In the human immune system, the HLA (human leucocyte antigen) family of genes plays an important role in defending against foreign invaders such as viruses.
The authors say that the origins of some HLA class 1 genes are proof that our ancient relatives interbred with Neanderthals and Denisovans for a period.
“Getting these genes by mating would have given an advantage to populations that acquired them.”
At least one variety of HLA gene occurs frequently in present day populations from West Asia, but is rare in Africans.
“The HLA genes that the Neanderthals and Denisovans had, had been adapted to life in Europe and Asia for several hundred thousand years, whereas the recent migrants from Africa wouldn't have had these genes,”said study leader Peter Parham from Stanford University School of Medicine in California.
“So getting these genes by mating would have given an advantage to populations that acquired them.”
Dr. Pinna says:
The HLA gene which provides our white cells in our immune system with the ability to recognize viruses and perhaps cancers was a gift from our Neanderthal ancestors.
Neanderthals interbred with Europeans and Chinese but not with Africans. This is very important from a medical point of view.
Since the HLA (HUMAN LEUKOCYTE (WHITE CELL) ANTIGEN) protects against viruses, we find the most deadly viruses in Africa. For example, the famous EBOLA virus.Why? Because Africans do not have the ability to defend against and eradicate this virus. The viruses found in Europe and China are rather mild, such as mumps, measles and German measles.Also, Africans have less defenses against cancers caused by viruses. Here is a report from the Guardian, U.K:
“The difference is that a disproportionate number of cancers in Africa are caused by infections, such as the hepatitis viruses (B and C), which cause liver cancer, or the human papillomavirus (HPV), which causes 98% of cervical cancers. The worldwide average for infection-related cancers is about 22%; in Africa, the figures are much higher: 40% of cases in women and 30% in men.”
European and Chinese interbreeding with Neanderthals was a gift from God. Not only did it give us red hair and big brains, but also a way to fight viral infection.
http://drpinna.com/neanderthal-genes-boosts-our-immune-system-23305
HLA B27 & Arthritis
Arthritis is a term for any of more than one hundred diseases that produce swelling in a joint, accompanied by pain and stiffness. The most common forms of arthritis are osteoarthritis (the degeneration of a joint) and rheumatoid arthritis ("the great crippler," inflammation of a joint that erodes bone and cartilage). Other forms include ankylosing spondylitis (inflammation of spinal joints, mainly affecting young men), infectious arthritis (caused by invading microorganisms), and chronic Lyme arthritis (which appears in some people who contract Lyme disease). Lupus, an autoimmune disease, also has elements of arthritis, with painful and often swollen joints.
Neanderthal skeletons show signs of arthritis, as do Egyptian mummies. Ancient Greek and Roman physicians wrote detailed descriptions of arthritic conditions and methods of treatment. In fourteenth- and fifteenth-century Europe, gout became common among members of the upper classes, and an outbreak of rheumatoid arthritis swept through the masses of Europe during the Industrial Revolution. By the early nineteenth century, rheumatoid arthritis had been recognized as a distinct condition, separate from gout. Augustin Landre-Beauvais gave rheumatoid arthritis its first complete clinical description in 1800; in 1859 Alfred Garrod (1819-1907) distinguished gout by the presence of uric acid.
While the disease had been known for centuries, its cause remained unknown. Some thought arthritis was the result of an infectious disease, such as gonorrhea or tuberculosis. In 1900 twophysicians, Frederick J. Poynton (1869-1943) and A. Paine, discovered a bacteria in a group of children afflicted with rheumatism. They speculated that rheumatic arthritis could be the result of an immune reaction to an invading microorganism. In 1940 researchers found an rheumatoid factor, an antibody-like substance, in the blood of arthritis patients. Further study showed that rheumatic infections were caused by a group A streptococcus, so the rheumatoid factor was indeed an immune system response to that bacteria. Current research focuses on the relationship between specific genetically coded HLA molecules (an element of the immune system) and the occurrence of various types of arthritis. For example, the HLA-B27 molecule is common in people with ankylosing spondylitis.[14]
HLA B27 & CCR5-Δ32
According to Randall Johnson at the Baylor College of Medicine in Houston, "Only 7% of the US population tests positive for the HLA-B27 gene; this gene, found only in persons with Rh-Negative blood, can trigger the immune system to operate overtime at WARP SPEED in times of medical emergency."
Note: HLA-B27 is also sometimes found in those who are Rh negative recessive.
The HLA-B27 Genetic Marker is said to have protective properties that guard against the progression of HIV. It is said, that people with this gene do not have the right proteins for the HIV virus to bind with. The HLA-B27 Marker is most often found in people with O- Blood.
CCR5-Δ32 is a deletion mutation of a gene that has a specific impact on the function of T cells. At least one copy of CCR5-Δ32 is found in about (5-14%) of people of Northern European and in those of Northern European descent. There also is a small minority (1%) with the same mutation amongst Southern Europeans or Balkan Peninsula. It has been hypothesized that this allele was favored by natural selection during the Black Death for Northern Europeans.
The allele has a negative effect upon T cell function, but appears to protect against smallpox and HIV. Yersinia pestis (the bubonic plague bacterium) was demonstrated in the laboratory not to associate with CCR5. Individuals with the Δ32 allele of CCR5 are healthy, suggesting that CCR5 is largely dispensable. However, CCR5 apparently plays a role in mediating resistance to West Nile virus infection in humans, as CCR5-Δ32 individuals have shown to be disproportionately at higher risk of West Nile virus in studies, indicating that not all of the functions of CCR5 may be compensated by other receptors.
While CCR5 has multiple variants in its coding region, the deletion of a 32-bp segment results in a nonfunctional receptor, thus preventing HIV R5 entry; two copies of this allele provide strong protection against HIV infection. This allele is found in 5–14% of Europeans but is rare in Africans and Asians.
HLA-B27 is an inherited gene marker that is associated with a number of related rheumatic diseases. They share in common, certain features like spinal and peripheral arthritis, skin and GI disorders, anterior chamber eye disease, psoriasis like skin lesions, as well as inflammation and joint pain. This gene is found with highest prevalence in patients with ankylosing spondylosis, reactive arthritis, and patients with the combination of peripheral arthritis and either psoriasis or inflammatory bowel disease.
Neanderthals have been found with skeletal deformities known to be caused be ankylosing spondylitis and Arthritis.[13]
CONCLUSION
Neanderthals carried HLA-B27 which offers protection from certain diseases, however it also causes autoimmune diseases. CCR5-Δ32 deletion is also linked in with O negative blood. They originate in Neanderthals and are not often found in Africa. If you have Rh negative blood, you are blessed with some of the genes from our most ancient families.
Research by Tia Douglass & Andre Heyrman of NADA.
REFERENCE:
Matt McGrath
http://rhnegativebloodsecrets.blogspot.com/2013/01/are-you-related-to-neanderthals.html?m=1
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