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CCR5-Delta32 and HIV/AIDS: evolution in action

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Hocus Locus

Joined: 22 Sep 2006
Posts: 850
Location: Lost in anamnesis, cannot forget my way out

PostPosted: Sat Oct 07, 2006 2:59 pm    Post subject: CCR5-Delta32 and HIV/AIDS: evolution in action Reply with quote

It seems we are witness to real genetic 'evolution in action', in recorded history. One of the greatest detective stories of all time.

CCR5-Delta 32 is a mutated aelle (considered 'defective' even if there is a health benefit!) of CCR5, an error in replication. An aelle is an specific expression of a gene (or defective gene) from either parent.

This defect seems to have first occurred in Caucasian Europenans in the time of the plague. The defect interferes with the mechanism by which HIV takes hold of the system.

If neither parent has the aelle: When exposed to HIV it will TAKE HOLD and AIDS will manifest 'quickly'.
One parent: A degree of immunity for a certain period, details not yet thoroughly studied.
BOTH parents have it, ('homozygous to this aelle'), apparent immunity to HIV/AIDS

10-12% of 'all' Caucasions decended from Bubonic Plague survivors, have this aelle. ('all' quoted because not much data yet); ranging down to nearly ZERO percent among Africa, Asia. Quite simply those who have gone 'all the way with' these Europeans in the last 700 years.

(by my reading), being 'immune' to HIV means that if exposed to it, you will have traces of it in your blood stream for a time period, but they will not 'take'. So upon exposure to HIV the potential still exists for anyone to pass it on to others, but it is 'short' (think someone guessed weeks but not sure).

One-aelle persons may represent the group who can carry HIV for years and remain able to infect others, because HIV has established a hold in their system.

Two-aelle Caucasian descendants may even be able to be donors of stem-cells that assist HIV/AIDS infected persons in their battle.

(Locus's Remedy for idiots opposed to stem cell research on purely religious grounds: (1) Start a rumor that vaccines for children contain stem cells and the Government has been secretly hiding that fact. (2) Wait one or two generations. For the record... I would much prefer to solve it some other way. ;-)


I think knowing this status is quite ethical; a child tested proven as a double carrier (homozygous) may consider it a natural calling for helping those with HIV. Or, if faced in a serious medical emergency response, be able to make a choice to 'go in' where others would more rightly fear to tread. It's not a end-all -- for such people, it seems that exposure to Hepatitis C might carry worse risk in the young.

I wanted to know if I possessed this aelle. If one tested positive for this, it would be possible to find a partner and produce children that are (very likely, it seems) to have a 'natural' immunity to AIDS. Or be able to tell your children exactly where they stand in the NO,SOME,YES issue.

So I sent emails to two gene test companies (most income derived from paternity tests).

1. Do you test for presence of the CCR5-Delta32 defect?
2. Have you done any tests that prove 'maternity'?

One of them did not respond at all. The other said,

"Sorry we do not test for CCR5D32, the gene that confers immunity to AIDS."

Just that. Nothing else. I was tempted to reply,

"Well ahm... how does that make you feel?"


[1] http://www.projinf.org/fs/ccr5.html
Understanding HIV: Co-Receptors—CCR5

"The study showed that when people inherited [CCR5-D32] from both parents, they appeared to be resistant to infection with HIV. (The gene is considered defective because a portion of it is missing, and it thus cannot produce a functional CCR5 receptor.) Some people may inherit a single defective version of the gene from one parent, but there is insufficient information to know whether this confers partial protection against infection.

It has been shown that people with the partial CCR5 defect may progress to HIV disease more slowly than someone without the CCR5 defect. This study was extremely small, however, and the defective receptor was found in only two of fifteen people who were thought to be exposed to HIV, yet remain uninfected.

[2] http://www.as.ua.edu/ant/bindon/ant475/Papers/Kampis.pdf
The detective story: recap on plague, the role of smallpox

During the time of the Black Death, a pathogen that like HIV-1 utilizes CCR5 established an immunity in ancestral Caucasian populations. This shows a link between the Black Death and AIDS. Descendants from a Caucasian who contracted the plague in the mid-fourteenth century and survived, may have complete immunity to HIV/AIDS. It is believed that up to fifteen percent of the population falls into this category.

Alison Galvani and Montgomery Slatkin from the University of California at Berkeley refute the claim that the CCR5- Delta 32 deletion mutation arose from the plague. Instead, their research indicates it arose during smallpox epidemics in Europe. They point out that although the allele has resistance against HIV-1, HIV has not existed long enough in the human population to account for this selective pressure. Galvani and Slatkin find that by using a population genetic framework that takes into account the temporal pattern and age-dependent nature of certain disease, they found that smallpox is more consistent with this historical role. The CCR5 chemokine receptor is fundamental to establishing HIV-1 infection. The receptor is exploited by HIV strains that predominate during the primary phase of infection to gain entry into immune system cells, including macrophages and CD4+T cells (Glavani & Slatkin, 2003). The CCR5- Delta 32 deletion produces resistance to HIV-1 by preventing the
expression of its receptor on the cell surface. The CCR5- Delta 32 allele provides complete resistance to HIV-1 in the homozygous state and partial resistance in the heterozygous state. The CCR5- Delta 32 allele is currently under intense selection in populations with a high occurrence of HIV-1. HIV-1 has not been affecting humans long enough to account for the selective rise of this resistance allele. The frequency of the allele is estimated at an average of ten percent in European populations and it is almost completely absent in African, Asian, Middle Eastern, and American Indian populations. This suggests a recent origin, estimated at around 700 years based on the coalescent theory (Galvani & Slatkin, 2003). The theory that the high frequency of the CCR5 allele arose in Europe through strong selection from the bubonic plague has become known as the classic example of historical selection on an important locus. This hypothesis has gained widespread acceptance in the medical world, but Galvani and Slatkin believe that the high frequency of CCR5 arose because of smallpox.
The plague epidemic was caused by an indirect transmission from rodents through fleas. By comparison, smallpox was transmitted directly between humans, resulting in more continuous transmission. The researchers found that bubonic plague could not generate sufficient selective pressure to account for current CCR5-Delta 32 frequencies. The 400-year period of plague epidemics in Europe did not remove enough people of high reproductive potential to generate a sufficient selection coefficient (Galvani & Slatkin, 2003). As illustrated by Figure 4, Galvani and Slatkin’s (2003) results suggest that the plague could not even have driven the resistance allele to one percent during the period it existed in Europe.

[...] the continuous mortality from smallpox on European children could have provided the selective pressure necessary to generate the rise of CCR5- Delta 32 deletion to current frequencies of ten percent (Galvani & Slatkin, 2003).
Conclusion: The Black Plague was a widespread epidemic that devastated Europe for nearly 400 years. It was caused in part by the uncleanness of the times coupled with overcrowding. There was nothing medieval medicine could have done because the disease was so advanced. Now, the plague is almost a forgotten memory, but many researchers believe that the one bright spot that came from it was the CCR5 deletion mutation that now protects some people from HIV. Much more research can be done on the CCR5 mutation and hopefully studies in the future will show how people without the CCR5 mutation can overcome HIV infection.

[3] http://www.hivandhepatitis.com/hiv_hcv_co_inf/020801.html
CCR5-Delta 32 Mutation Linked with More Severe Hepatitis C Virus Infection

[4] http://www.hivandhepatitis.com/recent/cxcr4/012203f.html
CCR5 Genotype Does Not Influence HIV Infection in Children with Hemophilia
The progression of HIV infection did differ, however, when age was taken into consideration. Although patients under age 20 were not protected by the CCR5-delta-32 mutation, the researchers note, heterozygous patients between the ages of 20 and 40 years seemed less likely than age-matched CCR5 homozygous patients to develop symptoms of AIDS and die. Patients over 40 years old also appeared to be protected by the variant allele.

"Why the protective effect of the CCR5-delta-32 mutation is not apparent in HIV-positive children is unknown," Dr. Iversen, now at The John Radcliffe Hospital in Oxford, UK, told Reuters Health. However, this might be "due to differences in CCR5 genotype being outweighed by age-related factors, such as a highly active immune system with high levels of beta-chemokines."

[5] http://www.sciencedaily.com/releases/2005/03/050325234239.htm
Biologists Discover Why 10 Percent Of Europeans Are Safe From HIV Infection

[5-1/2](SUSPECT) http://www.stewartsynopsis.com/boyd_ed_graves.htm

Tinfoil perhaps, but interesting in concept... maybe some hasty or broken science, innuendo, questionable +/- terms ('spectrum'...?)

Hocus: It's natural (even noble) to come up with theories that attempt to show that modern science created a monster. Because someday it will and scientists will throw the carcass, evidence and cultures into a river upstream from your location and burn their notes. Unlike Doctor Phibes, whose acid pit absorbed countless mistakes properly.

Perhaps it has... but with our gene machines themselves working overtime and the correlative effects of other diseases... modern civilation itself, not necessarily modern gene splicers, could also provide the 'thick soup' in which useful and bad mutations can occur. Technology and transport brings more diverse genomes into close proximity today than at any time in history.
"Luff... is the sweet comfut uff life. (Maharishi)

Dr. Phibes also had the way-coolest mechanical band.
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Hocus Locus

Joined: 22 Sep 2006
Posts: 850
Location: Lost in anamnesis, cannot forget my way out

PostPosted: Thu Oct 12, 2006 12:06 am    Post subject: Lung cancer: Another Caucasian gene alert Reply with quote

Lung cancer: Another Caucasian gene alert (unspecified) gene variants, insufficient enzyme 'GSTM1'

I am beginning to suspect that a number of the cancers attributed to 'second hand smoke' were in fact attributed thus because radon is odorless and invisible, and smokers are not.

Just as those antitheses to smoking, fresh air and exercise, get people out and about and away from their stagnant radon-infested homes.

Issues surrounding radon and second hand smoke are identical -- aggrivated by the push in the 1970s to seal homes for energy efficiency, greater concentrations of radon may accumulate (as less outside/inside ventilation occurs). An radon-safe home is a home with a hermetically sealed foundation, or an active vent and fan system that draws the gas up and away, presumeably to fall on someone else's home, since it is heavier than air.
Buzzword update: Reactive oxygen species are three: they include oxygen ions, free radicals and peroxides

EPA's radon page. But fer gosh sakes, don't be terrified of radiation. At least, ventilate your home so the parrot doesn't keep expiring -- your children will love you for it.

(URL deleted because it's just too damned long & ugly. Google it)

NEW YORK (Reuters Health) - Gene variants that lead to decreased amounts of an enzyme known as GSTM1 may raise the risk of lung cancer related to radon exposure, new research suggests. The gene variants also seem to increase the cancer-causing effect of secondhand smoke.

Both radon and secondhand smoke are thought to promote carcinogenesis through the formation of harmful molecules called reactive oxygen species. The enzyme GSTM1 detoxifies these species and their derivatives.
In an earlier study, Dr. Matthew R. Bonner, from the University at Buffalo in New York, and colleagues found that the "GSTM1 null genotype," which is estimated to be carried by 38 percent to 62 percent of Caucasians, increases the risk of lung cancer for never smokers exposed to secondhand smoke.

In the present analysis, the authors sought to confirm this association and look at the effect of this specific genotype on radon-related lung cancer.The study included data from 270 lung cancer patients drawn from previous case-control studies. Radon levels were determined using long-term alpha-track detectors.
As hypothesized, the presence of the GSTM1 null genotype strengthened the association between radon levels and lung cancer. The interaction between GSTM1 null genotype, secondhand smoke, and lung cancer seen in the researchers' previous study was again confirmed.

"This may be the first study to provide evidence of a GSTM1 and radon interaction in risk of lung cancer," write the researchers.

SOURCE: International Journal of Cancer September 15, 2006.

Reactive oxygen species (ROS) include oxygen ions, free radicals and peroxides both inorganic and organic. They are generally very small molecules and are highly reactive due to the presence of unpaired valence shell electrons. ROSs form as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling. However, during times of environmental stress ROS levels can increase dramatically which can result in significant damage to cell structures. This cumulates into a situation known as oxidative stress. Cells are normally able to defend themselves against ROS damage through the use of enzymes such as superoxide dismutases and catalases. Small molecule antioxidants such as Ascorbic acid (vitamin-C),uric acid, and glutathione also play important roles as cellular antioxidants. Similarly, Polyphenol antioxidants assist in preventing ROS damage by scavenging free radicals. In contrast, the antioxidant ability of the extracellular space in relatively less. E.g., the most important plasma antioxidant in humans is probably uric acid.

The effects of ROS on cell metabolism have been well documented in a variety of species. These include not only roles in programmed cell death and apoptosis, but also positive effects such as the induction of host defence genes and mobilisation of ion transport systems. This is implicating them more frequently with roles in redox signaling or oxidative signaling. In particular, platelets involved in wound repair and blood homeostasis release ROS to recruit additional platelets to sites of injury. These also provide a link to the adaptive immune system via the recruitment of leukocytes.

Reactive oxygen species are implicated in cellular activity to a variety of inflammatory responses including cardiovascular disease. They may also be involved in hearing impairment via cochlear damage induced by elevated sound levels, ototoxicity of drugs such as cis-platin and in congenital deafness in both animals and humans. Redox signaling is also implicated in mediation of apoptosis or programmed cell death and ischaemic injury. Specific examples include stroke and heart attack.

Great Lover, n.:A man who can breathe through his ears.
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Damian Flynn

Joined: 29 Jan 2006
Posts: 219
Location: Australia

PostPosted: Sat Oct 21, 2006 2:06 pm    Post subject: Reply with quote

All that stuff about HIV is just psycho babble mate. You're wasting your time. I don't think you'll find many believers on this forum. They're always trying to focus the AIDS psyop on Negros. This is just another example.
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