Native Africans did not have delta 32 at all," O'Brien says, "and when we
looked at East Asians and Indians, they were also flat zero." In fact, the levels
of delta 32 found in Eyam were only matched in regions of Europe that had been
affected by the plague and in America, which was, for the most part, settled by
European plague survivors and their descendents.

Meanwhile, recent work with another disease strikingly similar to the plague, AIDS,
suggests O'Brien was on the right track. HIV, the virus that causes AIDS, tricks the
immune system in a similar manner as the plague bacterium, targeting and taking over
white blood cells. Virologist Dr. Bill Paxton at the Aaron Diamond AIDS Research
Center in New York City noticed, "the center had no study of people who were exposed
to HIV but who had remained negative." He began testing the blood of high-risk,
HIV-negative individuals like Steve Crohn, exposing their blood to three thousand
times the amount of HIV normally needed to infect a cell. Steve's blood never
became infected. "We thought maybe we had infected the culture with bacteria or
whatever," says Paxton. "So we went back to Steve. But it was the same result.
We went back again and again. Same result." Paxton began studying Crohn's DNA, and
concluded there was some sort of blocking mechanism preventing the virus from
binding to his cells. Further research showed that that mechanism was delta 32.

Scientists studying HIV first learned about the gateway-blocking capacity of the
CCR5 mutation in 1996. Several drug companies, then, quickly began exploring the
possibility of developing pharmaceuticals that would mimic delta 32 by binding to
CCR5 and blocking the attachment of HIV. Previous methods of treatment interfered
with HIV's ability to replicate after the virus has already entered a cell. This new
class of HIV treatment, called early-inhibitor -- or fusion-inhibitor -- drugs seek
to prevent the virus from ever attaching at all. These pharmaceuticals are still in
relatively early stages of development, but certainly stand as a hopeful new method
of approaching HIV treatment.


You may possess a genetic mutation. Most people would probably be aghast to learn
that one of their genes is malformed. But before you start asking, "What does that
mean? Will it make me sick someday? Will I pass it on to my children?" bear in mind
that a mutation of the CCR5 gene -- called "delta 32" in its mutated form -- has no
adverse effect on humans. In fact, possessing delta 32 could save your life, and the
lives of your children.

"It's highly unusual," says Dr. Stephen J. O'Brien of the National Institutes of
Health in Washington D.C. "Most genes, if you knock them out, cause serious diseases
like cystic fibrosis or sickle cell anemia or diabetes. But CCR5-delta32 is rather
innocuous to its carriers. The reason seems to be that the normal function of CCR5
is redundant in our genes; that several other genes can perform the same function."

"The non-mutated form is what's called a chemokine receptor," he says. Chemokines
are protein distress calls released by an injured region of your body. "The normal
function of the CCR5 gene is to act as a retriever of the chemokine distress signal
from these bruises, which will then be alleviated by the chemokines."

This may not sound exciting, but delta 32 is a powerful mistake. HIV, the virus that
causes AIDS, attacks the human immune system, infecting the white blood cells sent
to destroy it. The delta 32 mutation, however, effectively blocks the crucial
gateway into human cells the virus needs. In the case of Steve Crohn, whose partner
was the fifth person to die from AIDS, possessing the CCR5 mutation has prevented
him from contracting the virus.

O'Brien explains further, "In order to have total resistance to HIV, you have to
carry two doses of the mutated gene -- one from each parent. If you get only one
dose, you will not be resistant to infection. However, you may be able to delay the
onset of HIV once you become infected. That's because, in patients with one copy of
the mutation, the amount of 'portals' or 'doorways' that HIV can use is reduced by
about 50 percent. That slows down virus replication, which is the most important
factor in AIDS progression."

O'Brien's work on AIDS led him to another disease that delta 32 could prevent, the
plague. "They both, upon entering the body, infect the macrophages, which are the
first line of defense against bacterial infections," he says. "Over the course of
evolution, many bugs and pathogens have become extinct because the body learned how
to defend itself against them. So the ones that are around today, like HIV and the
plague, are pretty savvy -- HIV, for example, specifically attacks and kills the
very cells that are designed to kill it. Both these pathogens have developed very
clever ways around our immunological defenses."

The results of the Eyam study suggest that delta 32 may have helped save Europe from
the bubonic plague pandemic. It seems logical, then, that this could be confirmed by
an experiment in which the plague bacterium is injected into the cells of someone
possessing the delta 32 mutation. "We have attempted to design experiments that
allow us to expose the plague to the lymphocytes of different people, including
Steve Crohn," O'Brien says. "But so far we haven't been able to design that kind of
experiment ... to do that experiment, you would need to isolate that particular
kind of cell. You would need to isolate the exact strain of the plague, and you
would need to expose them together."

Nevertheless, delta 32 seems to be a formidable defense the human body has developed
in response to ages of pathogenic exposure. And though we may just be getting
acquainted with it, delta 32 has been protecting humans for ages. O'Brien suspects
the mutation has been around since long before the Black Death. "There have been
human remains dug up from graves in Scandinavia -- bodies 3,000 and 4,000 years old
-- in which they actually found the mutation, through DNA typing. So there are all
kinds of pieces in this puzzle that are coming together."

August 6, 2007—The FDA approved maraviroc, the first in a new class of anti-HIV drugs, for the treatment of patients who are not responding
to other AIDS drugs. A study of more than 600 patients showed that adding maraviroc to combination antiretroviral therapy was twice as
likely to result in undetectable virus levels. The drug acts by blocking the virus from accessing the CCR5 receptor protein on the
surface of susceptible cells. The development of the drug was made possible by initial work from amfAR grantee Dr. Nathaniel Landau, who first described the vital role of CCR5 in HIV infection and the likelihood that blocking it would not be detrimental to human health.
Later in 2007, the FDA approved another new class of anti-HIV drugs (see October 12).
Peace and love to all that lived the reading of that.

Thank you for your most interesting article, Patricia.

Now the CDC is trying to sweep another retrovirus - XMRV- under the carpet.

XMRV is associated with chronic fatigue syndrome, a very insulting name for a seriously debilitating disease. Some epidemics have been noted back in the 1980's notably in Incline Village, Nevada. The CDC went and investigate and returned home with the idea that these 200 people and the 2 doctors were all hysterical. Some people have been sick with this, with no health care, for over 30 years. They have tested positive for XMRV.

There is a lot of secrets to be unfolded, I would really appreciate you investigate and ask lots of questions. It's a huge story of corruption and like I said, sweeping the shameful disease under the carpet.

I would be more than interested to share with you the big players in that story.

Thank you

Derrick Tibbetts | November 24, 2010 6:45 AM

I currently live in sacramento CA.ive had htlv1 for around or diagnosed with it for 6 years now.its funny how all these people write about their knowledge on it ,but actually livivg with it is a complete different story.i may not type all that well but i just want to get my story on baclofin all day,was on oxycontin,now on vicodin,i have bladder problems so i take oxybutynin, you see my picture.Ive been hospitalized 7 or8 times with infections where they have used pik lines because i have no veins anymore,but recentlystarted getting them back.ive been out of the hospitalfor about 8 months now...thats great.i have lower limb problems all day, problems.i was using a walker..but have graduated to a cane,yippee!! 36 and was a floorcoverer for 14 years.i way around 220.muscular.Where i got it ,i have no idea.I have tattoos so maybe there,but i think from laying floors and picking up nasty peoples toilets,and refrigerators..dirty filthy peoplescarpet with urineandfeal matter.As you can tell if i dont keep myself in check i can get very frusterated with peoples lack of cleanliness and bad attitudes toward it.Ive been cut ,scraped by urine filled tackstrip(for carpets that was rusted by urine)and so on.Its a hard life but im a jahovas witness and a family man that wont give up .im active as i can be get as much walkin as i can .take my vitamins,eat healthy... I can say that im very upset there is next to none support system from a gov. that is payed for by us to help us.But we all know where the money goes ,dont we?I believe in a heavenly gov.ruled by Jesus and his Father Jahovah.Its plain as day in the bible yu just have to read and believe.Well gotta go my back is about to bust..oh htlv1 eats away at the sheathing around the spinal cord...sounds fun huh?yup nerve problems.well ciao.