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1. Bud Powell Transcription Pdf Files

Jan 28, 2015. Anyways, I can't deny the joy I'm having to gradually discover Bud Powell's artistry. This is a deep dive into bebop.Hold your breath, hope you'll like it. Full transcript below and also pdf https://www.dropbox.com/s/8s40k4t12z5u0wd/Anthropology%20-Bud%20Powell%20Lausanne%2062.pdf?dl=0. May 26, 2017. Solos - Jazz Solo Transcriptions. PDFs at the Bottom of the page. Gingerbread Boy. Complete Studio Recordings (with Clark Terry). With the Duke Ellington Orchestra. And the necessary references are in general noted in the pdf. Their support helps keep this program free. Table of Contents General.

The human immunodeficiency viruses (HIV) are two species of Lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).^[1][2] AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.^[3] In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of blood, pre-ejaculate, semen, and vaginal fluids. Research has shown (for both same-sex and opposite-sex couples) that HIV is untransmissable through condomless sexual intercourse if the HIV-positive partner has a consistently undetectable viral load.^[4][5] Non-sexual transmission can occur from an infected mother to her infant during pregnancy, during childbirth by exposure to her blood or vaginal fluid, and through breast milk.^[6][7][8][9] Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.

HIV infects vital cells in the human immune system, such as helper T cells (specifically CD4⁺ T cells), macrophages, and dendritic cells.^[10] HIV infection leads to low levels of CD4⁺ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,^[11]apoptosis of uninfected bystander cells,^[12] direct viral killing of infected cells, and killing of infected CD4⁺ T cells by CD8⁺ cytotoxic lymphocytes that recognize infected cells.^[13] When CD4⁺ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections, leading to the development of AIDS.

• 1Virology
  • 1.4Replication cycle
• 5History

Virology

Classification

HIV is a member of the genusLentivirus,^[14] part of the family Retroviridae.^[15] Lentiviruses have many morphologies and biological properties in common. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.^[16] Lentiviruses are transmitted as single-stranded, positive-sense, envelopedRNA viruses. Upon entry into the target cell, the viral RNAgenome is converted (reverse transcribed) into double-stranded DNA by a virally encoded enzyme, reverse transcriptase, that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded enzyme, integrase, and host co-factors.^[17] Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system, for an indeterminate amount of time.^[18] The HIV virus can remain dormant in the human body for up to ten years after primary infection; during this period the virus does not cause symptoms. Alternatively, the integrated viral DNA may be transcribed, producing new RNA genomes and viral proteins, using host cell resources, that are packaged and released from the cell as new virus particles that will begin the replication cycle anew.

Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both lymphadenopathy associated virus (LAV) and human T-lymphotropic virus 3 (HTLV-III). HIV-1 is more virulent and more infective than HIV-2,^[19] and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2, compared to HIV-1, implies that fewer of those exposed to HIV-2 will be infected per exposure. Due to its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.^[20]

Structure and genome

HIV is different in structure from other retroviruses. It is roughly spherical^[21] with a diameter of about 120 nm, around 60 times smaller than a red blood cell.^[22] It is composed of two copies of positive-sensesingle-strandedRNA that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein p24.^[23] The single-stranded RNA is tightly bound to nucleocapsid proteins, p7, and enzymes needed for the development of the virion such as reverse transcriptase, proteases, ribonuclease and integrase. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle.^[23]

This is, in turn, surrounded by the viral envelope, that is composed of the lipid bilayer taken from the membrane of a human host cell when the newly formed virus particle buds from the cell. The viral envelope contains proteins from the host cell and relatively few copies of the HIV Envelope protein,^[23] which consists of a cap made of three molecules known as glycoprotein (gp) 120, and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope.^[24][25] The Envelope protein, encoded by the HIV env gene, allows the virus to attach to target cells and fuse the viral envelope with the target cell's membrane releasing the viral contents into the cell and initiating the infectious cycle.^[24]

As the sole viral protein on the surface of the virus, the Envelope protein is a major target for HIV vaccine efforts.^[26] Over half of the mass of the trimeric envelope spike is N-linked glycans. The density is high as the glycans shield the underlying viral protein from neutralisation by antibodies. This is one of the most densely glycosylated molecules known and the density is sufficiently high to prevent the normal maturation process of glycans during biogenesis in the endoplasmic and Golgi apparatus.^[27][28] The majority of the glycans are therefore stalled as immature 'high-mannose' glycans not normally present on human glycoproteins that are secreted or present on a cell surface.^[29] The unusual processing and high density means that almost all broadly neutralising antibodies that have so far been identified (from a subset of patients that have been infected for many months to years) bind to, or are adapted to cope with, these envelope glycans.^[30]

The molecular structure of the viral spike has now been determined by X-ray crystallography^[31] and cryogenic electron microscopy.^[32] These advances in structural biology were made possible due to the development of stable recombinant forms of the viral spike by the introduction of an intersubunit disulphide bond and an isoleucine to prolinemutation (radical replacement of an amino acid) in gp41.^[33] The so-called SOSIP trimers not only reproduce the antigenic properties of the native viral spike, but also display the same degree of immature glycans as presented on the native virus.^[34] Recombinant trimeric viral spikes are promising vaccine candidates as they display less non-neutralising epitopes than recombinant monomeric gp120, which act to suppress the immune response to target epitopes.^[35]

The RNA genome consists of at least seven structural landmarks (LTR, TAR, RRE, PE, SLIP, CRS, and INS), and nine genes (gag, pol, and env, tat, rev, nef, vif, vpr, vpu, and sometimes a tenth tev, which is a fusion of tat, env and rev), encoding 19 proteins. Three of these genes, gag, pol, and env, contain information needed to make the structural proteins for new virus particles.^[23] For example, env codes for a protein called gp160 that is cut in two by a cellular protease to form gp120 and gp41. The six remaining genes, tat, rev, nef, vif, vpr, and vpu (or vpx in the case of HIV-2), are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus (replicate), or cause disease.^[23]

The two tat proteins (p16 and p14) are transcriptional transactivators for the LTR promoter acting by binding the TAR RNA element. The TAR may also be processed into microRNAs that regulate the apoptosis genes ERCC1 and IER3.^[36][37] The rev protein (p19) is involved in shuttling RNAs from the nucleus and the cytoplasm by binding to the RRE RNA element. The vif protein (p23) prevents the action of APOBEC3G (a cellular protein that deaminatescytidine to uridine in the single-stranded viral DNA and/or interferes with reverse transcription^[38]). The vpr protein (p14) arrests cell division at G2/M. The nef protein (p27) down-regulates CD4 (the major viral receptor), as well as the MHC class I and class II molecules.^[39][40][41]

Nef also interacts with SH3 domains. The vpu protein (p16) influences the release of new virus particles from infected cells.^[23] The ends of each strand of HIV RNA contain an RNA sequence called a long terminal repeat (LTR). Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell. The Psi element is involved in viral genome packaging and recognized by gag and rev proteins. The SLIP element (TTTTTT) is involved in the frameshift in the gag-polreading frame required to make functional pol.^[23]

Tropism

The term viral tropism refers to the cell types a virus infects. HIV can infect a variety of immune cells such as CD4⁺ T cells, macrophages, and microglial cells. HIV-1 entry to macrophages and CD4⁺ T cells is mediated through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells' membrane and also with chemokineco-receptors.^[24][42]

Macrophage-tropic (M-tropic) strains of HIV-1, or non-syncytia-inducing strains (NSI; now called R5 viruses^[43]) use the β-chemokine receptor, CCR5, for entry and are thus able to replicate in both macrophages and CD4⁺ T cells.^[44] This CCR5 co-receptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. Indeed, macrophages play a key role in several critical aspects of HIV infection. They appear to be the first cells infected by HIV and perhaps the source of HIV production when CD4⁺ cells become depleted in the patient. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In the tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.

T-tropic strains of HIV-1, or syncytia-inducing strains (SI; now called X4 viruses^[43]) replicate in primary CD4⁺ T cells as well as in macrophages and use the α-chemokine receptor, CXCR4, for entry.^[44][45][46]

Dual-tropic HIV-1 strains are thought to be transitional strains of HIV-1 and thus are able to use both CCR5 and CXCR4 as co-receptors for viral entry.

The α-chemokine SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this by down-regulating the expression of CXCR4 on the surface of HIV target cells. M-tropic HIV-1 isolates that use only the CCR5 receptor are termed R5; those that use only CXCR4 are termed X4, and those that use both, X4R5. However, the use of co-receptors alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection^[44] and HIV can also infect a subtype of myeloid dendritic cells,^[47] which probably constitute a reservoir that maintains infection when CD4⁺ T cell numbers have declined to extremely low levels.

Some people are resistant to certain strains of HIV.^[48] For example, people with the CCR5-Δ32 mutation are resistant to infection by the R5 virus, as the mutation leaves HIV unable to bind to this co-receptor, reducing its ability to infect target cells.

Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid, which enables the virus to be transmitted from a male to his sexual partner. The virions can then infect numerous cellular targets and disseminate into the whole organism. However, a selection process^{[further explanation needed]} leads to a predominant transmission of the R5 virus through this pathway.^[49][50][51] In patients infected with subtype B HIV-1, there is often a co-receptor switch in late-stage disease and T-tropic variants that can infect a variety of T cells through CXCR4.^[52] These variants then replicate more aggressively with heightened virulence that causes rapid T cell depletion, immune system collapse, and opportunistic infections that mark the advent of AIDS.^[53] Thus, during the course of infection, viral adaptation to the use of CXCR4 instead of CCR5 may be a key step in the progression to AIDS. A number of studies with subtype B-infected individuals have determined that between 40 and 50 percent of AIDS patients can harbour viruses of the SI and, it is presumed, the X4 phenotypes.^[54][55]

HIV-2 is much less pathogenic than HIV-1 and is restricted in its worldwide distribution to West Africa. The adoption of 'accessory genes' by HIV-2 and its more promiscuous pattern of co-receptor usage (including CD4-independence) may assist the virus in its adaptation to avoid innate restriction factors present in host cells. Adaptation to use normal cellular machinery to enable transmission and productive infection has also aided the establishment of HIV-2 replication in humans. A survival strategy for any infectious agent is not to kill its host, but ultimately become a commensal organism. Having achieved a low pathogenicity, over time, variants that are more successful at transmission will be selected.^[56]

Replication cycle

Entry to the cell

The HIV virion enters macrophages and CD4⁺T cells by the adsorption of glycoproteins on its surface to receptors on the target cell followed by fusion of the viral envelope with the target cell membrane and the release of the HIV capsid into the cell.^[57][58]

Entry to the cell begins through interaction of the trimeric envelope complex (gp160 spike) on the HIV viral envelope and both CD4 and a chemokine co-receptor (generally either CCR5 or CXCR4, but others are known to interact) on the target cell surface.^[57][58] Gp120 binds to integrin α₄β₇ activating LFA-1, the central integrin involved in the establishment of virological synapses, which facilitate efficient cell-to-cell spreading of HIV-1.^[59] The gp160 spike contains binding domains for both CD4 and chemokine receptors.^[57][58]

The first step in fusion involves the high-affinity attachment of the CD4 binding domains of gp120 to CD4. Once gp120 is bound with the CD4 protein, the envelope complex undergoes a structural change, exposing the chemokine receptor binding domains of gp120 and allowing them to interact with the target chemokine receptor.^[57][58] This allows for a more stable two-pronged attachment, which allows the N-terminal fusion peptide gp41 to penetrate the cell membrane.^[57][58]Repeat sequences in gp41, HR1, and HR2 then interact, causing the collapse of the extracellular portion of gp41 into a hairpin shape. This loop structure brings the virus and cell membranes close together, allowing fusion of the membranes and subsequent entry of the viral capsid.^[57][58]

After HIV has bound to the target cell, the HIV RNA and various enzymes, including reverse transcriptase, integrase, ribonuclease, and protease, are injected into the cell.^{[57][failed verification]} During the microtubule-based transport to the nucleus, the viral single-strand RNA genome is transcribed into double-strand DNA, which is then integrated into a host chromosome.

HIV can infect dendritic cells (DCs) by this CD4-CCR5 route, but another route using mannose-specific C-type lectin receptors such as DC-SIGN can also be used.^[60] DCs are one of the first cells encountered by the virus during sexual transmission. They are currently thought to play an important role by transmitting HIV to T cells when the virus is captured in the mucosa by DCs.^[60] The presence of FEZ-1, which occurs naturally in neurons, is believed to prevent the infection of cells by HIV.^[61]

HIV-1 entry, as well as entry of many other retroviruses, has long been believed to occur exclusively at the plasma membrane. More recently, however, productive infection by pH-independent, clathrin-mediated endocytosis of HIV-1 has also been reported and was recently suggested to constitute the only route of productive entry.^{[62][63][64][65][66]}

Replication and transcription

Shortly after the viral capsid enters the cell, an enzyme called reverse transcriptase liberates the positive-sense single-stranded RNA genome from the attached viral proteins and copies it into a complementary DNA (cDNA) molecule.^[67] The process of reverse transcription is extremely error-prone, and the resulting mutations may cause drug resistance or allow the virus to evade the body's immune system. The reverse transcriptase also has ribonuclease activity that degrades the viral RNA during the synthesis of cDNA, as well as DNA-dependent DNA polymerase activity that creates a sense DNA from the antisense cDNA.^[68] Together, the cDNA and its complement form a double-stranded viral DNA that is then transported into the cell nucleus. The integration of the viral DNA into the host cell's genome is carried out by another viral enzyme called integrase.^[67]

The integrated viral DNA may then lie dormant, in the latent stage of HIV infection.^[67] To actively produce the virus, certain cellular transcription factors need to be present, the most important of which is NF-κB (nuclear factor kappa B), which is upregulated when T cells become activated.^[69] This means that those cells most likely to be targeted, entered and subsequently killed by HIV are those actively fighting infection.

During viral replication, the integrated DNA provirus is transcribed into RNA, some of which then undergo RNA splicing to produce mature messenger RNAs (mRNAs). These mRNAs are exported from the nucleus into the cytoplasm, where they are translated into the regulatory proteins Tat (which encourages new virus production) and Rev. As the newly produced Rev protein is produced it moves to the nucleus, where it binds to full-length, unspliced copies of virus RNAs and allows them to leave the nucleus.^[70] Some of these full-length RNAs function as new copies of the virus genome, while others function as mRNAs that are translated to produce the structural proteins Gag and Env. Gag proteins bind to copies of the virus RNA genome to package them into new virus particles.^[71]

HIV-1 and HIV-2 appear to package their RNA differently.^[72][73] HIV-1 will bind to any appropriate RNA.^[74] HIV-2 will preferentially bind to the mRNA that was used to create the Gag protein itself.^[75]

Recombination

Two RNA genomes are encapsidated in each HIV-1 particle (see Structure and genome of HIV). Upon infection and replication catalyzed by reverse transcriptase, recombination between the two genomes can occur.^[76][77] Recombination occurs as the single-strand, positive-sense RNA genomes are reverse transcribed to form DNA. During reverse transcription, the nascent DNA can switch multiple times between the two copies of the viral RNA. This form of recombination is known as copy-choice. Recombination events may occur throughout the genome. Anywhere from two to 20 recombination events per genome may occur at each replication cycle, and these events can rapidly shuffle the genetic information that is transmitted from parental to progeny genomes.^[77]

Viral recombination produces genetic variation that likely contributes to the evolution of resistance to anti-retroviral therapy.^[78] Recombination may also contribute, in principle, to overcoming the immune defenses of the host. Yet, for the adaptive advantages of genetic variation to be realized, the two viral genomes packaged in individual infecting virus particles need to have arisen from separate progenitor parental viruses of differing genetic constitution. It is unknown how often such mixed packaging occurs under natural conditions.^[79]

Bonhoeffer et al.^[80] suggested that template switching by reverse transcriptase acts as a repair process to deal with breaks in the single-stranded RNA genome. In addition, Hu and Temin^[76] suggested that recombination is an adaptation for repair of damage in the RNA genomes. Strand switching (copy-choice recombination) by reverse transcriptase could generate an undamaged copy of genomic DNA from two damaged single-stranded RNA genome copies. This view of the adaptive benefit of recombination in HIV could explain why each HIV particle contains two complete genomes, rather than one. Furthermore, the view that recombination is a repair process implies that the benefit of repair can occur at each replication cycle, and that this benefit can be realized whether or not the two genomes differ genetically. On the view that recombination in HIV is a repair process, the generation of recombinational variation would be a consequence, but not the cause of, the evolution of template switching.^[80]

HIV-1 infection causes chronic inflammation and production of reactive oxygen species.^[81] Thus, the HIV genome may be vulnerable to oxidative damages, including breaks in the single-stranded RNA. For HIV, as well as for viruses in general, successful infection depends on overcoming host defensive strategies that often include production of genome-damaging reactive oxygen species. Thus, Michod et al.^[82] suggested that recombination by viruses is an adaptation for repair of genome damages, and that recombinational variation is a byproduct that may provide a separate benefit.

Assembly and release

The final step of the viral cycle, assembly of new HIV-1 virions, begins at the plasma membrane of the host cell. The Env polyprotein (gp160) goes through the endoplasmic reticulum and is transported to the Golgi apparatus where it is cleaved by furin resulting in the two HIV envelope glycoproteins, gp41 and gp120.^[83] These are transported to the plasma membrane of the host cell where gp41 anchors gp120 to the membrane of the infected cell. The Gag (p55) and Gag-Pol (p160) polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begins to bud from the host cell. The budded virion is still immature as the gag polyproteins still need to be cleaved into the actual matrix, capsid and nucleocapsid proteins. This cleavage is mediated by the packaged viral protease and can be inhibited by antiretroviral drugs of the protease inhibitor class. The various structural components then assemble to produce a mature HIV virion.^[84] Only mature virions are then able to infect another cell.

Spread within the body

The classical process of infection of a cell by a virion can be called 'cell-free spread' to distinguish it from a more recently recognized process called 'cell-to-cell spread'.^[85] In cell-free spread (see figure), virus particles bud from an infected T cell, enter the blood or extracellular fluid and then infect another T cell following a chance encounter.^[85] HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread, for which two pathways have been described. Firstly, an infected T cell can transmit virus directly to a target T cell via a virological synapse.^[59][86] Secondly, an antigen-presenting cell (APC), such as a macrophage or dendritic cell, can transmit HIV to T cells by a process that either involves productive infection (in the case of macrophages) or capture and transfer of virions in trans (in the case of dendritic cells).^[87] Whichever pathway is used, infection by cell-to-cell transfer is reported to be much more efficient than cell-free virus spread.^[88] A number of factors contribute to this increased efficiency, including polarised virus budding towards the site of cell-to-cell contact, close apposition of cells, which minimizes fluid-phase diffusion of virions, and clustering of HIV entry receptors on the target cell towards the contact zone.^[86] Cell-to-cell spread is thought to be particularly important in lymphoid tissues where CD4⁺ T cells are densely packed and likely to interact frequently.^[85] Intravital imaging studies have supported the concept of the HIV virological synapse in vivo.^[89] The many spreading mechanisms available to HIV contribute to the virus' ongoing replication in spite of anti-retroviral therapies.^[85][90]

Genetic variability

HIV differs from many viruses in that it has very high genetic variability. This diversity is a result of its fast replication cycle, with the generation of about 10¹⁰ virions every day, coupled with a high mutation rate of approximately 3 x 10⁻⁵ per nucleotide base per cycle of replication and recombinogenic properties of reverse transcriptase.^[91][92][93]

This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day.^[91] This variability is compounded when a single cell is simultaneously infected by two or more different strains of HIV. When simultaneous infection occurs, the genome of progeny virions may be composed of RNA strands from two different strains. This hybrid virion then infects a new cell where it undergoes replication. As this happens, the reverse transcriptase, by jumping back and forth between the two different RNA templates, will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes.^[91] This recombination is most obvious when it occurs between subtypes.^[91]

The closely related simian immunodeficiency virus (SIV) has evolved into many strains, classified by the natural host species. SIV strains of the African green monkey (SIVagm) and sooty mangabey (SIVsmm) are thought to have a long evolutionary history with their hosts. These hosts have adapted to the presence of the virus,^[94] which is present at high levels in the host's blood, but evokes only a mild immune response,^[95] does not cause the development of simian AIDS,^[96] and does not undergo the extensive mutation and recombination typical of HIV infection in humans.^[97]

In contrast, when these strains infect species that have not adapted to SIV ('heterologous' or similar hosts such as rhesus or cynomologus macaques), the animals develop AIDS and the virus generates genetic diversity similar to what is seen in human HIV infection.^[98]Chimpanzee SIV (SIVcpz), the closest genetic relative of HIV-1, is associated with increased mortality and AIDS-like symptoms in its natural host.^[99] SIVcpz appears to have been transmitted relatively recently to chimpanzee and human populations, so their hosts have not yet adapted to the virus.^[94] This virus has also lost a function of the nef gene that is present in most SIVs. For non-pathogenic SIV variants, nef suppresses T cell activation through the CD3 marker. Nef's function in non-pathogenic forms of SIV is to downregulate expression of inflammatory cytokines, MHC-1, and signals that affect T cell trafficking. In HIV-1 and SIVcpz, nef does not inhibit T-cell activation and it has lost this function. Without this function, T cell depletion is more likely, leading to immunodeficiency.^[99][100]

Three groups of HIV-1 have been identified on the basis of differences in the envelope (env) region: M, N, and O.^[101] Group M is the most prevalent and is subdivided into eight subtypes (or clades), based on the whole genome, which are geographically distinct.^[102] The most prevalent are subtypes B (found mainly in North America and Europe), A and D (found mainly in Africa), and C (found mainly in Africa and Asia); these subtypes form branches in the phylogenetic tree representing the lineage of the M group of HIV-1. Co-infection with distinct subtypes gives rise to circulating recombinant forms (CRFs). In 2000, the last year in which an analysis of global subtype prevalence was made, 47.2% of infections worldwide were of subtype C, 26.7% were of subtype A/CRF02_AG, 12.3% were of subtype B, 5.3% were of subtype D, 3.2% were of CRF_AE, and the remaining 5.3% were composed of other subtypes and CRFs.^[103] Most HIV-1 research is focused on subtype B; few laboratories focus on the other subtypes.^[104] The existence of a fourth group, 'P', has been hypothesised based on a virus isolated in 2009.^[105] The strain is apparently derived from gorilla SIV (SIVgor), first isolated from western lowland gorillas in 2006.^[105]

HIV-2's closest relative is SIVsm, a strain of SIV found in sooty mangabees. Since HIV-1 is derived from SIVcpz, and HIV-2 from SIVsm, the genetic sequence of HIV-2 is only partially homologous to HIV-1 and more closely resembles that of SIVsm.^{[citation needed][106]}

Diagnosis

Many HIV-positive people are unaware that they are infected with the virus.^[107] For example, in 2001 less than 1% of the sexually active urban population in Africa had been tested, and this proportion is even lower in rural populations.^[107] Furthermore, in 2001 only 0.5% of pregnant women attending urban health facilities were counselled, tested or receive their test results.^[107] Again, this proportion is even lower in rural health facilities.^[107] Since donors may therefore be unaware of their infection, donor blood and blood products used in medicine and medical research are routinely screened for HIV.^[108]

HIV-1 testing is initially done using an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1. Specimens with a non-reactive result from the initial ELISA are considered HIV-negative, unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive ELISA result are retested in duplicate.^[109] If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., a polymerase chain reaction (PCR), western blot or, less commonly, an immunofluorescence assay (IFA)). Only specimens that are repeatedly reactive by ELISA and positive by IFA or PCR or reactive by western blot are considered HIV-positive and indicative of HIV infection. Specimens that are repeatedly ELISA-reactive occasionally provide an indeterminate western blot result, which may be either an incomplete antibody response to HIV in an infected person or nonspecific reactions in an uninfected person.^[110]

HIV deaths (other than U.S.) in 2014.^[111]

Although IFA can be used to confirm infection in these ambiguous cases, this assay is not widely used. In general, a second specimen should be collected more than a month later and retested for persons with indeterminate western blot results. Although much less commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA amplification method) can also help diagnosis in certain situations.^[109] In addition, a few tested specimens might provide inconclusive results because of a low quantity specimen. In these situations, a second specimen is collected and tested for HIV infection.

Modern HIV testing is extremely accurate, when the window period is taken into consideration. A single screening test is correct more than 99% of the time.^[112] The chance of a false-positive result in a standard two-step testing protocol is estimated to be about 1 in 250,000 in a low risk population.^[113] Testing post-exposure is recommended immediately and then at six weeks, three months, and six months.^[114]

The latest recommendations of the US Centers for Disease Control and Prevention (CDC) show that HIV testing must start with an immunoassay combination test for HIV-1 and HIV-2 antibodies and p24 antigen. A negative result rules out HIV exposure, while a positive one must be followed by an HIV-1/2 antibody differentiation immunoassay to detect which antibodies are present. This gives rise to four possible scenarios:

• 1. HIV-1 (+) & HIV-2 (−): HIV-1 antibodies detected
• 2. HIV-1 (−) & HIV-2 (+): HIV-2 antibodies detected
• 3. HIV-1 (+) & HIV-2 (+): both HIV-1 and HIV-2 antibodies detected
• 4. HIV-1 (−) or indeterminate & HIV-2 (−): Nucleic acid test must be carried out to detect the acute infection of HIV-1 or its absence.^[115]

Research

HIV/AIDS research includes all medical research that attempts to prevent, treat, or cure HIV/AIDS, as well as fundamental research about the nature of HIV as an infectious agent and AIDS as the disease caused by HIV.

Many governments and research institutions participate in HIV/AIDS research. This research includes behavioral health interventions, such as research into sex education, and drug development, such as research into microbicides for sexually transmitted diseases, HIV vaccines, and anti-retroviral drugs.^[116] Other medical research areas include the topics of pre-exposure prophylaxis, post-exposure prophylaxis, circumcision and HIV, and accelerated aging effects.

Treatment and transmission

The management of HIV/AIDS normally includes the use of multiple antiretroviral drugs. In many parts of the world, HIV has become a chronic condition in which progression to AIDS is increasingly rare.

HIV latency, and the consequent viral reservoir in CD4⁺ T cells, dendritic cells, as well as macrophages, is the main barrier to eradication of the virus.^[18]

It is important to note that although HIV is highly virulent, transmission does not occur through sex when an HIV-positive person has a consistently undetectable viral load (<50 copies/ml) due to anti-retroviral treatment. Previously it was said the chance of transmission was 'very low' or 'negligible' (The 'Swiss Statement').^[117] However, following multiple studies it is now clear that the chance of passing on HIV through sex is zero where the HIV-positive person has a consistently undetectable viral load, this is known as 'U=U' or 'Undetectable=Untransmittable', also phrased as 'can't pass it on'.^[118][119] The studies demonstrating U=U are: Opposites Attract,^[120] PARTNER 1,^[121] PARTNER 2,^[4][122] (for male-male couples)^[123] and HPTN052^[124] (for heterosexual couples) when 'the partner living with HIV had a durably suppressed viral load.'^[123] In these studies couples where one partner was HIV positive and one partner was HIV negative were enrolled and regular HIV testing completed. In total from the four studies, 4097 couples were enrolled over four continents and 151,880 acts of condomless sex were reported, there were zero phylogenetically linked transmissions of HIV where the positive partner had an undetectable viral load.^[125] Following this the U=U consensus statement advocating the use of 'zero risk' was signed by hundreds of individuals and organisations including the US CDC, British HIV Association and The Lancet medical journal.^[126] The importance of the final results of the PARTNER 2 study were described by the medical director of the Terrence Higgins Trust as 'impossible to overstate,' while lead author Alison Rodger declared that the message that 'undetectable viral load makes HIV untransmittable ... can help end the HIV pandemic by preventing HIV transmission.^[127] The authors summarised their findings in The Lancet as follows:^[4]

Our results provide a similar level of evidence on viral suppression and HIV transmission risk for gay men to that previously generated for heterosexual couples and suggest that the risk of HIV transmission in gay couples through condomless sex when HIV viral load is suppressed is effectively zero. Our findings support the message of the U=U (undetectable equals untransmittable) campaign, and the benefits of early testing and treatment for HIV.^[4]

This result is consistent with the conclusion presented by Anthony S. Fauci, the Director of the National Institute of Allergy and Infectious Diseases for the U.S. National Institutes of Health, and his team in a viewpoint published in the Journal of the American Medical Association, that U=U is an effective HIV prevention method when an undetectable viral load is maintained.^[5][123]

History

Discovery

AIDS was first clinically observed in 1981 in the United States.^[128] The initial cases were a cluster of injection drug users and gay men with no known cause of impaired immunity who showed symptoms of Pneumocystis jirovecii pneumonia (PJP), a rare opportunistic infection that was known to occur in people with very compromised immune systems.^[129] Soon thereafter, additional gay men developed a previously rare skin cancer called Kaposi's sarcoma (KS).^[130][131] Many more cases of PJP and KS emerged, alerting U.S. Centers for Disease Control and Prevention (CDC) and a CDC task force was formed to monitor the outbreak.^[132] The earliest retrospectively described case of AIDS is believed to have been in Norway beginning in 1966.^[133]

In the beginning, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.^[134][135] They also used Kaposi's Sarcoma and Opportunistic Infections, the name by which a task force had been set up in 1981.^[136] In the general press, the term GRID, which stood for gay-related immune deficiency, had been coined.^[137] The CDC, in search of a name, and looking at the infected communities coined 'the 4H disease', as it seemed to single out homosexuals, heroin users, hemophiliacs, and Haitians.^[138][139] However, after determining that AIDS was not isolated to the gay community,^[136] it was realized that the term GRID was misleading and AIDS was introduced at a meeting in July 1982.^[140] By September 1982 the CDC started using the name AIDS.^[141]

In 1983, two separate research groups led by American Robert Gallo and French investigators Françoise Barré-Sinoussi and Luc Montagnier independently declared that a novel retrovirus may have been infecting AIDS patients, and published their findings in the same issue of the journal Science.^{[142][143][144]} Gallo claimed that a virus his group had isolated from a person with AIDS was strikingly similar in shape to other human T-lymphotropic viruses (HTLVs) his group had been the first to isolate. Gallo's group called their newly isolated virus HTLV-III. At the same time, Montagnier's group isolated a virus from a patient presenting with swelling of the lymph nodes of the neck and physical weakness, two classic symptoms of primary HIV infection. Contradicting the report from Gallo's group, Montagnier and his colleagues showed that core proteins of this virus were immunologically different from those of HTLV-I. Montagnier's group named their isolated virus lymphadenopathy-associated virus (LAV).^[132] As these two viruses turned out to be the same, in 1986 LAV and HTLV-III were renamed HIV.^[145]

Another group working contemporaneously with the Montagnier and Gallo groups was that of Dr. Jay Levy at the University of California, San Francisco. He independently discovered the AIDS virus in 1983 and named it the AIDS associated retrovirus (ARV).^[146] This virus was very different from the virus reported by the Montagnier and Gallo groups. The ARV strains indicated, for the first time, the heterogeneity of HIV isolates and several of these remain classic examples of the AIDS virus found in the United States.^[147]

Origins

Both HIV-1 and HIV-2 are believed to have originated in non-human primates in West-central Africa, and are believed to have transferred to humans (a process known as zoonosis) in the early 20th century.^[148][149]

HIV-1 appears to have originated in southern Cameroon through the evolution of SIVcpz, a simian immunodeficiency virus (SIV) that infects wild chimpanzees (HIV-1 descends from the SIVcpz endemic in the chimpanzee subspecies Pan troglodytes troglodytes).^[150][151] The closest relative of HIV-2 is SIVsmm, a virus of the sooty mangabey (Cercocebus atys atys), an Old World monkey living in littoral West Africa (from southern Senegal to western Côte d'Ivoire).^[20]New World monkeys such as the owl monkey are resistant to HIV-1 infection, possibly because of a genomic fusion of two viral resistance genes.^[152]

HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O.^[153]

Bud Powell Transcription Pdf Files

There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV.^[154] However, SIV is a weak virus, and it is typically suppressed by the human immune system within weeks of infection. It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV.^[155] Furthermore, due to its relatively low person-to-person transmission rate, it can only spread throughout the population in the presence of one or more high-risk transmission channels, which are thought to have been absent in Africa prior to the 20th century.

Specific proposed high-risk transmission channels, allowing the virus to adapt to humans and spread throughout the society, depend on the proposed timing of the animal-to-human crossing. Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to circa 1910.^[156] Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including different patterns of sexual contact (especially multiple, concurrent partnerships), the spread of prostitution, and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities.^[157] While transmission rates of HIV during vaginal intercourse are typically low, they are increased manyfold if one of the partners suffers from a sexually transmitted infection resulting in genital ulcers. Early 1900s colonial cities were notable due to their high prevalence of prostitution and genital ulcers to the degree that as of 1928 as many as 45% of female residents of eastern Leopoldville were thought to have been prostitutes and as of 1933 around 15% of all residents of the same city were infected by one of the forms of syphilis.^[157]

An alternative view—unsupported by evidence—holds that unsafe medical practices in Africa during years following World War II, such as unsterile reuse of single-use syringes during mass vaccination, antibiotic, and anti-malaria treatment campaigns, were the initial vector that allowed the virus to adapt to humans and spread.^{[155][158][159]}

The earliest, well-documented case of HIV in a human dates back to 1959 in the Belgian Congo.^[160] The virus may have been present in the United States as early as the mid-to-late 1950s, as a sixteen-year-old male presented with symptoms in 1966 and died in 1969.^[161]

See also

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Further reading

• Berlier W, Bourlet T, Lawrence P, Hamzeh H, Lambert C, Genin C, Verrier B, Dieu-Nosjean MC, Pozzetto B, Delézay O (2005). 'Selective sequestration of X4 isolates by human genital epithelial cells: Implication for virus tropism selection process during sexual transmission of HIV'. Journal of Medical Virology. 77 (4): 465–74. doi:10.1002/jmv.20478. PMID16254974.
• Joint United Nations Programme on HIV/AIDS (UNAIDS) (2011). Global HIV/AIDS Response, Epidemic update and health sector progress towards universal access(PDF). Joint United Nations Programme on HIV/AIDS.

• Muciaccia B, Padula F, Vicini E, Gandini L, Lenzi A, Stefanini M (2005). 'Beta-chemokine receptors 5 and 3 are expressed on the head region of human spermatozoon'. The FASEB Journal. 19 (14): 2048–50. doi:10.1096/fj.05-3962fje. PMID16174786.

External links

• HIV/AIDS at Curlie

In music, the term swing has two main uses. Colloquially, it is used to describe the sense of propulsive rhythmic 'feel' or 'groove' created by the musical interaction between the performers, especially when the music creates a 'visceral response' such as feet-tapping or head-nodding (see pulse). The term is also used more specifically, to refer to a technique (most commonly associated with jazz but also used in other genres) that involves alternately lengthening and shortening the pulse-divisions in a rhythm.

• 2Swing as a rhythmic style

Swing as a 'feel'[edit]

Like the term 'groove', which is used to describe a cohesive rhythmic 'feel' in a funk or rock context, the concept of 'swing' can be hard to define. Indeed, some dictionaries use the terms as synonyms: 'Groovy ... denotes music that really swings.'^[1] The Jazz in America glossary defines it as 'when an individual player or ensemble performs in such a rhythmically coordinated way as to command a visceral response from the listener (to cause feet to tap and heads to nod); an irresistible gravitational buoyancy that defies mere verbal definition.'^[2]

Swing has been called 'the most debated word in jazz'. When jazz performer Cootie Williams was asked to define it, he joked, 'Define it? I'd rather tackle Einstein's theory!'^[3] When Louis Armstrong was asked on the Bing Crosby radio show what swing was, he said, 'Ah, swing, well, we used to call it syncopation—then they called it ragtime, then blues—then jazz. Now, it's swing. Ha! Ha! White folks, yo'all sho is a mess.'^[4]Benny Goodman, the 1930s-era bandleader nicknamed the 'King of Swing', called swing 'free speech in music', whose most important element is 'the liberty a soloist has to stand and play a chorus in the way he feels it'. His contemporary Tommy Dorsey gave a more ambiguous definition when he proposed that 'Swing is sweet and hot at the same time and broad enough in its creative conception to meet every challenge tomorrow may present.'^[3]Boogie-woogie pianist Maurice Rocco argues that the definition of swing 'is just a matter of personal opinion'.^[3] When asked for a definition of swing, Fats Waller replied, 'Lady, if you gotta ask, you'll never know.'^[5]

Treadwell stated:

What is Swing? Perhaps the best answer, after all, was supplied by the hep-cat who rolled her eyes, stared into the far-off and sighed, 'You can feel it, but you just can't explain it. Do you dig me?'

Stanley Dance, in The World of Swing, devoted the two first chapters of his work to discussions of the concept of swing with a collection of the musicians who played it. They described a kinetic quality to the music. It was compared to flying; 'take off' was a signal to start a solo. The rhythmic pulse continued between the beats, expressed in dynamics, articulation, and inflection. Swing was as much in the music anticipating the beat, like the swing of a jumprope anticipating the jump, as in the beat itself.^[5] Swing has been defined in terms of formal rhythmic devices, but according to the Jimmie Lunceford tune, 'T'aint whatcha do, it's the way thatcha do it' (say it so it swings).

Swing as a rhythmic style[edit]

In swing rhythm, the pulse is divided unequally, such that certain subdivisions (typically either eighth note or sixteenth note subdivisions) alternate between long and short durations. Certain music of the Baroque and Classical era is played using notes inégales, which is analogous to swing. In shuffle rhythm, the first note in a pair may be twice (or more) the duration of the second note. In swing rhythm, the ratio of the first note's duration to the second note's duration can take on a range of magnitudes. In traditional jazz, swing is typically applied to eighth notes. In other genres, such as funk and jazz-rock, swing is often applied to sixteenth notes.^[8][9]

In most jazz music, especially of the big band era and later, the second and fourth beats of a 4/4 measure are emphasized over the first and third, and the beats are lead-in—main-beat couplets (dah-DUM, dah-DUM....). The 'dah' anticipates, or leads into, the 'DUM.' The 'dah' lead-in may or may not be audible. It may be occasionally accented for phrasing or dynamic purposes. The first note of each pair is often understood to be twice as long as the second, implying a triplet feel, but in practice the ratio is less definitive and is often much more subtle.^[12]

The instruments of a swing rhythm section express swing in different ways from each other, and the devices evolved as the music developed. During the early development of swing music, the bass was often played with lead-in—main-note couplets, often with a percussive sound. Later, the lead-in note was dropped but incorporated into the physical rhythm of the bass player to help keep the beat 'solid.' Similarly, the rhythm guitar was played with the lead-in beat in the player's physical rhythm but inaudible. The piano was played with a variety of devices for swing. Chord patterns played in the rhythm of a dotted-eight—sixteenth couplet were characteristic of boogie-woogie playing (sometimes also used in boogie-woogie horn section playing). The 'swing bass' left hand, used by James P. Johnson, Fats Waller, and Earl Hines, used a bass note on the first and third beats, followed by a mid-range chord to emphasize the second and fourth beats. The lead-in beats were not audible, but expressed in the motion of the left arm. Swing bass piano also put the first and third beats a role anticipatory to the emphasized second and fourth beats in two-beat figures.^[13] As swing music developed, the role of the piano in the ensemble changed to emphasize accents and fills; these were often played on the lead-in to the main beat, adding a punch to the rhythm. Count Basie's style was sparse, played as accompaniment to the horn sections and soloists.^[14] The bass and snare drums started the swing era as the main timekeepers, with the snare usually used for either lead-ins or emphasis on the second and fourth beats. It was soon found that the high-hat cymbal could add a new dimension to the swing expressed by the drum kit when played in a two-beat 'ti-tshhh-SH' figure, with the 'ti' the lead-in to the 'tshhh' on the first and third beats, and the 'SH' the emphasized second and fourth beats. With that high-hat figure, the drummer expressed three elements of swing: the lead-in with the 'ti,' the continuity of the rhythmic pulse between the beats with the 'tshhh,' and the emphasis on the second and fourth beats with the 'SH'. Early examples of that high-hat figure were recorded by the drummer Chick Webb. Jo Jones carried the high-hat style a step further, with a more continuous-sounding 't'shahhh-uhh' two beat figure while reserving the bass and snare drum for accents. The changed role of the drum kit away from the heavier style of the earlier drumming placed more emphasis on the role of the bass in holding the rhythm.^[14]

Horn sections and soloists added inflection and dynamics to the rhythmic toolbox, 'swinging' notes and phrases. One of the characteristic horn section sounds of swing jazz was a section chord played with a strong attack, a slight fade, and a quick accent at the end, expressing the rhythmic pulse between beats. That device was used interchangeably or in combination with a slight downward slur between the beginning and the end of the note. Similarly, section arrangements sometimes used a series of triplets, either accented on the first and third notes or with every other note accented to make a 3/2 pattern. Straight eighth notes were commonly used in solos, with dynamics and articulation used to express phrasing and swing. Phrasing dynamics built swing across two or four measures or, in the innovative style of tenor saxophonist Lester Young, across odd sequences of measures, sometimes starting or stopping without regard to place in the measure.^[14]

The rhythmic devices of the swing era became subtler with bebop. Bud Powell and other piano players influenced by him mostly did away with left-hand rhythmic figures, replacing them with chords. The ride cymbal played in a 'ting-ti-ting' pattern took the role of the high-hat, the snare drum was mainly used for lead-in accents, and the bass drum was mainly used for occasional 'bombs.' But the importance of the lead-in as a rhythmic device was still respected. Drummer Max Roach emphasized the importance of the lead-in, audible or not, in 'protecting the beat.'^[15] Bebop soloists rose to the challenge of keeping a swinging feel in highly sophisticated music often played at a breakneck pace. The groundbreakers of bebop had come of age as musicians with swing and, while breaking the barriers of the swing era, still reflected their swing heritage.^[14]

• Various rhythmic swing approximations:
  • ≈1:1 = eighth note + eighth note, 'straight eighths.' play example
  • ≈3:2 = long eighth + short eighth. play example
  • ≈2:1 = triplet quarter note + triplet eighth, triple meter; play example
  • ≈3:1 = dotted eighth note + sixteenth note. play example

The subtler end of the range involves treating written pairs of adjacent eighth notes (or sixteenth notes, depending on the level of swing) as slightly asymmetrical pairs of similar values. On the other end of the spectrum, the 'dotted eighth – sixteenth' rhythm, consists of a long note three times as long as the short. Prevalent 'dotted rhythms' such as these in the rhythm section of dance bands in the mid-20th century are more accurately described as a 'shuffle';^[16] they are also an important feature of baroque dance and many other styles.

In jazz, the swing ratio typically lies somewhere between 1:1 and 3:1, and can vary considerably. Swing ratios in jazz tend to be wider at slower tempos and narrower at faster tempos.^[17] In jazz scores, swing is often assumed, but is sometimes explicitly indicated. For example, 'Satin Doll', a swing era jazz standard, was notated in ⁴
₄ time and in some versions includes the direction, medium swing.

Genres using swing rhythm[edit]

Swing is commonly used in blues, country, and jazz, and often appears in other genres such as rock, funk, and hip-hop. Much written music in jazz is assumed to be performed with a swing rhythm. Styles that always use traditional (triplet) rhythms, resembling 'hard swing', include foxtrot, quickstep and some other ballroom dances, Stride piano, and 1920s-era Novelty piano (the successor to Ragtime style).

See also[edit]

• Clave (rhythm) for the rhythms of Latin jazz and Latin dance
• Jig for the swung triplets of Celtic music – triplets with a swing feel to them – not to be confused with the swung duplets of 'triplet swing'.
• Folk hornpipe of the dotted note variety, often notated in ²
  ₄ (The Harvest Home, The Boys of Bluehill) for the 3:1 hard swing/shuffle of Celtic music.
• Notes inégales, a 17th-century French usage of similar meters and notation
• Schaffel music swing and shuffle beats in electronic music
• Swing music, a jazz-influenced genre of music

References[edit]

1. ^'Swing Slang'. Big Bands Database Plus.
2. ^'Jazz Resources: Glossary'. Jazz in America. The Thelonious Monk Institute of Jazz.
3. ^ ^abc'What Is Swing?'. Savoy Ballroom.
4. ^Argyle, Ray (1 April 2009). 'Scott Joplin and the Age of Ragtime'. Google Books. McFarland.
5. ^ ^abDance, Stanley, 1974, The World of Swing: An Oral History of Big Band Jazz (2001 edition) Da Capo Press, 436 p.
6. ^Treadwell, Bill (1946). 'Introduction: What Is Swing'. Big Book of Swing. pp. 8–10.
7. ^Savidge, Wilbur M.; Vradenburg, Randy L. (2002). Everything About Playing the Blues. Music Sales Distributed. p. 35. ISBN1-884848-09-5.
8. ^Frane, Andrew V. (2017). 'Swing rhythm in classic drum breaks from hip-hop's breakbeat canon'. Music Perception: An Interdisciplinary Journal. 34 (3): 291–302. doi:10.1525/mp.2017.34.3.291.
9. ^Pressing, Jeff (2002). 'Black Atlantic Rhythm. Its Computational and Transcultural Foundations'. Music Perception. 19: 285–310. doi:10.1525/mp.2002.19.3.285.
10. ^Mattingly, Rick (2006). All About Drums. Hal Leonard. p. 44. ISBN1-4234-0818-7.
11. ^Starr, Eric (2007). The Everything Rock & Blues Piano Book. p. 124. ISBN1-59869-260-7.
12. ^'Jazz Drummers' Swing Ratio in Relation to Tempo'. Acoustical Society of America. Archived from the original on 2008-05-18. Retrieved 2008-07-22.
13. ^Hadlock, Richard, Jazz Masters of the Twenties, New York, MacMillan, 1972, 255p.
14. ^ ^abcdRussell, Ross, Jazz Style in Kansas City and the Southwest, Berkeley, CA, University of California Press, 1972, 291 p.
15. ^Davis, Miles, and Troupe, Quincy, Miles: The Autobiography, New York, Simon and Schuster, 1989, 448 p.
16. ^Prögler, J. A. (1995). 'Searching for Swing: Participatory Discrepancies in the Jazz Rhythm Section'. Ethnomusicology. 39 (1): 26.
17. ^Friberg, Anders; Sundström, Andreas (2002). 'Swing Ratios and Ensemble Timing in Jazz Performance: Evidence for a Common Rhythmic Pattern'. Music Perception: An Interdisciplinary Journal. 19 (3): 344.

Further reading[edit]

• Floyd, Samuel A., Jr. (1991). 'Ring Shout! Literary Studies, Historical Studies, and Black Music Inquiry'. Black Music Research Journal. 11 (2): 265–268. doi:10.2307/779269. Featuring a socio-musicological description of swing in African American music.
• Rubin, Dave (1996). Art of the Shuffle. ISBN0-7935-4206-5. An exploration of shuffle, boogie, and swing rhythms for guitar.
• Clark, Mike; Paul, Jackson (1992). Rhythm Combination. ISBN0-7119-8049-7.
• Prögler, J. A. (1995). 'Searching for Swing. Participatory Discrepancies in the Jazz Rhythm Section'. Ethnomusicology. 39: 21–54. doi:10.2307/852199.
• Butterfield, Matthew W. 'Why Do Jazz Musicians Swing Their Eighth Notes?'(PDF). Yale University.

External links[edit]

• Video Resources – Swung Notes – more Swing Rhythm videos made with Bounce Metronome which can play swing rhythms
• 'Jeff Porcaro', Drummer World. The 'Rosanna shuffle' as played by the Toto drummer, including audio and transcription.