Mr. Steve Crohn, an admittedly promiscuous gay New Yorker who lost over 70 friends to AIDS in the '80s and '90s; has been nicknamed, "The man who can't catch AIDS".
Years of scientific study have shown that he is a descendant of a small population of people that survived the devastation of the Bubonic Plague or Black Death that devastated much of Europe during the Middle Ages. From these descendants, Steve inherited genes that made him largely immune to HIV.
Steve Crohns' gay partner was reportedly the 5th person in the US said to have died due to AIDS complications in the 80's. Steve Crohn went on to spend the next decade awaiting his own HIV related death sentence, which fortunately never came; as he continued to test HIV-Negative. After awhile, this very strange anomaly caught the attention of doctor & scientists who began looking for the reason for why Steve had never gotten HIV.
After some discovery about the genetics related to the people of Eyam, England an their survival of the Black Plague; Dr. Stephen O'Brien began testing the blood of some 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. Unbelievably, Steve's blood never became infected. "
According to one article, they thought maybe they had infected the culture with bacteria or whatever," said Mr. 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 finally revealed that the mechanism was delta 32.
Two doctors, Dr.David Ho and Stephen O'Brien have studied Mr. Steve Crohn. By studying the people like Steve Crohn, whose cells repeatedly resisted HIV infection, they eventually found a genetic mutation that prevents the HIV virus from entering the cell. HIV needs to enter white blood cells through the CD-4 and CCR-5 receptors on the cell's surface. There are some rare individuals who have no CCR-5 gene, which means HIV simply cannot enter their cells.
Further study showed that the individual like Mr. Steve Crohn, must be heterozygous for the Delta 32, CCR5 gene mutation, which means that they MUST have inherited the gene from BOTH parents and have two copies of the gene to have this resistance to HIV.
Scientists are using this new information in the development of an AIDS vaccine.
Over and over again through my research, you'll find that when the subject is researched and discussed statistically, often the conditions effect approximately 15% of the population or that approximately 15% are resistant to some condition or disease.
Could the Rh-Negative Factor & its' approximate 15% of the population be associated with these new genetic findings?
Of course, because we now have such a gene mixture in the US and because of the often recessive nature of the Rh Negative Factor; there will be a variance in the statistics.
In the article sited below, you will see the percentage, ethnic & regional association between a disease, genetics and the Rh Negative origin.
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 (Remember 14%) than anywhere else? To find out, Dr. 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, England 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 & their descendants.
Extended MHC haplotypes that are conserved and inherited across generations due to strong linkage disequilibrium are referred to as "Ancestral Haplotypes" (AH).
The classical Caucasian MHC haplotype, A-1-B8-DR3-DQ2 (AH8.1) has been reported to be associated with faster progression to AIDS.
It is known that healthy people carrying this haplotype are immunologically hyper-responsive and have a significantly higher risk of developing autoimmune diseases. This haplotype is absent in the Indian population.
Another extended haplotype that shows positive association with rapid progression to AIDS among Caucasians is A11-Cw4-B35-DR1-DQ1, apparently due to the specific peptide binding motifs of B*35Px alleles.
Are the Rh-Negative Factor and the CCR5 delta 32 mutation connected?
Read the article and related Patent Application information before you answer that question.
Abstract: Therapeutic and prophylactic methods using Rh antibodies for delaying the progression of infection with the Human Immunodeficiency Virus (HIV) in a subject who is exposed to HIV, or infected by HIV.
Doctors and Scientists are now looking to the "Elite Controllers" of HIV for answers on how to treat, fight and cure the disease in the rest of the general population.
According to this article, Scientists have honed in on certain parts of the HIV virus that could be the perfect targets for future drugs. In effect, they are looking for the "weak" spots rather than the whole disease to attack. By way of a mathematical method that the stock market employed, they are trying to find its' vulnerable spots.
One of those spots is where HIV is attacked by the natural immune systems of an "elite controllers". This is where these doctors and scientists are now looking for answers!
So what is an Elite Controller?
They are those HIV/AIDS positive patients who have the disease under control without medication, according to the study, published in the journal Proceedings of the NationalAcademies of Sciences. Unfortunately, HIV is evolving and mutating constantly, which makes a cure hard to develop. So now they are concentrating on the parts that mutate at a slower rate to find treatments that work better and longer, as well as continuing to search for a cure.
Profound Discoveries From Around the World on HIV Controllers and Long-Term Nonprogressors, Part 4
By Loreen Willenberg From The Body ~ July 23, 2010
This blog entry is the 4th in a series of reports on a few of the scientific abstracts submitted for presentation on the subject of "HIV Controllers (HCs)" and of "Long Term Nonprogressors (LTNPs) -- a small minority of HIV-positive people who control the virus in as-of-yet unexplained ways -- to the XVIII International AIDS Conference.
This page had been created to try and get to the bottom of the debate surrounding AIDS/HIV, the Rh-Negative Population and the genetics that make a person resistant to the virus.
Comments and questions are received daily related to this subject, like this one. Jonathan writes, "I found this document while doing some research on Rh- blood types and I was wondering if anyone here might be able to help me out with a question I was having. Does anyone here know of any cases where a Rh- person contracted HIV/AIDS? I have always believed that HIV/AIDS was an engineered disease to wipe off certain races of people and I thought that blood type would be a great way to target certain races since 95% of all African Americans and 99% of Asians are Rh+ and the bloodlines of the elites in the world seem to be Rh-Negative. Just a thought of mine and any info would be greatly appreciated."
It seems we need to compile the information available and try to come to a conclusion of opinions on this subject. Is it the CCR5 delta 32 mutation, does it so happen that more Rh-Negatives carry this genetic mutation,? Could it only be the O-Negative population that carries immunity? What is it about the proteins on the blood cells? Clearly there are a lot of questions to answered and information that needs to be reviewed.
Timothy Ray Brown suffered from both leukemia and HIV when he received a bone marrow stem cell transplant in Berlin, Germany in 2007. The transplant came from a man who was immune to HIV, which scientists say about 1 percent of Caucasians are. (According to San Francisco's CBS affiliate, the trait may be passed down from ancestors who became immune to the plague centuries ago. This Wired story says it was more likely passed down from people who became immune to a smallpox-like disease. What happened next has stunned the dozens of scientists who are closely monitoring Brown: His HIV went away.
The C-C chemokine receptor type 5 also known as CCR5 is a protein that in humans is encoded by the CCR5 gene. CCR5 is a member of the beta chemokine receptors family of integral membrane proteins. In Humans, the CCR5 gene location is on the short (p) arm at position 21 on chromosome 3. Certain populations have inherited the Delta 32 mutation resulting in the genetic deletion of a portion of the CCR5 gene. Homozygous carriers of this mutation are resistant to M-tropic strains of HIV-1 infection. To read more, click here.
"It's a story about ... a genetic mutation that arose in just one person who was probably living in the lost Kingdom of Khazars in southern Russia more than 1200 years ago. Today the mutation is widespread among Caucasians and helps protect carriers against infection with the AIDS virus. Marc Buhler, a Sydney geneticist, has pieced together this colourful history of the mutation's origins to explain its particularly high prevalence in populations as disparate as Jewish people in Australia and people living in Iceland. The mutation, in a gene known as CCR5, was discovered in 1996. People with one copy usually take several years to become ill if they acquire HIV. People with two copies rarely become infected. Mr Buhler ...tested DNA from about 1400 Australians and found about 15 per cent of Ashkenazi Jews (from Germany and Eastern Europe) were carriers, but only 6 per cent of Sephardic Jews (from southern Europe and Africa). ... he found about 20 per cent of Ashkenazi Jews had the mutation if their grandparents had come from Russia, Poland, Hungary or Czechoslovakia. ... But how to explain its prevalence in Iceland and other Nordic countries? ... If a person in Khazar had developed the CCR5 mutation it would have spread back to Scandinavia with the Vikings [suggested Buhler]."
Except found on RhesusNetwork.net, from Biomedical Research 2008; 19 (1): 41-44 AA Abdulazeez, EB Alo, SN Rebecca Department of Biological Sciences, Federal University of Technology, Yola, Nigeria. Accepted October 27, 2007
"prevalence of HIV serotypes is significantly higher (97.8%) among Rhesus D positive subjects than their Rhesus D negative counterparts in which 2.2% was recorded (P<0.05). This finding was in consonance with the results of Omoriegie et al.  which reported that Rhesus D positive subjects were more susceptible to infections."
Please Note ~ Rhesus D Positive means Rh+ and Rhesus D Negative means Rh-.
HIV Resistant Genes...Rhesus Negative, Excess PK & CCR5 Deletion
This is an interesting and detailed article found on Rense.com . It discusses the rumor that AIDS is a man-made disease. The article states that although this theory has been discredited by "scientific consensus," there is evidence linking the outbreak of this new disease to a vaccine experiment conducted on gay men in New York City, as well as in other U.S. cities, between 1978 and 1981.
The article starts by discussing the first epidemic cases of AIDS in America, that were uncovered exclusively in young, previously healthy, and mostly white gay men in Manhattan in 1979. However, the cause was apparently unknown until about 1984 when a virus, later named HIV (human immunodeficiency virus), was accepted as the infectious agent.
According to the author, beginning in 1974, workers in a bloodmobile provided by the New York Blood Center in Manhattan began soliciting 8, 906 gay men for a hepatitis B vaccine research study (Koblin et al, 1992). The article goes through the full details of the cause and effect of the vaccine exposure and the years that followed. Then the article goes on to covers the alternative theory of Simian Viruses and the connection and comparison of the two AIDS epidemic, the one here in the United States and the other in Africa.
According to Luc Montagnier in his book "Virus" (1999), the African AIDS epidemic did not begin until the Autumn of 1982 at the earliest. As well, it says there is no epidemiologic or sexual connection between gay cases and African AIDS cases. The article states, that there are strong connections between simian viruses and the experimental hep B vaccine, the gay participants, and the outbreak of AIDS. According to the author, "The vaccine given to gays was designed by Maurice Hilleman of Merck; and was "developed" by repeatedly injecting it into chimpanzees, as part of the safety testing of the vaccine".
So the question becomes... Could a chimp HIV-like virus have been transferred to the vaccine during the 65-week manufacturing process?
What is HIV-associated arthritis? How does it differ from the painful articular syndrome?
HIV-associated arthritis is characterized by extreme disability and pain in the knees and ankles. The synovial fluid is noninflammatory with negative cultures. The symptoms tend to last from 1 to 6 weeks to respond to rest, physical therapy, and NSAIDs and low-dose corticosteroids. There is no HLA-B27 association. Occasionally sulfasalazine may be necessary. Once the clinical disorder is resolved, the medications can be successfully discontinued. The painful articular syndrome typically involves the knees, shoulders, and elbows and lasts only 2-24 hours. It is speculated that this may represent transient bone ischemia; there is no evidence of synovitis.
Taken From: Rheumatic Syndromes Associated with HIV Infection (Pages 103-104): Read Full Story, Click Here >
It is believed that the plague bacteria entered Eyam, England, a very small town in the north and that it was carried in on a blanket shipped from "sick old Europe", where the plague began centuries earlier in a Sicilian port. During the Middle Ages, approximately 25 million Europeans died in agony, cause by the Black Plague. Researchers have since been interested in finding the people who didn't die and the reason why!
Apparently, the man who received the blanket noticed some dots on his wrist, and soon there after, he was dead. Not long after the first death, the whole town was quarantined and left to their own devices. During this quarantine many of the Eyamers' died, but there were survivors. Approximately half of the towns' population, about 433 people, are said to have survived the almost certain death they were facing from the black plague.
Many researchers and historians later began to wonder whether Eyam ever got the plague at all and why all of these people were able to avoid death. Some of the names of survivor families include; the Hancocks, the Furnesses, the Blackwells, and more. In the years following the plague, many of these families lived on in the town of Eyam, England. Genetically, this gave researchers a way to peer into the past by way of ancestral DNA typing.
Eventually, a Geneticist named Steven O'Brien from the National Institutes of Health, approached the descendants' of Eyman and asked if they would be willing to swab the inside of their cheeks and give up DNA for a genetic study. Many agreed to participate and the results showed that they had a special "anti-plague gene, Delta 32" which protects them from the effects of the Black Plague, just as it had for their ancestors.
O'Brien originally began this research through his study of AIDS, the HIV virus and Steve Crohn; dubbed the man who cannot catch AIDS. He and others in his field are responsible for the finding of the CCR5 Delta 32 mutation that gives a resistance to AIDS. He explains on the PBS special that "HIV, the virus that causes AIDS, attacks the human immune system, by 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."
I must interject here.... Again, please understand, we obviously have 3 sub-groups of humans, as shown above. Those who can get AIDS, those who have slow progression and those who are resistant.
It is +/+ vs. +/- vs. -/- There is a split genetically and it is NOT just + and -'s, there are those in the middle, those who are half breeds if you will - they are recessive - they are the +/- population.
Whether we're talking about the CCR5 delta 32 mutation or the Rh-Negative mutation; there needs to be an understanding that there are 3 subgroups to review....NOT 2! This pattern will repeat itself over & over again in my research.... It is not simple black or white - there are shades of gray in the middle, needing to be addressed.
Both the Plague and HIV, upon entering the body will 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. However, in the case of HIV it specifically attacks and kills the cells that are designed to and should kill it. Clever little pathogens they are!!
According to O'Brien, the results of the Eyam study suggest that delta 32 may have helped save Europe from the bubonic plague pandemic. Interestingly enough, delta 32 seems to not only to be a formidable defense of some human bodies against terrible diseases, plagues or viruses; but it has might also have been around since long before the black plague; as the delta 32 mutation has been found in 3,000 to 4,000 year old Scandinavian human remains dug up and DNA tested. There are all kinds of pieces in this puzzle that are coming together", says O'Brien.
Learn more on PBS.org, Secrets of the Dead - Case File: Mystery of the Black Plague, click here.
This man who created this video is foreign and bit hard to understand. Since I am NOT a geneticist or doctor, I do not know if what he is saying is correct or incorrect. However, there are a ton of great comments made about this video on YouTube as well to make your own judgement.
From my understanding of the video, he is saying that the CCR5 delta 32 mutation may have positive and negative effects on the health of a person. It appears that he is saying that those people who have the delta 32 mutation may not only be resistant to one of the two strains of the HIV/AIDS virus; but also to the positive effects of three forms of Chemotherapy. He says that this is because the deletion of the CCR5 gene takes away the receptors needed to "accept" these three types of chemotherapy treatment. So to say it plainly, those people with a delta 32 mutation may have lost the receptors needed to effective receive 3 chemotherapy treatments meant to fight other diseases. He also says that he is seeing this in his delta 32 mutation patients who are dying from failed health, breast cancer, leukemia, Wegener's disease and more. He quotes studies that say there is an increased susceptibility to Hepatitis C and the health problems that go with it.
Finally, he explains regarding HIV/AIDS, that there are 2 receptors on the CD4 Lymphocyte that HIV/AIDS enters the cell through and it is like having two doors into the home to accept HIV/AIDS, the CCr5 and the CXCR4. People with the double dose of the delta 32 mutation have shut the CCR5 door, but HIV/AIDS will still look for a route to walk in through the CXCR4 receptor door. He states that there are two strains of HIV/AIDS and the Delta 32 mutation only gives protection against the one knocking on the CCR5 door. He says that gene deletions always cause some negative effects on the body.
HIV status and blood groups determination (Rhesus and ABO groups) in 3691 pregnant women attending antenatal clinic at a Mission Hospital and Maternity and 1199 non-pregnant women visiting the same institution for marriage-related matters, or blood donation, or out-patient department between 1999 – 2002 were studied. Blood sample from each subject was screened for HIV using the quick test kits and tested for blood group types with anti-sera A,B,AB, and D. Overall, the prevalence of blood group O+ was higher than in the general population with highest rate of 62.9% in HIV+ pregnant women followed by 58.4% in HIV- pregnant women and 58.0% in non-pregnant women. No difference was observed in groups A+, B+, AB+, O- for the three categories of subjects studied. Blood groups B-, AB- were conspicuously absent in HIV+ pregnant women but non-significant in HIV pregnant women and the control. Type A- was very few in all the categories.
Rh-Negative accounted for 3.16%(HIV+), 3.46%( HIV-) and 2.67%(Control) while Rh-Positive were 96.84%( HIV+), 96.06% ( HIV-) and 97.33%( Control). Thus, the higher than normal prevalence of group O+ in HIV+ pregnant women is indicative of the population size for this group.
The very low prevalence of Rh–Negative in type A (Type A-) suggests that incompatibility could be higher than in this population and protective in HIV infection contrary to the previous report in apparently healthy population. The obvious absence of Rh-Negative in AB group suggests that AB may have a higher percentage of protection against immunization. Hence in group B, less incidence of Rh incompatibility and haemolytic disease of the young in the mothers in blood group AB will occur.
Table 1 shows the percentage prevalence of Rh within the ABO Groups in non-pregnant women (Control) while
Table 2 shows the prevalence among HIV+ and HIV- pregnant women.
Overall Rh Positive (Rh+) for HIV+ pregnant women was 96.84%; for HIV- pregnant Women, it was 96.06% and for non-pregnant women-97.33%
while Rh-Negative Factor for HIV+ pregnant women was 3.16%; for HIV- group - 3.46% and non-pregnant women– 2.67%.
In the combined test, blood group O+ was the most numerous (62.9% for HIV+; 58.4% for HIV-; 58.0% for non-pregnant),
followed by A+ (19.4% for HIV+; 22.5% for HIV-; 22.3% for non-pregnant women), and B+ (13.4% for HIV+; 14.0% for HIV-; 16.0% for non-pregnant) while O-, AB+ B-, A- were few for HIV- andAB- and B- were not found among HIV+ pregnant women.