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CCR5
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CCR5
Available structures
PDB
Ortholog search: PDBe RCSB
[show]List of PDB id codes
2L87, 2RLL, 2RRS, 2MZX, 4MBS
Identifiers
Aliases
CCR5, CC-CKR-5, CCCKR5, CCR-5, CD195, CKR-5, CKR5, CMKBR5, IDDM22, C-C motif chemokine receptor 5 (gene/pseudogene)
External IDs
OMIM: 601373 MGI: 107182 HomoloGene: 37325 GeneCards: CCR5
[hide]Gene location (Human)
Chr.
Chromosome 3 (human)[1]
Band
3p21.31
Start
46,370,854 bp[1]
End
46,376,206 bp[1]
[show]Gene location (Mouse)
Chr.
Chromosome 9 (mouse)[2]
Band
9 F4|9 75.05 cM
Start
124,121,543 bp[2]
End
124,147,699 bp[2]
[show]Gene ontology
Molecular function
• G-protein coupled receptor activity
• coreceptor activity
• chemokine (C-C motif) ligand 5 binding
• virus receptor activity
• signal transducer activity
• protein binding
• chemokine receptor activity
• C-C chemokine receptor activity
• actin binding
• phosphatidylinositol phospholipase C activity
• C-C chemokine binding
Cellular component
• cytoplasm
• integral component of membrane
• endosome
• membrane
• plasma membrane
• integral component of plasma membrane
• external side of plasma membrane
• cell surface
Biological process
• G-protein coupled receptor signaling pathway
• signaling
• response to cholesterol
• release of sequestered calcium ion into cytosol by sarcoplasmic reticulum
• positive regulation of cytosolic calcium ion concentration
• cell-cell signaling
• dendritic cell chemotaxis
• MAPK cascade
• chemotaxis
• cellular defense response
• cell surface receptor signaling pathway
• immune response
• inflammatory response
• cellular response to lipopolysaccharide
• calcium ion transport
• calcium-mediated signaling
• entry into host cell
• signal transduction
• fusion of virus membrane with host plasma membrane
• chemokine-mediated signaling pathway
• viral process
• defense response
• negative regulation of macrophage apoptotic process
Sources:Amigo / QuickGO
Orthologs
Species
Human Mouse
Entrez
1234
12774
Ensembl
ENSG00000160791
ENSMUSG00000079227
UniProt
P51681
P51682
RefSeq (mRNA)
NM_001100168
NM_000579
NM_009917
RefSeq (protein)
NP_000570
NP_001093638
NP_034047
Location (UCSC)
Chr 3: 46.37 – 46.38 Mb Chr 3: 124.12 – 124.15 Mb
PubMed search
[3] [4]
Wikidata
View/Edit Human View/Edit Mouse
Attachment of HIV to a CD4+ T-helper cell: 1) the gp120 viral protein attaches to CD4. 2) gp120 variable loop attaches to a coreceptor, either CCR5 or CXCR4. 3) HIV enters the cell.
C-C chemokine receptor type 5, also known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines. This is the process by which T cells are attracted to specific tissue and organ targets. Many forms of HIV, the virus that causes AIDS, initially use CCR5 to enter and infect host cells. Certain individuals carry a mutation known as CCR5-Δ32 in the CCR5 gene, protecting them against these strains of HIV.
In humans, the CCR5 gene that encodes the CCR5 protein is located 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.[5][6][7][8][9][10]
Contents
[hide]
1 Function
2 HIV
3 CCR5-Δ32
3.1 Evolutionary history and age of the allele
3.2 Evidence for a single mutation
3.3 Positive selection
3.4 Potential costs
3.5 Medical applications
4 See also
5 References
6 Further reading
7 External links
Function[edit]
The CCR5 protein belongs to the beta chemokine receptors family of integral membrane proteins.[11][12] It is a G protein–coupled receptor[11] which functions as a chemokine receptor in the CC chemokine group.
CCR5's cognate ligands include CCL3, CCL4 (also known as MIP 1α and 1β, respectively), and CCL3L1.[13][14] CCR5 furthermore interacts with CCL5 (a chemotactic cytokine protein also known as RANTES).[13][15][16]
CCR5 is predominantly expressed on T cells, macrophages, dendritic cells, eosinophils, microglia and a subpopulation of ether breast or prostate cancer cells.[17][18] It is likely that CCR5 plays a role in inflammatory responses to infection, though its exact role in normal immune function is unclear. Regions of this protein are also crucial for chemokine ligand binding, functional response of the receptor, and HIV co-receptor activity.[19]
Primary Protein Sequence
HIV[edit]
Further information: HIV tropism and Entry inhibitor
HIV-1 most commonly uses the chemokine receptors CCR5 and/or CXCR4 as co-receptors to enter target immunological cells.[20] These receptors are located on the surface of host immune cells whereby they provide a method of entry for the HIV-1 virus to infect the cell.[21] The HIV-1 envelope glycoprotein structure is essential in enabling the viral entry of HIV-1 into a target host cell.[21] The envelope glycoprotein structure consists of two protein subunits cleaved from a Gp160 protein precursor encoded for by the HIV-1 env gene: the Gp120 external subunit, and the Gp41 transmembrane subunit.[21] This envelope glycoprotein structure is arranged into a spike-like structure located on the surface of the virion and consists of a trimer of three Gp120-Gp41 hetero-dimers.[21] The Gp120 envelope protein is a chemokine mimic.[20] It lacks the unique structure of a chemokine, however it is still capable of binding to the CCR5 and CXCR4 chemokine receptors.[20] During HIV-1 infection, the Gp120 envelope glycoprotein subunit binds to a CD4 glycoprotein and a HIV-1 co-receptor expressed on a target cell- forming a heterotrimeric complex.[20] The formation of this complex stimulates the release of a fusogenic peptide inducing the fusion of the viral membrane with the membrane of the target host cell.[20] Because binding to CD4 alone can sometimes result in gp120 shedding, gp120 must next bind to co-receptor CCR5 in order for fusion to proceed. The tyrosine sulfated amino terminus of this co-receptor is the "essential determinant" of binding to the gp120 glycoprotein.[22] Co-receptor recognition also include the V1-V2 region of gp120, and the bridging sheet (an antiparallel, 4-stranded β sheet that connects the inner and outer domains of gp120). The V1-V2 stem can influence "co-receptor usage through its peptide composition as well as by the degree of N-linked glycosylation." Unlike V1-V2 however, the V3 loop is highly variable and thus is the most important determinant of co-receptor specificity.[22] The normal ligands for this receptor, RANTES, MIP-1β, and MIP-1α, are able to suppress HIV-1 infection in vitro. In individuals infected with HIV, CCR5-using viruses are the predominant species isolated during the early stages of viral infection,[23] suggesting that these viruses may have a selective advantage during transmission or the acute phase of disease. Moreover, at least half of all infected individuals harbor only CCR5-using viruses throughout the course of infection.
CCR5 is the primary co-receptor used by gp120 sequentially with CD4. This bind results in gp41, the other protein product of gp160, to be released from its metastable conformation and insert itself into the membrane of the host cell. Although it hasn't been finalized as a proven theory yet, binding of gp120-CCR5 involves two crucial steps: 1) The tyrosine sulfated amino terminus of this co-receptor is an "essential determinant" of binding to gp120 (as stated previously) 2) Following step 1., there must be reciprocal action (synergy, intercommunication) between gp120 and the CCR5 transmembrane domains [22]
CCR5 is essential for the spread of the R5-strain of the HIV-1 virus.[24] Knowledge of the mechanism by which this strain of HIV-1 mediates infection has prompted research into the development of therapeutic interventions to block CCR5 function.[25] A number of new experimental HIV drugs, called CCR5 receptor antagonists, have been designed to interfere with the associative binding between the Gp120 envelope protein and the HIV co-receptor CCR5.[24] These experimental drugs include PRO140 (CytoDyn), Vicriviroc (Phase III trials were cancelled in July 2010) (Schering Plough), Aplaviroc (GW-873140) (GlaxoSmithKline) and Maraviroc (UK-427857) (Pfizer). Maraviroc was approved for use by the FDA in August 2007.[24] It is the only one thus far approved by the FDA for clinical use, thus becoming the first CCR5 inhibitor.[22] A problem of this approach is that, while CCR5 is the major co-receptor by which HIV infects cells, it is not the only such co-receptor. It is possible that under selective pressure HIV will evolve to use another co-receptor. However, examination of viral resistance to AD101, molecular antagonist of CCR5, indicated that resistant viruses did not switch to another coreceptor (CXCR4) but persisted in using CCR5, either through binding to alternative domains of CCR5, or by binding to the receptor at a higher affinity. However, because there is still another co-receptor available, this indicates that lacking the CCR5 gene doesn't make one immune to the virus; it simply implies that it would be more challenging for the individual to contract it. Also, the virus still has access to the CD4. Unlike CCR5, which the body apparently doesn't really need due to those still living healthy lives even with the lack of/or absence of the gene (as a result of the delta 32 mutation), CD4 is critical in the body's defense system (fighting against infection).[26] Even without the availability of either co-receptors (even CCR5), the virus can still invade cells if gp41 were to go through an alteration (including its cytoplasmic tail), resulting in the independence of CD4 without the need of CCR5 and/or CXCR4 as a doorway.[27]
CCR5-Δ32[edit]
CCR5-Δ32 (or CCR5-D32 or CCR5 delta 32) is an allele of CCR5.[28][29]
CCR5 Δ32 is a 32-base-pair deletion that introduces a premature stop codon into the CCR5 receptor locus, resulting in a nonfunctional receptor.[30][31] CCR5 is required for M-tropic HIV-1 virus entry.[32] Individuals homozygous for CCR5 Δ32 do not express functional CCR5 receptors on their cell surfaces and are resistant to HIV-1 infection, despite multiple high-risk exposures.[32] Individuals heterozygous for the mutant allele have a greater than 50% reduction in functional CCR5 receptors on their cell surfaces due to dimerization between mutant and wild-type receptors that interferes with transport of CCR5 to the cell surface.[33] Heterozygote carriers are resistant to HIV-1 infection relative to wild types and when infected, heterozygotes exhibit reduced viral loads and a 2-3-year-slower progression to AIDS relative to wild types.[30][32][34] Heterozygosity for this mutant allele also has shown to improve one's virological response to anti-retroviral treatment.[35] CCR5 Δ32 has an (heterozygote) allele frequency of 10% in Europe, and a homozygote frequency of 1%.
Evolutionary history and age of the allele[edit]
The CCR5 Δ32 allele is notable for its recent origin, unexpectedly high frequency, and distinct geographic distribution,[36] which together suggest that (a) it arose from a single mutation, and (b) it was historically subject to positive selection.
Two studies have used linkage analysis to estimate the age of the CCR5 Δ32 deletion, assuming that the amount of recombination and mutation observed on genomic regions surrounding the CCR5 Δ32 deletion would be proportional to the age of the deletion.[29][37] Using a sample of 4000 individuals from 38 ethnic populations, Stephens et al. estimated that the CCR5-Δ32 deletion occurred 700 years ago (275-1875, 95% confidence interval). Another group, Libert et al. (1998), estimated the age of the CCR5 Δ32 mutation is based on the microsatellite mutations to be 2100 years (700-4800, 95% confidence interval). On the basis of observed recombination events, they estimated the age of the mutation to be 2250 years (900-4700, 95% confidence interval).[37] A third hypothesis relies on the north-to-south gradient of allele frequency in Europe which shows that the highest allele frequency occurred in Nordic regions such as Iceland, Norway and Sweden and lowest allele frequency in the south. Because the Vikings historically occupied these countries, it may be possible that the allele spread throughout Europe was due to the Viking dispersal in the 8th to 10th century.[38] Vikings were later replaced by the Varangians in Russia, which migrated East which may have contributed to the observed east-to-west cline of allele frequency.[36][38]
HIV-1 was initially transmitted from chimpanzees (Pan troglodytes) to humans in the early 1900s in Southeast Cameroon, Africa,[39] through exposure to infected blood and body fluids while butchering bushmeat.[40] However, HIV-1 was effectively absent from Europe until the late 1980s.[41] Therefore, given the average age of roughly 1000 years for the CCR5-Δ32 allele, it can be established that HIV-1 did not exert selection pressure on the human population for long enough to achieve the current frequencies.[36] Hence, other pathogens have been suggested agents of positive selection for CCR5 Δ32. The first major one being bubonic plague (Yersinia pestis), and later, smallpox (Variola major). Other data suggest that the allele frequency resulted as a negative selection pressure as a result of pathogens that became more widespread during Roman expansion.[42] The idea that negative selection played a role in its low frequency is also supported by experiments using knockout mice and Influenza A, which demonstrated that the presence of the CCR5 receptor is important for efficient response to a pathogen.[43][44]
Evidence for a single mutation[edit]
Several lines of evidence suggest that the CCR5 Δ32 allele evolved only once.[36] First, CCR5 Δ32 has a relatively high frequency in several different Caucasian populations but is comparatively absent in Asian, Middle Eastern and American Indian populations,[29] suggesting that a single mutation occurred after divergence of Caucasians from their African ancestor.[29][30][45] Second, genetic linkage analysis indicates that the mutation occurs on a homogenous genetic background, implying that inheritance of the mutation occurred from a common ancestor.[37] This was demonstrated by showing that the CCR5 Δ32 allele is in strong linkage disequilibrium with highly polymorphic microsatellites. More than 95% of CCR5 Δ32 chromosomes also carried the IRI3.1-0 allele, while 88% carried the IRI3.2 allele. By contrast, the microsatellite markers IRI3.1-0 and IRI3.2-0 were found in only 2 or 1.5% of chromosomes carrying a wild-type CCR5 allele.[37] This evidence of linkage disequilibrium supports the hypothesis that most, if not all, CCR5 Δ32 alleles arose from a single mutational event. Finally, the CCR5 Δ32 allele has a unique geographical distribution indicating a single Northern origin followed by migration. A study measuring allele frequencies in 18 European populations found a North-to-South gradient, with the highest allele frequencies in Finnish and Mordvinian populations (16%), and the lowest in Sardinia (4%).[37]
Positive selection[edit]
In the absence of selection, a single mutation would take an estimated 127,500 years to rise to a population frequency of 10%.[29] Estimates based on genetic recombination and mutation rates place the age of the allele between 1000 and 2000 years. This discrepancy is a signature of positive selection.
It is estimated that HIV-1 entered the human population in Africa in the early 1900s,[39] symptomatic infections were not reported until the 1980s. The HIV-1 epidemic is therefore far too young to be the source of positive selection that drove the frequency of CCR5 Δ32 from zero to 10% in 2000 years. In 1998, Stephens et al. suggested that bubonic plague (Yersinia pestis) had exerted positive selective pressure on CCR5 Δ32.[29] This hypothesis was based on the timing and severity of the Black Death pandemic, which killed 30% of the European population of all ages between 1346 and 1352.[46] After the Black Death, there were less severe, intermittent, epidemics. Individual cities experienced high mortality, but overall mortality in Europe was only a few percent.[46][47][48] In 1655-1656 a second pandemic called the "Great Plague" killed 15-20% of Europe’s population.[46][49] Importantly, the plague epidemics were intermittent. Bubonic plague is a zoonotic disease, primarily infecting rodents and spread by fleas and only occasionally infecting humans.[50] Human-to-human infection of bubonic plague does not occur, though it can occur in pneumonic plague, which infects the lungs.[51] Only when the density of rodents is low are infected fleas forced to feed on alternative hosts such as humans, and under these circumstances a human epidemic may occur.[50] Based on population genetic models, Galvani and Slatkin (2003) argue that the intermittent nature of plague epidemics did not generate a sufficiently strong selective force to drive the allele frequency of CCR5 Δ32 to 10% in Europe.[28]
To test this hypothesis, Galvani and Slatkin (2003) modeled the historical selection pressures produced by plague and smallpox.[28] Plague was modeled according to historical accounts,[52][53] while age-specific smallpox mortality was gleaned from the age distribution of smallpox burials in York (England) between 1770 and 1812.[47] Smallpox preferentially infects young, pre-reproductive members of the population since they are the only individuals who are not immunized or dead from past infection. Because smallpox preferentially kills pre-reproductive members of a population, it generates stronger selective pressure than plague.[28] Unlike plague, smallpox does not have an animal reservoir and is only transmitted from human to human.[54][55] The authors calculated that if plague were selecting for CCR5 Δ32, the frequency of the allele would still be less than 1%, while smallpox has exerted a selective force sufficient to reach 10%.
The hypothesis that smallpox exerted positive selection for CCR5 Δ32 is also biologically plausible, since poxviruses, like HIV, are viruses that enter white blood cells by using chemokine receptors.[56] By contrast, Yersinia pestis is a bacterium with a very different biology.
Although Caucasians are the only population with a high frequency of CCR5 Δ32, they are not the only population that has been subject to selection by smallpox, which had a worldwide distribution before it was declared eradicated in 1980. The earliest unmistakable descriptions of smallpox appear in the 5th century A.D. in China, the 7th century A.D. in India and the Mediterranean, and the 10th century A.D. in southwestern Asia.[55] By contrast, the CCR5 Δ32 mutation is found only in European, West Asian, and North African populations.[57] The anomalously high frequency of CCR5 Δ32 in these populations appears to require both a unique origin in Northern Europe and subsequent selection by smallpox.
Potential costs[edit]
Research has not yet revealed a cost of carrying the CCR5 null mutation that is as dramatic as the benefit conferred in the context of HIV-1 exposure. In general, research suggests that the CCR5 Δ32 mutation protects against diseases caused by certain pathogens but may also play a deleterious role in postinfection inflammatory processes, which can injure tissue and create further pathology.[58] The best evidence for this proposed antagonistic pleiotropy is found in flavivirus infections. In general many viral infections are asymptomatic or produce only mild symptoms in the vast majority of the population. However, certain unlucky individuals experience a particularly destructive clinical course, which is otherwise unexplained but appears to be genetically mediated. Patients homozygous for CCR5 Δ32 were found to be at higher risk for a neuroinvasive form of tick-borne encephalitis (a flavivirus).[59] In addition, functional CCR5 may be required to prevent symptomatic disease after infection with West Nile virus, another flavivirus; CCR5 Δ32 was associated with early symptom development and more pronounced clinical manifestations after infection with West Nile virus.[60]
This finding in humans confirmed a previously-observed experiment in an animal model of CCR5 Δ32 homozygosity. After infection with West Nile Virus, CCR5 Δ32 mice had markedly increased viral titers in the central nervous system and had increased mortality[61] compared with that of wild-type mice, thus suggesting that CCR5 expression was necessary to mount a strong host defense against West Nile virus.
CCR5 Δ32 can be beneficial to the host in some infections (e.g., HIV-1, possibly smallpox), but detrimental in others (e.g., tick-borne encephalitis, West Nile virus). Whether CCR5 function is helpful or harmful in the context of a given infection depends on a complex interplay between the immune system and the pathogen.
Medical applications[edit]
A genetic approach involving intrabodies that block CCR5 expression has been proposed as a treatment for HIV-1 infected individuals.[62] When T-cells modified so they no longer express CCR5 were mixed with unmodified T-cells expressing CCR5 and then challenged by infection with HIV-1, the modified T-cells that do not express CCR5 eventually take over the culture, as HIV-1 kills the non-modified T-cells. This same method might be used in vivo to establish a virus-resistant cell pool in infected individuals.[62]
This hypothesis was tested in an AIDS patient who had also developed myeloid leukemia, and was treated with chemotherapy to suppress the cancer. A bone marrow transplant containing stem cells from a matched donor was then used to restore the immune system. However, the transplant was performed from a donor with 2 copies of CCR5-Δ32 mutation gene. After 600 days, the patient was healthy and had undetectable levels of HIV in the blood and in examined brain and rectal tissues.[6][63] Before the transplant, low levels of HIV X4, which does not use the CCR5 receptor, were also detected. Following the transplant, however, this type of HIV was not detected either, further baffling doctors.[6] However, this is consistent with the observation that cells expressing the CCR5-Δ32 variant protein lack both the CCR5 and CXCR4 receptors on their surfaces, thereby conferring resistance to a broad range of HIV variants including HIV X4.[64] After over six years, the patient has maintained the resistance to HIV and has been pronounced cured of the HIV infection.[7]
Enrollment of HIV-positive patients in a clinical trial was started in 2009 in which the patients' cells were genetically modified with a zinc finger nuclease to carry the CCR5-Δ32 trait and then reintroduced into the body as a potential HIV treatment.[65][66] Results reported in 2014 were promising.[10]
Inspired by the first person ever to be cured of HIV, The Berlin Patient, StemCyte began collaborations with Cord blood banks worldwide to systematically screen Umbilical cord blood samples for the CCR5 mutation beginning in 2011.[67] [68][69]
Further information: Long-term nonprogressor
See also[edit]
Discovery and development of CCR5 receptor antagonists
Entry inhibitor
HIV tropism
Stephen Crohn
HIV immunity
References[edit]
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Jump up ^ Michael NL, Louie LG, Rohrbaugh AL, Schultz KA, Dayhoff DE, Wang CE, Sheppard HW (Oct 1997). "The role of CCR5 and CCR2 polymorphisms in HIV-1 transmission and disease progression". Nature Medicine. 3 (10): 1160–2. doi:10.1038/nm1097-1160. PMID 9334732.
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^ Jump up to: a b Keele BF, Van Heuverswyn F, Li Y, Bailes E, Takehisa J, Santiago ML, Bibollet-Ruche F, Chen Y, Wain LV, Liegeois F, Loul S, Ngole EM, Bienvenue Y, Delaporte E, Brookfield JF, Sharp PM, Shaw GM, Peeters M, Hahn BH (Jul 2006). "Chimpanzee reservoirs of pandemic and nonpandemic HIV-1". Science. 313 (5786): 523–6. doi:10.1126/science.1126531. PMC 2442710  . PMID 16728595.
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Jump up ^ Faure E, Royer-Carenzi M (2008). "Is the European spatial distribution of the HIV-1-resistant CCR5-Δ32 allele formed by a breakdown of the pathocenosis due to the historical Roman expansion?". Infection, Genetics and Evolution. 8 (6): 864–874. doi:10.1016/j.meegid.2008.08.007. PMID 18790087.
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Jump up ^ O'Brien SJ, Dean M (Sep 1997). "In search of AIDS-resistance genes". Scientific American. 277 (3): 44–51. doi:10.1038/scientificamerican0997-44. PMID 9274039.
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Jump up ^ Hatcher J (1977). Plague, Population, and the English Economy 1348-1530. London: MacMillan.
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Jump up ^ Appleby AB (1980). "The disappearance of plague: a continuing puzzle". The Economic History Review. 33 (2): 161–73. doi:10.2307/2595837. JSTOR 2595837. PMID 11614424.
Jump up ^ Russel J (1948). British Mediaeval Population. Albequerque: University of New Mexico Press.
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Jump up ^ Chapin C (1913). "Variation in the type of infectious diseases as shown by the history of smallpox in the United States, 1815-1912". J Infect Dis. 13 (2): 171–196. doi:10.1093/infdis/13.2.171.
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Jump up ^ Novembre J, Galvani AP, Slatkin M (Nov 2005). "The geographic spread of the CCR5 Delta32 HIV-resistance allele". PLoS Biology. 3 (11): e339. doi:10.1371/journal.pbio.0030339. PMC 1255740  . PMID 16216086.
Jump up ^ Klein RS (Jan 2008). "A moving target: the multiple roles of CCR5 in infectious diseases". The Journal of Infectious Diseases. 197 (2): 183–6. doi:10.1086/524692. PMID 18179384.
Jump up ^ Kindberg E, Mickiene A, Ax C, Akerlind B, Vene S, Lindquist L, Lundkvist A, Svensson L (Jan 2008). "A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis". The Journal of Infectious Diseases. 197 (2): 266–9. doi:10.1086/524709. PMID 18179389.
Jump up ^ Lim JK, Louie CY, Glaser C, Jean C, Johnson B, Johnson H, McDermott DH, Murphy PM (Jan 2008). "Genetic deficiency of chemokine receptor CCR5 is a strong risk factor for symptomatic West Nile virus infection: a meta-analysis of 4 cohorts in the US epidemic". The Journal of Infectious Diseases. 197 (2): 262–5. doi:10.1086/524691. PMID 18179388.
Jump up ^ Glass WG, Lim JK, Cholera R, Pletnev AG, Gao JL, Murphy PM (Oct 2005). "Chemokine receptor CCR5 promotes leukocyte trafficking to the brain and survival in West Nile virus infection". The Journal of Experimental Medicine. 202 (8): 1087–98. doi:10.1084/jem.20042530. PMC 2213214  . PMID 16230476.
^ Jump up to: a b Steinberger P, Andris-Widhopf J, Bühler B, Torbett BE, Barbas CF (Jan 2000). "Functional deletion of the CCR5 receptor by intracellular immunization produces cells that are refractory to CCR5-dependent HIV-1 infection and cell fusion". Proceedings of the National Academy of Sciences of the United States of America. 97 (2): 805–10. Bibcode:2000PNAS...97..805S. doi:10.1073/pnas.97.2.805. PMC 15412  . PMID 10639161.
Jump up ^ Schoofs M (2008-11-07). "A Doctor, a Mutation and a Potential Cure for AIDS". The Wall Street Journal. Retrieved 2010-12-15.
Jump up ^ Agrawal L, Lu X, Qingwen J, VanHorn-Ali Z, Nicolescu IV, McDermott DH, Murphy PM, Alkhatib G (Mar 2004). "Role for CCR5Delta32 protein in resistance to R5, R5X4, and X4 human immunodeficiency virus type 1 in primary CD4+ cells". Journal of Virology. 78 (5): 2277–87. doi:10.1128/JVI.78.5.2277-2287.2004. PMC 369216  . PMID 14963124.
Jump up ^ "Autologous T-Cells Genetically Modified at the CCR5 Gene by Zinc Finger Nucleases SB-728 for HIV (Zinc-Finger)". U.S. National Institutes of Health. 2009-12-09. Retrieved 2009-12-30.
Jump up ^ Wade N (2009-12-28). "Zinc Fingers Could Be Key to Reviving Gene Therapy". The New York Times. Retrieved 2009-12-30.
Jump up ^ Corbyn Z (July 2012). "Plan launched to find HIV cure". Lancet. 380 (9838): 203–4. PMID 22826833.
Jump up ^ Gonzalez G, Park S, Chen D, Armitage S, Shpall E, Behringer R (September 2011). "Identification and frequency of CCR5Δ32/Δ32 HIV-resistant cord blood units from Houston area hospitals". HIV Medicine. 12 (8): 481–6. doi:10.1111/j.1468-1293.2010.00911.x. PMID 21375684.
Jump up ^ Petz LD, Burnett JC, Li H, Li S, Tonai R, Bakalinskaya M, Shpall EJ, Armitage S, Kurtzberg J, Regan DM, Clark P, Querol S, Gutman JA, Spellman SR, Gragert L, Rossi JJ (2015). "Progress toward curing HIV infection with hematopoietic cell transplantation". Stem Cells and Cloning. 8: 109–16. doi:10.2147/SCCAA.S56050. PMC 4524463  . PMID 26251620.
Further reading[edit]
Wilkinson D (Sep 1996). "Cofactors provide the entry keys. HIV-1". Current Biology. 6 (9): 1051–3. doi:10.1016/S0960-9822(02)70661-1. PMID 8805353.
Broder CC, Dimitrov DS (1996). "HIV and the 7-transmembrane domain receptors". Pathobiology. 64 (4): 171–9. doi:10.1159/000164032. PMID 9031325.
Choe H, Martin KA, Farzan M, Sodroski J, Gerard NP, Gerard C (Jun 1998). "Structural interactions between chemokine receptors, gp120 Env and CD4". Seminars in Immunology. 10 (3): 249–57. doi:10.1006/smim.1998.0127. PMID 9653051.
Sheppard HW, Celum C, Michael NL, O'Brien S, Dean M, Carrington M, Dondero D, Buchbinder SP (Mar 2002). "HIV-1 infection in individuals with the CCR5-Delta32/Delta32 genotype: acquisition of syncytium-inducing virus at seroconversion". Journal of Acquired Immune Deficiency Syndromes. 29 (3): 307–13. doi:10.1097/00042560-200203010-00013. PMID 11873082.
Freedman BD, Liu QH, Del Corno M, Collman RG (2003). "HIV-1 gp120 chemokine receptor-mediated signaling in human macrophages". Immunologic Research. 27 (2–3): 261–76. doi:10.1385/IR:27:2-3:261. PMID 12857973.
Esté JA (Sep 2003). "Virus entry as a target for anti-HIV intervention". Current Medicinal Chemistry. 10 (17): 1617–32. doi:10.2174/0929867033457098. PMID 12871111.
Gallo SA, Finnegan CM, Viard M, Raviv Y, Dimitrov A, Rawat SS, Puri A, Durell S, Blumenthal R (Jul 2003). "The HIV Env-mediated fusion reaction". Biochimica et Biophysica Acta. 1614 (1): 36–50. doi:10.1016/S0005-2736(03)00161-5. PMID 12873764.
Zaitseva M, Peden K, Golding H (Jul 2003). "HIV coreceptors: role of structure, posttranslational modifications, and internalization in viral-cell fusion and as targets for entry inhibitors". Biochimica et Biophysica Acta. 1614 (1): 51–61. doi:10.1016/S0005-2736(03)00162-7. PMID 12873765.
Lee C, Liu QH, Tomkowicz B, Yi Y, Freedman BD, Collman RG (Nov 2003). "Macrophage activation through CCR5- and CXCR4-mediated gp120-elicited signaling pathways". Journal of Leukocyte Biology. 74 (5): 676–82. doi:10.1189/jlb.0503206. PMID 12960231.
Yi Y, Lee C, Liu QH, Freedman BD, Collman RG (2004). "Chemokine receptor utilization and macrophage signaling by human immunodeficiency virus type 1 gp120: Implications for neuropathogenesis". Journal of Neurovirology. 10 Suppl 1: 91–6. doi:10.1080/753312758. PMID 14982745.
Seibert C, Sakmar TP (2004). "Small-molecule antagonists of CCR5 and CXCR4: a promising new class of anti-HIV-1 drugs". Current Pharmaceutical Design. 10 (17): 2041–62. doi:10.2174/1381612043384312. PMID 15279544.
Cutler CW, Jotwani R (2006). "Oral mucosal expression of HIV-1 receptors, co-receptors, and alpha-defensins: tableau of resistance or susceptibility to HIV infection?". Advances in Dental Research. 19 (1): 49–51. doi:10.1177/154407370601900110. PMC 3750741  . PMID 16672549.
Ajuebor MN, Carey JA, Swain MG (Aug 2006). "CCR5 in T cell-mediated liver diseases: what's going on?". Journal of Immunology. 177 (4): 2039–45. doi:10.4049/jimmunol.177.4.2039. PMID 16887960.
Lipp M, Müller G (2003). "Shaping up adaptive immunity: the impact of CCR7 and CXCR5 on lymphocyte trafficking". Verhandlungen Der Deutschen Gesellschaft Für Pathologie. 87: 90–101. PMID 16888899.
Balistreri CR, Caruso C, Grimaldi MP, Listì F, Vasto S, Orlando V, Campagna AM, Lio D, Candore G (Apr 2007). "CCR5 receptor: biologic and genetic implications in age-related diseases". Annals of the New York Academy of Sciences. 1100: 162–72. Bibcode:2007NYASA1100..162B. doi:10.1196/annals.1395.014. PMID 17460174.
Madsen HO, Poulsen K, Dahl O, Clark BF, Hjorth JP (Mar 1990). "Retropseudogenes constitute the major part of the human elongation factor 1 alpha gene family". Nucleic Acids Research. 18 (6): 1513–6. doi:10.1093/nar/18.6.1513. PMC 330519  . PMID 2183196.
Uetsuki T, Naito A, Nagata S, Kaziro Y (Apr 1989). "Isolation and characterization of the human chromosomal gene for polypeptide chain elongation factor-1 alpha". The Journal of Biological Chemistry. 264 (10): 5791–8. PMID 2564392.
Whiteheart SW, Shenbagamurthi P, Chen L, Cotter RJ, Hart GW (Aug 1989). "Murine elongation factor 1 alpha (EF-1 alpha) is posttranslationally modified by novel amide-linked ethanolamine-phosphoglycerol moieties. Addition of ethanolamine-phosphoglycerol to specific glutamic acid residues on EF-1 alpha". The Journal of Biological Chemistry. 264 (24): 14334–41. PMID 2569467.
Ann DK, Wu MM, Huang T, Carlson DM, Wu R (Mar 1988). "Retinol-regulated gene expression in human tracheobronchial epithelial cells. Enhanced expression of elongation factor EF-1 alpha". The Journal of Biological Chemistry. 263 (8): 3546–9. PMID 3346208.
Brands JH, Maassen JA, van Hemert FJ, Amons R, Möller W (Feb 1986). "The primary structure of the alpha subunit of human elongation factor 1. Structural aspects of guanine-nucleotide-binding sites". European Journal of Biochemistry / FEBS. 155 (1): 167–71. doi:10.1111/j.1432-1033.1986.tb09472.x. PMID 3512269.
External links[edit]
Crystal Structure of the CCR5 Chemokine Receptor A rotatable, zoomable 3-D image from rcsb.org
Video and text from a PBS documentary about the discovery of CCR5
"Chemokine Receptors: CCR5". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology.
HuGENavigator literature on HIV Infections and CCR5 from CDC - (note, authors may not be CDC employees, and there is no public domain notice on the page, so this cannot be assumed to be public domain)
Schering-Plough Initiates Phase III Studies with CCR5-Vicriviroc in Treatment- Experienced HIV Patients.
HIVcoPred A server for prediction of HIV coreceptor usage (CCR5). PLoS ONE 8(4): e61437
Human CCR5 genome location and CCR5 gene details page in the UCSC Genome Browser.
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CD329
CD331
CD332
CD333
CD334
CD335
CD336
CD337
CD338
CD339
CD340
CD344
CD349
CD350
[show]
v
t
e
Chemokine receptor modulators
CC
CCR1
Agonists: CCL4 (MIP-1β)
CCL5 (RANTES)
CCL6
CCL9 (CCL10)
CCL14
CCL15
CCL16
CCL23
CCR2
Agonists: CCL2
CCL8
CCL12
CCL16
NAMs: Cenicriviroc (TAK-652, TBR-652)
CCR3
Agonists: CCL5 (RANTES)
CCL7
CCL11
CCL13
CCL15
CCL18
CCL24
CCL26
CCL28
CCR4
Agonists: CCL3 (MIP-1α)
CCL5 (RANTES)
CCL17
CCL22
Antibodies: Mogamulizumab (against CCR4)
CCR5
Agonists: CCL3 (MIP-1α)
CCL4 (MIP-1β)
CCL5 (RANTES)
CCL8
CCL11
CCL13
CCL14
CCL16
NAMs: Aplaviroc
Cenicriviroc (TAK-652, TBR-652)
INCB009471
Maraviroc
Vicriviroc
Antibodies: PRO-140
CCR6
Agonists: CCL20
CCR7
Agonists: CCL19
CCL21
CCR8
Agonists: CCL1
CCL16
CCR9
Agonists: CCL25
CCR10
Agonists: CCL27
CCL28
CCR11
Agonists: CCL19
CCL21
CCL25
Ungrouped
Antibodies: Bertilimumab (against CCL11)
Carlumab (against CCL2)
CXC
CXCR1
(IL-8Rα)
Agonists: CXCL6
Emoctakin
Interleukin-8 (CXCL8, GCP-1)
Antagonists: Navarixin
NAMs: Ladarixin
Reparixin (repertaxin)
CXCR2
(IL-8Rβ)
Agonists: CXCL1 (MGSA)
CXCL2
CXCL3
CXCL5
CXCL6
CXCL7
Emoctakin
Garnocestim
Interleukin-8 (CXCL8, GCP-1)
Antagonists: Danirixin
Elubrixin
Navarixin
NAMs: Ladarixin
Reparixin (repertaxin)
CXCR3
Agonists: CXCL4 (PF4)
CXCL9 (MIG)
CXCL10 (IP-10)
CXCL11 (I-TAC)
Iroplact
Antibodies: Eldelumab (against CXCL10)
CXCR4
Agonists: MIF
SDF-1 (CXCL12)
Ubiquitin
Antagonists: Plerixafor (AMD3100)
Antibodies: Ulocuplumab (against CXCR4)
CXCR5
Agonists: CXCL13
CXCR6
Agonists: CXCL16
CXCR7
Agonists: CXCL11 (I-TAC)
SDF-1 (CXCL12)
PAMs: Plerixafor (AMD3100)
C (XC)
XCR1
Agonists: Lymphotactin-α (XCL1)
Lymphotactin-β (XCL2)
Antibodies: Pateclizumab
CX3C
CX3CR1
Agonists: Fractalkine (CX3CL1)
Others
CCBP2
Agonists: CC (β) chemokines
CMKLR1
Agonists: Chemerin
Resolvin E1
See also
Receptor/signaling modulators
Signaling peptide/protein receptor modulators
Cytokine receptor modulators
Retrieved from "https://en.wikipedia.org/w/index.php?title=CCR5&oldid=813042265"
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text:
Feed Jake
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"Feed Jake"
Single by Pirates of the Mississippi
from the album Pirates of the Mississippi
Released
February 25, 1991
Format
CD single, cassette single
Genre
Country
Length
4:00
Label
Capitol
Songwriter(s)
Danny "Bear" Mayo [1]
Producer(s)
Rich Alves, James Stroud
Pirates of the Mississippi singles chronology
"Rollin' Home"
(1990) "Feed Jake"
(1991) "Speak of the Devil"
(1991)
"Rollin' Home"
(1990) "Feed Jake"
(1991) "Speak of the Devil"
(1991)
"Feed Jake" is a song written by Danny "Bear" Mayo, and recorded by the American country music band Pirates of the Mississippi. It was released in February 1991 as the third single from the band's self-titled debut album. The song is also the band's highest chart peak, having reached number 15 on the Billboard Hot Country Singles & Tracks (now Hot Country Songs) charts.
Contents
[hide]
1 Content
2 Music video
3 Critical reception
4 Chart performance
5 Other versions
6 References
7 External links
Content[edit]
"Feed Jake" is a mid-tempo accompanied mainly by guitar and synthesized strings.[1] In the chorus, the male narrator reminisces on his childhood friend, a dog named Jake ("If I die before I wake / Feed Jake..."). The narrator also addresses societal stereotypes toward homeless people and homosexuals, of whom the latter are addressed in the final verse.[2]
Guitarist Rich Alves said of the song that it "means something different to everyone who hears it."[3]
Music video[edit]
Robert Deaton and George J. Flanigen IV, both of whom lead the film and video production team of Deaton Flanigen, directed the song's music video, which was one of the first of its kind in the country music industry to not feature the artist at all.[4] Most of the music video was filmed southwest of Nashville, Tennessee on Tennessee State Route 100 as well as on Highway 70 in White Bluff, Tennessee. It tells the song's story through two men, who are childhood friends, as shown in flashbacks. Later on, one of the men is attending the other's funeral, and the surviving man goes to meet his dog, which he and the deceased friend adopted together, at the cemetery. Upon its release, the music video was believed by some members of the gay community to have a gay theme; the two men were said to be lovers, one of whom dies from AIDS at the end.[2] Kimberly Lansing, then the executive producer of Deaton-Flanigen Productions, said that the video was "not meant one way or another" regarding the back story or the one man's death. Lansing also said that the video is about returning home and not fitting in anymore. Additionally, because of the Persian Gulf War, some people have also assumed that the man's death is war-related.[2]
Critical reception[edit]
In the book The Encyclopedia of Country Music, Tom Roland wrote that the final verse, with its theme of tolerance towards homosexuals, showed a shift in political beliefs for the typically conservative country music audience.[5]
Chart performance[edit]
"Feed Jake" debuted on the U.S. Billboard Hot Country Singles & Tracks for the week of March 16, 1991. It spent 20 weeks on the Billboard Hot Country Singles & Tracks (now Hot Country Songs) charts, peaking at number 15.
Chart (1991)
Peak
position
Canada Country Tracks (RPM)[6] 12
US Hot Country Songs (Billboard)[7] 15
Other versions[edit]
A live recording appeared on the band's 1995 album Paradise for Giant Records. This version was produced by David Malloy.[8]
References[edit]
^ Jump up to: a b Pirates of the Mississippi (Media notes). Pirates of the Mississippi. Capitol Records Nashville. 1990. C2-94389.
^ Jump up to: a b c Smith, Russell (4 July 1991). ""Feed Jake" video clip gives rise to questions". Dallas Morning News. Retrieved 21 August 2009.
Jump up ^ Asker, Jim (6 April 1991). "Pirate Power: After a rough start, it's smooth sailing for band". The Free-Lance Star. Retrieved 21 August 2009.
Jump up ^ "Inventive images on the increase". USA Today. 17 April 1991. Retrieved 21 August 2009.
Jump up ^ Kingsbury, Paul; et al. (2004). The Encyclopedia of Country Music. Sourcebooks, Inc. p. 417. ISBN 0-19-517608-1.
Jump up ^ "Top RPM Country Tracks: Issue 1544." RPM. Library and Archives Canada. June 15, 1991. Retrieved August 16, 2013.
Jump up ^ "Pirates of the Mississippi Chart History (Hot Country Songs)". Billboard.
Jump up ^ Paradise (CD booklet). Pirates of the Mississippi. Giant Records. 1995. 24603.
External links[edit]
Lyrics of this song at MetroLyrics
[hide]
v
t
e
Pirates of the Mississippi
Studio albums
Pirates of the Mississippi
Walk the Plank
A Street Man Named Desire
Dream You
Paradise
Heaven and a Dixie Night
Compilation albums
The Best of Pirates of the Mississippi
Notable singles
"Honky Tonk Blues"
"Feed Jake"
"Speak of the Devil"
"Til I'm Holding You Again"
"Too Much"
Retrieved from "https://en.wikipedia.org/w/index.php?title=Feed_Jake&oldid=789217712"
Categories:
1991 singles
Music videos directed by Deaton-Flanigen Productions
Pirates of the Mississippi songs
Songs written by Danny Mayo
Song recordings produced by James Stroud
Capitol Records Nashville singles
LGBT-related songs
Song recordings produced by David Malloy
1991 songs
Hidden categories:
Articles with hAudio microformats
Singlechart usages for Canadacountry
Singlechart called without artist
Singlechart called without song
Singlechart usages for Billboardcountrysongs
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