VDO Freshy

HIV new therapies _ CCR5 antagonist

While evolutionists adore CCR5Delta 32 mutation as an evidence for evolution, they ignore the negative side effects of this mutation.

Barry Zingman, M.D., of Montefiore Medical Center in New York http://www.medpagetoday.com BOSTON -- Comforting data about the safety of the second major drug aimed at blocking HIV entry to target cells were revealed here today.

O HIV entra no linfócito auxiliar T CD4+ ao ligar-se à molécula CXCR4 ou às moléculas CXCR4 e CCR5, dependendo do estágio no qual a infecção pelo HIV se encontra. Uma proteína cofator (fusina) é requerida para auxiliar na ligação do vírus à membrana da célula T. Durante as fases iniciais de uma típica infecção pelo HIV, as duas moléculas CCR5 e CXCR4 estão ligadas, enquanto que um estágio mais avançado da infecção geralmente envolve mutações do HIV que apenas ligam-se à molécula CXCR4. Uma vez que o HIV está ligado ao linfócito T CD4+, um estrutura viral conhecida como GP41 penetra na membrana celular e o RNA do HIV e várias enzimas, incluindo (mas não limitada) à transcriptase reversa, integrase e protease são injetadas na célula. Uma vez que a célula T hospedeira não processa o RNA em proteínas, o próximo passo é gerar um DNA a partir do RNA do HIV usando a enzima transcritase reversa para que ocorra a transcripção reversa. Se bem sucedida, o DNA pró-viral deve ser então integrado ao DNA da célula hospedeira usando a enzima integrase. Se o DNA pró-viral é integrado ao DNA da célula hospedeira, a célula torna-se altamente infectada, mas não produzindo ativamente proteínas do HIV. Esse é o estágio latente do HIV, uma infecção durante a qual a célula infectada pode ser uma "bomba não explodida" potencialmente por um longo tempo.

Just a bit of clearing up on the CCR5delta32 issue, and a plea for GERONAMI to watch the whole the whole of the "Selective Evidence" video. In-depth article on CCR5 with regards to HIV and Hepatitis C: http://jac.oxfordjournals.org/cgi/content/full/53/6/895 Phenotypes are affected by environmental factors (in this case, the phenotype is resistance to HIV): http://en.wikipedia.org/wiki/Phenotype R5 is the most common strain of HIV: http://www.mcld.co.uk/hiv/?q=CCR5 Speciation: http://en.wikipedia.org/wiki/Speciation

Exibe a entrada do HIV em um LT CD4+, sua replicação e a farmacodinâmica dos principais anti-retrovirais: Inibidores de TR, de protease, de integrase e de fusão. Legendas e tradução feitas por mim.

Mecanismo de entrada do hiv na celula hospedeira e mudanca de tropismo

For several years, Boyd Graves and Leonard Horowitz have spoken about HIV AIDS being manufactured and funded by the US government with the knowledge that it could be used to kill massive populations of humans. Since the mid-1980s, I have maintained that it is a race-specific weapon and even wrote about it being such in 1990-91. It was in 1996 that some scientists found this to be the case, linked to the CCR5 Delta 32 negative genetic mutation making it impossible for millions of whites to contract HIV AIDS. Such is not the case for Africans and Asians, the highest birthrate groups. I also indicated they manufactured a strain of the virus that targeted certain genetic characteristics with white homosexual men. The reason for the targeting of this group was because eugenists discovered that where there is high homosexuality among whites, the birthrates are lower. The case I quoted in 1988-89 was with Denmark and Sweden, having the highest homosexuality rate and the lowest negative birthrate of all Western European countries. This videos main theme is about the patent, proported to be a cure for HIV AIDS. The text of this patent in this video is clear and readable. Barack Obama has stated publicly that it is obsurd to believe the US government created the HIV AIDS. We did not press him about his wrong assumption because had he stated the truth, as most blacks know it to be, it would have politically stopped his run for the presidency. You can't bring about big changes if you're not the president. It is now different and we're going to press this very, very serious issue far more devastating to Blacks around the world. I promise that we shall make this a key agenda in America, far beyond gays wanting to be married. I'm sure millions of blacks dying in Africa, in America and elsewhere is a much more important issue. It is crippling economies all across the African continent with millions of orphaned children and adults too sick to work and build economies.

CNN report on HIV AIDS among Blacks in America with commentary.

Le core viral est appelé capside. Le core viral contient : Un génome constitué de deux copies identiques d' ARN, qui contiennent les informations génétiques permettant au virus de se répliquer, et trois enzymes qui sont nécéssaires à la réplication du virus : la transcriptase inverse, l'intégrase et la protéase.

It is a very excellent animation which explains the hiv replication very clearly. For free download of this video please visit my webpage http://rufusrajadurai.wetpaint.com/ And other 3D animation videos visit http://rufusrajadurai.wetpaint.com/page/3D+Medical+Animation+Library Regards, Dr.Rufus The Lyrics of this video is here Targeting HIV replication The replication of HIV 1 is a multi-stage process. Each step is crucial to successful replication and is therefore a potential target of antiretroviral drugs. Step one is the infection of a suitable host-cell, such as a CD4-positive T-lymphocyte. Entry of HIV into the cell requires the presence of certain receptors on the cell surface, CD4 -- receptors and co-receptors such as CCR5 or CXCR4. These receptors interact with protein-complexes, which are embedded in the viral envelope. These complexes are composed of two glycoproteins: an extracellular gp 120 and a transmembrane gp 41 When HIV approaches the target cell gp120 binds to the CD4-receptors. This process is termed attachment. It promotes further binding to a co-receptor. Co-receptor binding results in a conformational change in gp120. This allows gp41 to unfold and insert its hydrophobic terminus into the cell membrane. Gp 41 then folds back on itself. This draws the virus towards the cell and facilitates the fusion of their membranes. The viral nucleocapsid enters the host cell and breaks open releasing two viral RNA-strands and 3 essential replication enzymes: Integrase, Protease and Reverse Transcriptase. Reverse Transcriptase begins the reverse transcription of viral RNA. It has two catalytic domains: The Ribonuclease-H active site And the polymerase active site Here single stranded viral RNA is transcribed into an RNA-DNA double helix. Ribonuclease- H breaks down the RNA. The polymerase then completes the remaining DNA-strand to form a DNA -- double helix. Now Integrase goes into action. It cleaves a dinucleotide from each 3-prime end of the DNA creating two sticky ends. Integrase then transfers the DNA into the cell nucleus and facilitates its integration into the host cell genome. The host cell genome now contains the genetic information of HIV. Activation of the cell induces transcription of proviral DNA into messenger RNA. The viral messenger RNA migrates into the cytoplasm where building blocks for a new virus are synthesised. Some of them have to be processed by the viral protease. Protease cleaves longer proteins into smaller core proteins. This step is crucial to create an infectious virus. Two viral RNA-strands and the replication enzymes then come together and core proteins assemble around them forming the capsid. This immature particle leaves the cell acquiring a new envelope of host and viral proteins. The virus matures and becomes ready to infect other cells. HIV replicates billions of times per day destroying the hosts` immune cells and eventually causing disease progression. Drugs which interfere with the key steps of viral replication can stop this fatal process. Entry into the host cell can be blocked by fusion inhibitors for example. Inhibition of reverse transcriptase by nucleoside inhibitors or by non-nucleoside Reverse Transcriptase- inhibitors is part of standard antiretroviral regimens. The action of Integrase can be blocked. Protease inhibitors are also part of standard antiretroviral therapy. Each blocked step in viral replication is a step towards better control of HIV disease. Script, Storyboard, Art Direction by: Frank Schauder, MD Animation: MACKEVISION Publicity: Dr.Rufus Rajadurai.MD.,D.DENS.,

It is a very excellent animation which explains the hiv replication very clearly The Lyrics of this video is here Targeting HIV replication The replication of HIV 1 is a multi-stage process. Each step is crucial to successful replication and is therefore a potential target of antiretroviral drugs. Step one is the infection of a suitable host-cell, such as a CD4-positive T-lymphocyte. Entry of HIV into the cell requires the presence of certain receptors on the cell surface, CD4 -- receptors and co-receptors such as CCR5 or CXCR4. These receptors interact with protein-complexes, which are embedded in the viral envelope. These complexes are composed of two glycoproteins: an extracellular gp 120 and a transmembrane gp 41 When HIV approaches the target cell gp120 binds to the CD4-receptors. This process is termed attachment. It promotes further binding to a co-receptor. Co-receptor binding results in a conformational change in gp120. This allows gp41 to unfold and insert its hydrophobic terminus into the cell membrane. Gp 41 then folds back on itself. This draws the virus towards the cell and facilitates the fusion of their membranes. The viral nucleocapsid enters the host cell and breaks open releasing two viral RNA-strands and 3 essential replication enzymes: Integrase, Protease and Reverse Transcriptase. Reverse Transcriptase begins the reverse transcription of viral RNA. It has two catalytic domains: The Ribonuclease-H active site And the polymerase active site Here single stranded viral RNA is transcribed into an RNA-DNA double helix. Ribonuclease- H breaks down the RNA. The polymerase then completes the remaining DNA-strand to form a DNA -- double helix. Now Integrase goes into action. It cleaves a dinucleotide from each 3-prime end of the DNA creating two sticky ends. Integrase then transfers the DNA into the cell nucleus and facilitates its integration into the host cell genome. The host cell genome now contains the genetic information of HIV. Activation of the cell induces transcription of proviral DNA into messenger RNA. The viral messenger RNA migrates into the cytoplasm where building blocks for a new virus are synthesised. Some of them have to be processed by the viral protease. Protease cleaves longer proteins into smaller core proteins. This step is crucial to create an infectious virus. Two viral RNA-strands and the replication enzymes then come together and core proteins assemble around them forming the capsid. This immature particle leaves the cell acquiring a new envelope of host and viral proteins. The virus matures and becomes ready to infect other cells. HIV replicates billions of times per day destroying the hosts` immune cells and eventually causing disease progression. Drugs which interfere with the key steps of viral replication can stop this fatal process. Entry into the host cell can be blocked by fusion inhibitors for example. Inhibition of reverse transcriptase by nucleoside inhibitors or by non-nucleoside Reverse Transcriptase- inhibitors is part of standard antiretroviral regimens. The action of Integrase can be blocked. Protease inhibitors are also part of standard antiretroviral therapy. Each blocked step in viral replication is a step towards better control of HIV disease. Script, Storyboard, Art Direction by: Frank Schauder, MD Animation: MACKEVISION Publicity: Dr.Rufus Rajadurai.M.D.,D.DENS.,

The commission to create what later was dubbed as HIV/AIDS was in 1969-70 via a US government law entitled Public Law 91-171. This is known by all American presidents, including Barack Obama. All of them fear having to deal with it and prefer to mask it through the motions of throwing a few billion dollars at Africa, primarily, and then Asia. There is a extraordinarily high rate in the United States among targeted non-whites. We are demanding a national public discussion, a "Truth & Resolution" Commission with Public Law 91-171 as the central discussion point. It is not good enough for foundations, even the Clinton Foundation to collect hundreds of millions of dollars without acknowledging that there is a growing suspicion of covering up the genesis of this "mass killer of populations", especially Africans and Asians. We demand that an investigation be done with regards to this being more of a "race-specific weapon" with intent to reduce populations and even the existence of certain groups. We also demand specific detailed accountability of the $15 billion the Bush Administration has committed to fight this "mass killer of populations".

CNN reporting on HIV AIDS in Black America along with commentary.

In this video I show how GERONAMI selectively chooses the evidence that supports his claims, and otherwise ignores or distorts the evidence that supports evolution. CCR5delta32 as a result of smallpox and/or Bubonic plague. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=299980 Homo/heterozygote sickle-cell anemia carriers: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16001361 Positive mutation of brain size: http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0020126&ct=1 Edit: I occassionally misread my own notes so I'd like to correct an error. Zygosity is not to do with the double helix, but alleles, which are viable genetic codings for a paticular gene. Homozygotes have the same alleles in both chromsomes, and heterozygotes have different alleles (in which one can be dominant.) The CCR5 deletion (and all mutations) happens at the level of the base pairs that make up the double helix, but zygosity is determined at the level of the allele. Sorry for the mistake :-)

Acquired immunodeficiency syndrome (AIDS) Classification and external resources The Red ribbon is a symbol for solidarity with HIV-positive people and those living with AIDS. ICD-10 B24. ICD-9 042 DiseasesDB 5938 MedlinePlus 000594 eMedicine emerg/253 MeSH D000163 List of abbreviations used in this article AIDS: Acquired immune deficiency syndrome HIV: Human immunodeficiency virus CD4+: T helper cells CCR5: Chemokine (C-C motif) receptor 5 CDC: Centers for Disease Control and Prevention WHO: World Health Organization PCP: Pneumocystis pneumonia TB: Tuberculosis MTCT: Mother-to-child transmission HAART: Highly active antiretroviral therapy STI/STD: Sexually transmitted infection/disease Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS or Aids) is a set of symptoms and infections resulting from the damage to the human immune system caused by the human immunodeficiency virus (HIV).[1] This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and breast milk.[2][3] This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, or breastfeeding, or other exposure to one of the above bodily fluids. AIDS is now a pandemic.[4] In 2007, an estimated 33.2 million people lived with the disease worldwide, and it killed an estimated 2.1 million people, including 330,000 children.[5] Over three-quarters of these deaths occurred in sub-Saharan Africa,[5] retarding economic growth and destroying human capital.[6] Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century.[7] AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified by American and French scientists in the early 1980s.[8] Although treatments for AIDS and HIV can slow the course of the disease, there is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries.[9] Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS epidemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus.

We will soon blow the lid off of what some of us have known since the 1980s, that HIV/AIDS was produced in American labs funded by the Department of Defense dating all the way back to the 1960s. This is a piece from CNN with commentary regarding why genes play a huge part as to why far many more blacks get HIV/AIDS than whites. It's time to demand that U.S. Congress investigate PUBLIC LAW 91-171, the smoking gun for the creation and mass production of what later became known as GRIDS and then HIV. We also demand discussion about the difference between HIV1 and HIV2 with HIV2 having an appetite for gay white men. However, the attack on that group dropped dramatically while it continued to rise among blacks all around the world. Yes, it is genocide at a scale never ever seen. America and Britain should leave Zimbabwe alone because it is a part of ground zero for this biological warfare attack by the U.S. and some of its European allies.

DOWNLOAD VIDEO...SPREAD THE WORD http://blip.tv/file/get/RalphBuckley-HIVAids504.mpg *IF YOU HAVEN'T BEEN EXPOSED TO THE WORK OF DR. BOYD E. GRAVES...PLEASE RESEARCH: http://www.boydgraves.com/ (FinalCall.com) - After beginning his research on the AIDS pandemic in 1992, Dr. Boyd Graves discovered in February 1999 the greatest evidence, to date, of records and reports of the experiments that led to the development of what the world now knows as the AIDS virus. That document is the "1971 Flow Chart of the Special Virus Program of the United States." Dr. Graves submitted this flowchart as evidence to the Sixth Circuit Federal Court in a case which named the President of the United States as a defendant to answer a petition acknowledging the authenticity of the Flow Chart. On January 12, 2001, the case was dismissed as "frivolous," and then referred to the District's Appellate Court, which ruled in favor of the lower court. Eventually, it went to the Supreme Court, which refused to hear it without giving comment as to why. "The 1971 flowchart makes it perfectly clear, the design, intent and purpose of the U.S. Special Virus program. As Dr. Peter Piot, Executive Director of UNAIDS says, 'The HIV/AIDS virus is the result of many steps in the laboratory, it was no accident.' The 1971 flowchart provides absolute evidence of the United States' intent to kill its own citizens and others." http://www.stewartsynopsis.com/boyd_ed_graves.htm U.S. Public Law 91-213 signed March 16, 1970, by Richard Nixon states: "In the United States' effort to 'stabilize the population of Sub-Saharan Africa' and thus, increase the national security of future United States, Nixon proclaims there would be 'explosive events' (relative to John D. Rockefeller, III's oversight on the problem of African overpopulation). To date nary a single U.S. official will address the 'peculiar' public law that authorizes the United States to kill its own citizens and others in the name of the national security of future (White) Americas. If the United States is above board, then the President should take immediate corrective action to fully disclose this secret (Manhattan-style) program. J. Craig Venter, Jr., holds the patent to the gene called the "African American HIV/AIDS Entryway." This is the same gene that early U.S. science used on African children in the late 50's (CCR5 Delta 32 positive). *********************************** LIFE IS PRECIOUS... KEEP FREEDOM ALIVE!!! http://www.ralphbuckley.com http://www.ronpaul2008.com/ http://www.prisonplanet.com/ http://www.infowars.com/ http://www.redicecreations.com/ http://www.stewartsynopsis.com/boyd_ed_graves.htm "9/11 Conspiracy Blues" CD http://cdbaby.com/cd/ralphbuckley2

It is a very excellent animation which explains the hiv replication very clearly. For free download of this video please visit my webpage http://rufusrajadurai.wetpaint.com/ And other 3D animation videos visit http://rufusrajadurai.wetpaint.com/pa... Regards, Dr.Rufus The Lyrics of this video is here Targeting HIV replication The replication of HIV 1 is a multi-stage process. Each step is crucial to successful replication and is therefore a potential target of antiretroviral drugs. Step one is the infection of a suitable host-cell, such as a CD4-positive T-lymphocyte. Entry of HIV into the cell requires the presence of certain receptors on the cell surface, CD4 -- receptors and co-receptors such as CCR5 or CXCR4. These receptors interact with protein-complexes, which are embedded in the viral envelope. These complexes are composed of two glycoproteins: an extracellular gp 120 and a transmembrane gp 41 When HIV approaches the target cell gp120 binds to the CD4-receptors. This process is termed attachment. It promotes further binding to a co-receptor. Co-receptor binding results in a conformational change in gp120. This allows gp41 to unfold and insert its hydrophobic terminus into the cell membrane. Gp 41 then folds back on itself. This draws the virus towards the cell and facilitates the fusion of their membranes. The viral nucleocapsid enters the host cell and breaks open releasing two viral RNA-strands and 3 essential replication enzymes: Integrase, Protease and Reverse Transcriptase. Reverse Transcriptase begins the reverse transcription of viral RNA. It has two catalytic domains: The Ribonuclease-H active site And the polymerase active site Here single stranded viral RNA is transcribed into an RNA-DNA double helix. Ribonuclease- H breaks down the RNA. The polymerase then completes the remaining DNA-strand to form a DNA -- double helix. Now Integrase goes into action. It cleaves a dinucleotide from each 3-prime end of the DNA creating two sticky ends. Integrase then transfers the DNA into the cell nucleus and facilitates its integration into the host cell genome. The host cell genome now contains the genetic information of HIV. Activation of the cell induces transcription of proviral DNA into messenger RNA. The viral messenger RNA migrates into the cytoplasm where building blocks for a new virus are synthesised. Some of them have to be processed by the viral protease. Protease cleaves longer proteins into smaller core proteins. This step is crucial to create an infectious virus. Two viral RNA-strands and the replication enzymes then come together and core proteins assemble around them forming the capsid. This immature particle leaves the cell acquiring a new envelope of host and viral proteins. The virus matures and becomes ready to infect other cells. HIV replicates billions of times per day destroying the hosts` immune cells and eventually causing disease progression. Drugs which interfere with the key steps of viral replication can stop this fatal process. Entry into the host cell can be blocked by fusion inhibitors for example. Inhibition of reverse transcriptase by nucleoside inhibitors or by non-nucleoside Reverse Transcriptase- inhibitors is part of standard antiretroviral regimens. The action of Integrase can be blocked. Protease inhibitors are also part of standard antiretroviral therapy. Each blocked step in viral replication is a step towards better control of HIV disease. Script, Storyboard, Art Direction by: Frank Schauder, MD Animation: MACKEVISION Publicity: Dr.Rufus Rajadurai.MD.,D.DENS

In this video I will address some of the misconceptions, lies, and other false claims made by creationists regarding mutations. Due to time constraints I will only be addressing the most commonly used creationist arguments regarding mutations. Throughout this video I will use superscripted numbers to indicate sources. At the end of the video I will list my references; the superscripted numbers will correspond to particular sources Claim 1: Mutations are Rare Actually mutations are fairly common. Consider the following facts: -In humans, the average mutation rate per genome per replication is 0.0041. -We must also take into consideration that the mutation rate may actually be higher than this, because mutations with very small effects may be hard to detect. -This number may seem small to some people, but consider the following: -- in humans, the number of cell divisions prior to sperm formation in a male of age 30 is about 4002. -- This works out to about 1.6 mutations per sperm cell. -Including neutral mutations, each human zygote has approximately 64 new mutations1. -Also, mutation rates are generally higher, and life cycles shorter, in lower organisms. This is why bacteria, and other lower organisms, evolve faster than humans do. -Even if many of these mutations occur in 'junk' DNA (by some estimates 'junk' DNA accounts for 90% of human DNA2), mutations are not nearly as rare as many creationists would like people to believe. Claim 2: Most Mutations are Harmful Most mutations are actually neutral. One study estimated around 3 deleterious mutations out of 175 per generation in humans3. Many non-neutral mutations are harmful, but a small fraction are beneficial. Harmful mutations are removed from the gene pool via natural selection; beneficial mutations stay in the gene pool via natural selection. Claim 3: Mutations are purely random, random processes never build anything. This claim completely ignores the fact that natural selection is a non-random process. Mutations may be random, but natural selection is not. To put it simply: if a mutation helps the organism survive in its environment, then it will go on to reproduce and pass on its genetic material; if a mutation does not help the organism survive (if the mutation is harmful), then the organism dies out and does not pass that mutation on (the harmful mutation is removed from the gene pool). Claim 4: Mutations do not add information, traits, etc. Most creationists make this claim, but refuse to define what they mean by information. Since creationists refuse to define what they mean by 'information', I will tackle the possibilities that could apply to genetics and evolution. If they are talking about each nucleotide (or set of nucleotides) as being 'information', then frameshift mutations CAN add information4. If they are referring to new traits being added, then mutations DO add information. Here are a few examples: -The development of nylonase in Flavobacterium Sp. K1725. -Adaptation to high and low temperatures by E. Coli6. -Some mutations in humans provide resistance to HIV7. - Eero Mäntyranta, among other members of his family, has naturally aberrant high blood hemoglobin due to a mutation in the erythropoietin receptor (EPOR) gene8. This list could on for quite a while, but you get the point... By any definition of information that can be applied to evolution, mutations DO add information. As you can clearly see, creationist claims regarding mutations are false. Creationists simply choose to ignore the scientific evidence in favor of their dogmatic beliefs. References 1) JW Drake et al, "Rates of Spontaneous Mutation",Genetics 148:1667-1686, April 1998 http://www.genetics.org/cgi/content/full/148/4/1667 2) Harter, R., "Are Mutations Harmful?". Retrieved August 1, 2007, from http://www.talkorigins.org/faqs/mutations.html#append_1 3) Nachman, M. W. and S. L. Crowell. 2000. Estimate of the mutation rate per nucleotide in humans. Genetics 156(1): 297-304. 4) Johnson, G. B. (2006). The Living World, Fourth Edition. The McGraw-Hill Companies, Inc. 5) Prijambada, I. D., S. Negoro, T. Yomo and I. Urabe. 1995. Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution. Applied and Environmental Microbiology 61(5): 2020-2022. 6) Bennett, A.F., Lenski, R.E., & Mittler, J.E. (1992). Evolutionary adaptation to temperature I. Fitness responses of Escherichia coli to changes in its thermal environment. Evolution, 46:16-30. 7) Sullivan, Amy D., Janis Wigginton and Denise Kirschner. 2001. The coreceptor mutation CCR5-delta-32 influences the dynamics of HIV epidemics and is selected for by HIV. Proceedings of the National Academy of Science USA 98: 10214-10219. 8) de la Chapelle A, Traskelin AL, Juvonen E. (1993). "Truncated erythropoietin receptor causes dominantly inherited benign human erythrocytosis." Proc Natl Acad Sci U S A. 90(10):4495-9.