document_title: HIV

question_text: based on the large number of hiv replicates produced it is common to find

text: HIV

text: Virology

text: Classification

text:
Comparison of HIV species

Species
Virulence
Infectivity
Prevalence
Inferred origin

HIV-1
High
High
Global
Common chimpanzee

HIV-2
Lower
Low
West Africa
Sooty mangabey

text: HIV is a member of the genus Lentivirus,[8] part of the family Retroviridae.[9] 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.[10] Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded 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 integrase and host co-factors.[11] Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system. Alternatively, the virus may be transcribed, producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew.

text: Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both LAV and HTLV-III. It is more virulent, more infective,[12] 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. Because of its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.[13]

text: Structure and genome

text: HIV is different in structure from other retroviruses. It is roughly spherical[14] with a diameter of about 120 nm, around 60 times smaller than a red blood cell.[15] It is composed of two copies of positive single-stranded RNA that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein p24.[16] 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.[16]

text: This is, in turn, surrounded by the viral envelope, that is composed of the lipid bilayer taken from the membrane of a human 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,[16] which consists of a cap made of three molecules known as glycoprotein (gp) 120, and a stem consisting of three gp41 molecules which anchor the structure into the viral envelope.[17][18] 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 membrane releasing the viral contents into the cell and initiating the infectious cycle.[17] As the sole viral protein on the surface of the virus, the Envelope protein is a major target for HIV vaccine efforts.[19] 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.[20][21] The majority of the glycans are therefore stalled as immature 'high-mannose' glycans not normally present on secreted or cell surface human glycoproteins.[22] 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.[23]

text: The molecular structure of the viral spike has now been determined by X-ray crystallography[24] and cryo-electron microscopy.[25] 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 proline mutation in gp41.[26] 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.[27] 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.[28]

text: 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.[16] 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.[16]

text: 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.[29][30] 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 deaminates Cytidine to Uridine in the single stranded viral DNA and/or interferes with reverse transcription[31]). 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.[32][33][34]

text: Nef also interacts with SH3 domains. The Vpu protein (p16) influences the release of new virus particles from infected cells.[16] The ends of each strand of HIV RNA contain an RNA sequence called the 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-Pol reading frame required to make functional Pol.[16]

text: Tropism

text: 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 and also with chemokine coreceptors.[17][35]

text: Macrophage (M-tropic) strains of HIV-1, or non-syncytia-inducing strains (NSI; now called R5 viruses[36] ) use the β-chemokine receptor CCR5 for entry and are, thus, able to replicate in macrophages and CD4+ T cells.[37] This CCR5 coreceptor 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 tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.

text: T-tropic isolates, or syncytia-inducing (SI; now called X4 viruses[36] ) strains replicate in primary CD4+ T cells as well as in macrophages and use the α-chemokine receptor, CXCR4, for entry.[37][38][39] 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.

text: 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 these cells. HIV 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 coreceptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection[37] and HIV can also infect a subtype of myeloid dendritic cells,[40] which probably constitute a reservoir that maintains infection when CD4+ T cell numbers have declined to extremely low levels.

text: Some people are resistant to certain strains of HIV.[41] For example, people with the CCR5-Δ32 mutation are resistant to infection with R5 virus, as the mutation stops HIV from binding to this coreceptor, reducing its ability to infect target cells.

text: Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid, which is passed 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 leads to a predominant transmission of the R5 virus through this pathway.[42][43][44] In patients infected with subtype B HIV-1, there is often a co-receptor switch in late-stage disease and T-tropic variants appear that can infect a variety of T cells through CXCR4.[45] 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.[46] 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.[47][48]

text: HIV-2 is much less pathogenic than HIV-1 and is restricted in its worldwide distribution. The adoption of "accessory genes" by HIV-2 and its more promiscuous pattern of coreceptor 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 more successful at transmission will be selected.[49]

text: Replication cycle

text: Entry to the cell

text: 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 cell membrane and the release of the HIV capsid into the cell.[50][51]

text: Entry to the cell begins through interaction of the trimeric envelope complex (gp160 spike) and both CD4 and a chemokine receptor (generally either CCR5 or CXCR4, but others are known to interact) on the cell surface.[50][51] 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.[52] The gp160 spike contains binding domains for both CD4 and chemokine receptors.[50][51]

text: 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.[50][51] This allows for a more stable two-pronged attachment, which allows the N-terminal fusion peptide gp41 to penetrate the cell membrane.[50][51] Repeat sequences in gp41, HR1, and HR2 then interact, causing the collapse of the extracellular portion of gp41 into a hairpin. This loop structure brings the virus and cell membranes close together, allowing fusion of the membranes and subsequent entry of the viral capsid.[50][51]

text: 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.[50][not in citation given] 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.

text: 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.[53] 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.[53] The presence of FEZ-1, which occurs naturally in neurons, is believed to prevent the infection of cells by HIV.[54]

text: 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-dependent endocytosis of HIV-1 has also been reported and was recently suggested to constitute the only route of productive entry.[55][56][57][58][59]

text: Replication and transcription

text: Shortly after the viral capsid enters the cell, an enzyme called reverse transcriptase liberates the single-stranded (+)RNA genome from the attached viral proteins and copies it into a complementary DNA (cDNA) molecule.[60] 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.[61] 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.[60]

text: This integrated viral DNA may then lie dormant, in the latent stage of HIV infection.[60] To actively produce the virus, certain cellular transcription factors need to be present, the most important of which is NF-κB (NF kappa B), which is upregulated when T-cells become activated.[62] This means that those cells most likely to be killed by HIV are those currently fighting infection.

text: During viral replication, the integrated DNA provirus is transcribed into RNA, some of which then undergo RNA splicing to produce mature 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 accumulates in the nucleus, it binds to full-length, unspliced copies of virus RNAs and allows them to leave the nucleus.[63] 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.[64]

text: HIV-1 and HIV-2 appear to package their RNA differently.[65][citation needed] HIV-1 will bind to any appropriate RNA[citation needed]. HIV-2 will preferentially bind to the mRNA that was used to create the Gag protein itself.[66]

text: Recombination

text: 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.[67][68] Recombination occurs as the single-strand (+)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. From 2 to 20 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.[68]

text: Viral recombination produces genetic variation that likely contributes to the evolution of resistance to anti-retroviral therapy.[69] 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.[70]

text: Bonhoeffer et al.[71] suggested that template switching by the reverse transcriptase acts as a repair process to deal with breaks in the ssRNA genome. In addition, Hu and Temin[67] 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 ssRNA 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 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.[71]

text: HIV-1 infection causes chronic ongoing inflammation and production of reactive oxygen species.[72] Thus, the HIV genome may be vulnerable to oxidative damages, including breaks in the single-stranded RNA. For HIV, as well as for viruses generally, successful infection depends on overcoming host defensive strategies that often include production of genome-damaging reactive oxygen. Thus, Michod et al.[73] 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.

text: Assembly and release

text: 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 complex where it is cleaved by furin resulting in the two HIV envelope glycoproteins, gp41 and gp120.[74] 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.[75] Only mature virions are then able to infect another cell.

text: Spread within the body

text: HIV is now known to spread between CD4+ T cells by two parallel routes: cell-free spread and cell-to-cell spread, i.e. it employs hybrid spreading mechanisms.[76] In the cell-free spread, virus particles bud from an infected T cell, enter the blood/extracellular fluid and then infect another T cell following a chance encounter.[76] HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread. Two pathways of cell-to-cell transmission have been reported. Firstly, an infected T cell can transmit virus directly to a target T cell via a virological synapse.[52][77] Secondly, an antigen presenting cell (APC) can also 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).[78] Whichever pathway is used, infection by cell-to-cell transfer is reported to be much more efficient than cell-free virus spread.[79] 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 to the contact zone.[77] Cell-to-cell spread is thought to be particularly important in lymphoid tissues where CD4+ T lymphocytes are densely packed and likely to frequently interact.[76] Intravital imaging studies have supported the concept of the HIV virological synapse in vivo.[80] The hybrid spreading mechanisms of HIV contribute to the virus's ongoing replication against antiretroviral therapies.[76][81]

text: Genetic variability

text: 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.[82][83][84]

text: This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day.[82] 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.[82] This recombination is most obvious when it occurs between subtypes.[82]

text: 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,[85] which is present at high levels in the host's blood but evokes only a mild immune response,[86] does not cause the development of simian AIDS,[87] and does not undergo the extensive mutation and recombination typical of HIV infection in humans.[88]

text: In contrast, when these strains infect species that have not adapted to SIV ("heterologous" 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.[89] Chimpanzee SIV (SIVcpz), the closest genetic relative of HIV-1, is associated with increased mortality and AIDS-like symptoms in its natural host.[90] SIVcpz appears to have been transmitted relatively recently to chimpanzee and human populations, so their hosts have not yet adapted to the virus.[85] 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.[90][91]

text: Three groups of HIV-1 have been identified on the basis of differences in the envelope (env) region: M, N, and O.[92] Group M is the most prevalent and is subdivided into eight subtypes (or clades), based on the whole genome, which are geographically distinct.[93] 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. Coinfection 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.[94] Most HIV-1 research is focused on subtype B; few laboratories focus on the other subtypes.[95] The existence of a fourth group, "P", has been hypothesised based on a virus isolated in 2009.[96] The strain is apparently derived from gorilla SIV (SIVgor), first isolated from western lowland gorillas in 2006.[96]

text: 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][97]

text: Diagnosis

text: Many HIV-positive people are unaware that they are infected with the virus.[98] 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.[98] Furthermore, in 2001 only 0.5% of pregnant women attending urban health facilities were counselled, tested or receive their test results.[98] Again, this proportion is even lower in rural health facilities.[98] 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.[99]

text: HIV-1 testing is initially by an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1. Specimens with a nonreactive 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.[100] 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., western blot or, less commonly, an immunofluorescence assay (IFA)). Only specimens that are repeatedly reactive by ELISA and positive by IFA 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.[101]

text: HIV deaths (other than U.S.) in 2014.[102]

text: 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.[100] 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.

text: Modern HIV testing is extremely accurate. A single screening test is correct more than 99% of the time.[103][needs update] The chance of a false-positive result in standard two-step testing protocol is estimated to be about 1 in 250,000 in a low risk population.[103] Testing post exposure is recommended initially and at six weeks, three months, and six months.[104]

text: The latest recommendations of the 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 is present. This gives rise to four possible scenarios:

text:
1. HIV-1 (+) & HIV-2 (-): HIV-1 antibodies detected
2. HIV-1 (-) & HIV-2 (+): HIV-2 antibodies detected
3. HIV-1 (+) & HIV-2 (+): HIV 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.[105]

text: An updated algorithm published by the CDC in June 2014 recommends that diagnosis starts with the p24 antigen test. A negative result rules out infection, while a positive one must be followed by an HIV-1/2 antibody differentiation immunoassay. A positive differentiation test confirms diagnosis, while a negative or indeterminate result must be followed by nucleic acid test (NAT). A positive NAT result confirms HIV-1 infection whereas a negative result rules out infection (false positive p24).[106]

text: Research

text: 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.

text: 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 antiretroviral drugs.[107] Other medical research areas include the topics of pre-exposure prophylaxis, post-exposure prophylaxis, circumcision and HIV, and accelerated aging effects.

text: After many years of research an untested HIV vaccine has been created.[108] Bi-specific antibodies that target both the surface of T-cells and viral epitopes can prevent entry of the virus into somatic cells.[109] Another group has utilised the same technology to develop a bi-specific antibody that neutralises viral particles by cross linking of envelope glycoproteins.[110]

text: History

text: Discovery

text: AIDS was first clinically observed in 1981 in the United States.[111] 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 carinii pneumonia (PCP), a rare opportunistic infection that was known to occur in people with very compromised immune systems.[112] Soon thereafter, additional gay men developed a previously rare skin cancer called Kaposi's sarcoma (KS).[113][114] Many more cases of PCP and KS emerged, alerting U.S. Centers for Disease Control and Prevention (CDC) and a CDC task force was formed to monitor the outbreak.[115] The earliest retrospectively described case of AIDS is believed to have been in Norway beginning in 1966.[116]

text: 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.[117][118] They also used Kaposi's Sarcoma and Opportunistic Infections, the name by which a task force had been set up in 1981.[119] In the general press, the term GRID, which stood for gay-related immune deficiency, had been coined.[120] 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.[121][122] However, after determining that AIDS was not isolated to the gay community,[119] it was realized that the term GRID was misleading and AIDS was introduced at a meeting in July 1982.[123] By September 1982 the CDC started using the name AIDS.[124]

text: In 1983, two separate research groups led by Robert Gallo 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.[125][126] 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 AIDS. 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).[115] As these two viruses turned out to be the same, in 1986 LAV and HTLV-III were renamed HIV.[127]

text: 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).[128] 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.[129]

text: Origins

text: 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.[130][131]

text: HIV-1 appears to have originated in southern Cameroon through the evolution of SIV(cpz), a simian immunodeficiency virus (SIV) that infects wild chimpanzees (HIV-1 descends from the SIV(cpz) endemic in the chimpanzee subspecies Pan troglodytes troglodytes).[132][133] The closest relative of HIV-2 is SIV (smm), a virus of the sooty mangabey (Cercocebus atys atys), an Old World monkey living in litoral West Africa (from southern Senegal to western Côte d'Ivoire).[13] 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.[134] 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.[135]

text: There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV.[136] 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.[137] 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.

text: 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.[138] 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 a higher degree of sexual promiscuity, the spread of prostitution, and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities.[139] While transmission rates of HIV during vaginal intercourse are typically low, they are increased many fold 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.[139]

text: An alternative view 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.[137][140][141]

text: The earliest well documented case of HIV in a human dates back to 1959 in the Belgian Congo.[142] 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 died in 1969.[143]


document_title: Tommy Flanagan (actor)

question_text: how did chibs on sons of anarchy get the scars on his face

root

text: Tommy Flanagan (actor)

text: Personal life[edit]

text: Flanagan was born in Easterhouse, Glasgow, the third of five children. He was an altar boy as a child.[1][2][3] His facial scars are the result of a knife attack outside a nightclub where he had been working as a DJ.[4]

tag: p

text: Flanagan is married to Dina, and together they have a daughter born in 2012.[5] He is a supporter of Celtic F.C.[6]

text: Career[edit]

text: His first television roles were in Screen One (1992) and Taggart (1993). Flanagan worked in Robert Carlyle's Raindog Theatre for three years before being cast in Braveheart (1995). He has had roles in Face/Off (1997), The Game (1997), Sunset Strip (2000), Gladiator (2000), All About the Benjamins (2002), Charlie's Angels: Full Throttle (2003), Alien vs. Predator (2004), Sin City (2005), Smokin' Aces (2006), When a Stranger Calls (2006), The Last Drop (2006), Smokin' Aces 2: Assassins' Ball (2010) and the TV mini-series Attila.

text: He portrayed arms dealer Gabriel Schecter in the first episode of 24's seventh season and appeared in the episode "Headlock" of Lie to Me, aired in the U.S. on Monday 2 August 2010. He was one of the main cast members of Sons of Anarchy, in which he plays an outlaw biker named Filip "Chibs" Telford.[7] In October 2010, Flanagan was revealed as the spokesperson for the Scottish soft drink Irn-Bru. In July 2016, he appeared in the music video for the song "Rotting in Vain" by Korn.

text: Filmography[edit]

text: Film[edit]

text:
Year
Title
Role
Notes

1995
Braveheart
Morrison

1997
The Saint
Scarface

1997
Face/Off
Leo

1997
The Detail

1997
The Game
Solicitor/Taxi driver

1999
Plunkett & Macleane
Eddie

1999
Ratcatcher
Da

2000
Gladiator
Cicero

2000
Sunset Strip
Duncan

2000
Hidden
McCracken
Short film

2001
Strictly Sinatra
Michelangelo

2001
Dead Dogs Lie
Michael

2002
All About the Benjamins
Williamson

2003
Charlie's Angels: Full Throttle
Irish Henchman

2004
Trauma
Tommy

2004
Alien vs. Predator
Mark Verheiden

2005
Sin City
Brian

2006
The Last Drop
Pvt. Dennis Baker

2006
When a Stranger Calls
The Stranger

2006
Smokin' Aces
Lazlo Soot

2008
Hero Wanted
Derek
Credited as Thomas Flannigan

2010
Luster
Les

2010
Smokin' Aces 2: Assassins' Ball
Lazlo Soot

2010
Swifty & Veg
Swifty
Short film

2011
Grace and Danger

2012
Officer Down
Father Reddy

2015
Winter
Woods Weston

2016
Running Wild
Jon Kilpatrick

2016
Sand Castle
SG Major McGregor

2017
Guardians of the Galaxy Vol. 2
Tullk Ul-Zyn

2017
Papillon
Masked Breton

2017
The Ballad of Lefty Brown

tag: table

text: Television[edit]

text:
Year
Title
Role
Notes

1992
Screen One

Episode: "Black and Blue"

1993
Tis the Season to be Jolly
Prisoner
TV film

1993
Taggart
Tam McLeod
Episode: "Instrument of Justice"

1995
Jolly: A Life
Man at grotto
TV film

1996
Rab C. Nesbitt
Sean
Episode: "Lottery"

1996
A Mug's Game
Paul

1996
Bad Boys
Harry
Episode: "The Bonny Bonny Banks"

2000
Rebus
Thomas Telford
Episode: "The Hanging Garden"

2001
Attila
Bleda
TV miniseries

2008–2014
Sons of Anarchy
Filip "Chibs" Telford
90 episodes

2009
24
Gabriel Schector
Episode: "Day 7: 8:00 a.m.-9:00 a.m."

2010
Lie to Me
Ron Marshall
Episode: "Headlock"

2011
Detroit 1-8-7
Albert Stram
2 episodes

2012
Law & Order: Special Victims Unit
Murphy
Episode: "Home Invasions"

2013
Peaky Blinders
Arthur Shelby Snr
Episode: "Episode 5"

2015
Revenge
Malcolm Black
3 episodes

2015
Gotham
Tom "The Knife"
1 episode "Rise of the Villains: The Son of Gotham"

2016
Motive
Jack Stoker
4 episodes


document_title: American Horror Story

question_text: when did season 1 of ahs come out

question_tokens: when did season 1 of ahs come out

text: American Horror Story

text: Episodes[edit]

text: SeasonTitleEpisodesOriginally airedFirst airedLast aired1Murder House12October 5, 2011 (2011-10-05)December 21, 2011 (2011-12-21)2Asylum13October 17, 2012 (2012-10-17)January 23, 2013 (2013-01-23)3Coven13October 9, 2013 (2013-10-09)January 29, 2014 (2014-01-29)4Freak Show13October 8, 2014 (2014-10-08)January 21, 2015 (2015-01-21)5Hotel12October 7, 2015 (2015-10-07)January 13, 2016 (2016-01-13)6Roanoke10September 14, 2016 (2016-09-14)November 16, 2016 (2016-11-16)7Cult11September 5, 2017 (2017-09-05)November 14, 2017 (2017-11-14)8ApocalypseTBASeptember 12, 2018 (2018-09-12)TBA

text: Murder House (2011)[edit]

text: Set in the year 2011, the season follows the Harmons, consisting of psychiatrist Ben (Dylan McDermott), his wife Vivien (Connie Britton), and their teenage daughter Violet (Taissa Farmiga), as they move from Boston to Los Angeles to make a fresh start after Vivien's miscarriage led to Ben having an affair with one of his students, which almost tore their family apart. They move into a restored mansion and soon encounter the residence's housekeeper, Moira O'Hara (Frances Conroy and Alexandra Breckenridge), as well as their neighbors – the eccentric Langdon family consisting of Constance (Jessica Lange) and her daughter Adelaide (Jamie Brewer). The Harmons' lives are troubled by the meddling Langdons, the incompetent realtor Marcy (Christine Estabrook), as well as by the disfigured Larry Harvey (Denis O'Hare), a former resident of the mansion who is secretly in love with Constance, and the scorned Hayden McClaine (Kate Mara), Ben's student who follows him to Los Angeles and is pregnant from their affair. Ben and Vivien try to rekindle their relationship as Violet, suffering from depression, finds comfort with Tate (Evan Peters), the ghost of Constance's psychopathic son. The family soon discovers that the home is haunted by the ghosts of anyone who has ever died on the property, including its creators Charles (Matt Ross) and Nora Montgomery (Lily Rabe); and their deformed son Thaddeus (Ben Woolf). Flashbacks depict the mansion's previous homeowners throughout the last century, dating back to its construction in the 1920s.

text: Asylum (2012–13)[edit]

text: Set in the year 1964, the season follows the patients and staff members of the church-owned Briarcliff Manor, located in Massachusetts, which was founded to treat and house the criminally insane. Kit Walker (Evan Peters), accused of being prolific serial killer "Bloody Face" after the disappearance of his wife Alma (Britne Olford)—though he claims she was abducted by aliens—is incarcerated at Briarcliff. This piques the interest of ambitious journalist Lana Winters (Sarah Paulson), who is yearning to find a story for her big break. At Briarcliff, Kit meets the other patients, many of whom claim to be unjustly institutionalized, including microcephalic Pepper (Naomi Grossman), who was framed for her nephew's murder; nymphomaniac Shelley (Chloe Sevigny); and the unassuming Grace Bertrand (Lizzie Brocheré) from France, who appears to be harboring a deep secret of her own. Believed to be a violent serial killer, he becomes the subject of interest of pragmatic psychiatrist Oliver Thredson (Zachary Quinto) and the sadistic Dr. Arthur Arden (James Cromwell), the latter of whom routinely conducts scientific operations on patients. The institution is run under the watchful eye of the stern Sister Jude (Jessica Lange), as well as her second-in-command, the naive Sister Mary Eunice (Lily Rabe), and the founder of the institution, Monsignor Timothy Howard (Joseph Fiennes). Briarcliff's inhabitants are routinely subject to supernatural and scientific influences, including demonic possession and extraterrestrial abduction.

text: Coven (2013–14)[edit]

text: Set in the year 2013, the season follows the dwindling descendants of the witches who survived the Salem Witch Trials and their struggle to hide their identity in the modern world. Those who share this genetic affliction are being subjected to violent attacks from outside forces, such as religious townspeople and witch hunters. Zoe Benson (Taissa Farmiga), a young teenager completely unaware of the existence of witches, discovers her identity as a Salem descendant after a violent accident that causes the death of her boyfriend. She is sent to an all-girls boarding school in New Orleans which aims to protect and house young women who carry this unique bloodline, and keep them from the dangers of the outside world. There, she meets the other students, narcissistic film star Madison Montgomery (Emma Roberts), outspoken Queenie (Gabourey Sidibe), and enigmatic Nan (Jamie Brewer), and gets romantically entangled with Kyle Spencer (Evan Peters), a non-witch and good-natured college student. The school is run by headmistress Cordelia Foxx (Sarah Paulson), head of the Witches Council and eccentric fashionista Myrtle Snow (Frances Conroy), and the mute butler Spalding (Denis O'Hare). Cordelia's mother, Fiona Goode (Jessica Lange), is the Supreme and most powerful witch of her generation, though she regularly avoids her responsibilities, much to the chagrin of Cordelia and her long-time rival Myrtle. After a mob of townspeople discover and nearly kill a young witch living in the swamps named Misty Day (Lily Rabe), Fiona returns to the school to ensure the safety of the other young witches, but also to fulfill her own hidden agenda. Events reveal a long-held rivalry between the witches of Salem and the voodoo practitioners of New Orleans, as well as a historic grudge between Voodoo Queen Marie Laveau (Angela Bassett) and socialite serial killer Delphine LaLaurie (Kathy Bates).

text: Freak Show (2014–15)[edit]

text: Set in the year 1952, the season follows a struggling freak show led by Elsa Mars (Jessica Lange) in the quiet town of Jupiter, Florida. Decades have passed since the public has looked upon freak shows as a form of entertainment, but Elsa dreams of finding a home for her "monsters", as well as for her own fame and fortune. Other members of her troupe include Jimmy Darling (Evan Peters), a boy born with syndactyly who dreams of living a normal life, and his mother Ethel (Kathy Bates), a bearded lady who is Elsa's second-in-command by maintaining law and order under the tent. A strongman from Ethel's troubled past named Dell Toledo (Michael Chiklis), and his three-breasted wife Desiree Dupree (Angela Bassett), make waves when they arrive to join the freak show. To drum up business and save her troupe once and for all, Elsa also recruits conjoined twin sisters Bette and Dot Tattler (Sarah Paulson) to perform for her show. In a time when the era of television is beginning to reign high above sideshow acts, these individuals must overcome those who persecute them based on their looks. However, as events unfold, it is revealed that multiple dark entities have taken up residence in Jupiter, with all of their eyes being set on the freaks. A conman named Stanley (Denis O'Hare), posing as a Hollywood executive, arrives with his young protege Maggie Esmerelda (Emma Roberts), with the intention of murdering the freaks and sending their bodies to a museum for profit. The wealthy and spoiled Dandy Mott (Finn Wittrock), enabled by his doting mother Gloria (Frances Conroy), develops an unhealthy obsession with the freaks, particularly Bette and Dot. Perhaps most dangerous of all is a mysterious, deformed killer clown, only known as Twisty (John Carroll Lynch), who wreaks havoc among the town and appears to be targeting freaks and townspeople alike.

text: Hotel (2015–16)[edit]

text: Set in the year 2015, the season follows the strange and dangerous happenings that seem to center around the retro Hotel Cortez in downtown Los Angeles, California, initially built as a secret torture chamber to fulfill the violent desires of founder James March (Evan Peters). Detective John Lowe (Wes Bentley) arrives at the hotel, based on intel from an anonymous tip, to investigate a grisly string of murders, each of which exemplify a sin in violation of one of the Ten Commandments. He has become estranged from his wife Alex (Chloe Sevigny), who suffers from depression, and his daughter Scarlett (Shree Crooks), after the disappearance of their son Holden (Lennon Henry). As the season unfolds, the Lowes discover that the disappearance of Holden may be related to the strange activities at the hotel, led by March's fashionista widow Elizabeth Johnson (Lady Gaga), also known as the Countess—who was turned into a vampire by her former lovers, actor Rudolph Valentino (Finn Wittrock) and his wife Natacha Rambova (Alexandra Daddario)—and her current lover Donovan (Matt Bomer). Throughout his investigation, John also becomes entangled with the spirits of heroin junkie named Sally (Sarah Paulson), hotel maid Hazel Evers (Mare Winningham), and James March, who is looking for a protege to continue the violent acts he started when he was alive. The hotel's tireless staff includes the surly front desk manager Iris (Kathy Bates), Donovan's mother who took the job to be close to her son, and her best friend, the transgender bartender Liz Taylor (Denis O'Hare), both of whom hesitantly cater to Elizabeth and her vampiric children. Elizabeth's relationship with Donovan becomes troubled with the arrival of male model and cocaine addict Tristan Duffy (Wittrock), New York fashion designer Will Drake (Cheyenne Jackson), and her scorned ex-lover Ramona Royale (Angela Bassett), all of whom become entangled in her violent life.

text: Roanoke (2016)[edit]

text: Set in the years 2014-2016, the season follows the supernatural events that occur in a renovated farmhouse in North Carolina, which is situated on the land where the Roanoke Colony moved after their infamous 1580s disappearance. In 2015, Shelby Miller (Lily Rabe), her husband Matt (André Holland), along with Matt's sister Lee Harris (Adina Porter) recount their harrowing experience living in the farmhouse a year prior in a popular documentary series titled My Roanoke Nightmare, including their encounters with the ghosts of the house's previous residents, the violent ghosts of the Roanoke Colony, the cannibalistic Polk family who live nearby, and the beautiful, yet terrifying Celtic goddess, Scáthach (Lady Gaga). The documentary becomes a huge success, featuring dramatic reenactments of the Millers' story starring Audrey Tindall (Sarah Paulson) as Shelby, Dominic Banks (Cuba Gooding Jr.) as Matt, Monet Tumusiime (Angela Bassett) as Lee, Agnes Mary Winstead (Kathy Bates) as Thomasin White, leader of the ghost colony, Audrey's husband Rory Monahan (Evan Peters) as Edward Philippe Mott, the creator and first owner of the house, William van Henderson (Denis O'Hare) as Dr. Elias Cunningham, a professor who becomes entranced with the paranormal happenings of the area, and Dylan (Wes Bentley) as Ambrose White, Thomasin's son and accomplice. In 2016, the success of the documentary leads to a sequel titled Return to Roanoke: Three Days In Hell, spearheaded by the producer of the original series, Sidney Aaron James (Cheyenne Jackson), who invites the Millers, as well as many of the reenactment actors, to return to the farmhouse for three days, where all their actions will be captured by hidden cameras. Although the Millers are aware of the entities that reside in the house, all three agree to return, each with their own agenda. The production eventually descends into disaster, however, as cast and crew alike are quickly targeted when the violent entities begin to surface.

text: Cult (2017)[edit]

text: Set in the year 2017, the fictional town of Brookfield Heights, Michigan, is left divided upon the wake of Donald Trump's presidential election. Local restaurant owner Ally Mayfair-Richards (Sarah Paulson) is left utterly distraught, along with her wife Ivy (Alison Pill). Despite the help of her psychiatrist, Dr. Rudy Vincent Anderson (Cheyenne Jackson), Ally becomes increasingly unstable in the following weeks, her long repressed phobias begin to re-emerge, and they begin to affect her relationships with her wife as well as their son Oz (Cooper Dodson). Across town, misogynistic alt-righter Kai Anderson (Evan Peters) rejoices at the election results, enticing him to pursue political power by running for city council, led by Bebe Babbitt (Frances Conroy), an old-school feminist, with the help of his reluctant, liberal sister Winter (Billie Lourd), who was also hired by the Mayfair-Richards household as their nanny. As Ally attempts to adjust to regular life despite her growing anxiety and paranoia, she becomes terrorized by a group of masked assailants in clown attire who are only present when she is alone, leaving those around her to wonder if she was truly attacked, or if they were merely hallucinations. Kai's faithful followers include Ally's eccentric neighbors Harrison (Billy Eichner) and Meadow Wilton (Leslie Grossman), newscast reporter Beverly Hope (Adina Porter), rogue detective Jack Samuels (Colton Haynes), as well as local grocery cashier Gary K. Longstreet (Chaz Bono). With Kai's rise to power revealing sinister motives, Ally starts to draw connections between her alleged clown attackers and the many strange incidents occurring in Brookfield Heights. She begins to fear that everyone in town is out to get her, amplifying her growing distrust of those around her, especially her neighbors.

text: Apocalypse (2018)[edit]

text: In the year 2020, nuclear holocaust breaks out and results in the collapse of human civilization. Billionaire-heiress Coco St. Pierre Vanderbilt (Leslie Grossman), her personal assistant Mallory (Billie Lourd), hairstylist Mr. Gallant (Evan Peters) and Gallant's grandmother Evie (Joan Collins) board a private jet and are taken to a secret underground bunker known as Outpost 3, where they meet fellow survivors Dinah Stevens (Adina Porter), Andre (Jeffrey Bowyer-Chapman), Timothy Campbell (Kyle Allen) and Emily (Ash Santos). Wilhelmina Venable (Sarah Paulson) and Miriam Mead (Kathy Bates) run the Outpost with an iron fist, punishing its residents for all manners of indiscretions, including unauthorized copulation. After 18 months, Emily and Timothy, who were selected by the "Cooperative" for their unique genetic makeup, have established a secret relationship, and along with the other survivors are living off a single gelatinous cube of nutrients per day. Before long, Michael Langdon (Cody Fern), the Antichrist, arrives at the Outpost to evaluate the necessity of its survivors, and lead the valuable ones to the "Sanctuary". It is soon that the Outpost is shaken up by the arrival of Cordelia Goode, Madison Montgomery (Emma Roberts) and Myrtle Snow (Frances Conroy) as well as the other Coven witches, Zoe (Taissa Farmiga), Misty (Lily Rabe) and Queenie (Gabourey Sidibe). Their arrival not only changes the course of the season but also provides the background and events leading up to the apocalypse, with the inclusion of characters from Murder House.

text: Future seasons[edit]

text: On January 12, 2017, the series was renewed for a ninth season, with a two-season renewal alongside Apocalypse.[7] Subsequently, on August 3, 2018, the series was renewed for a tenth season.[8]

text: Production[edit]

text: Conception[edit]

text:
What you saw in the finale was the end of the Harmon house. The second season of the show will be a brand-new home or building to haunt. Just like this year, every season of this show will have a beginning, middle and end. [The second season] won't be in L.A. It will obviously be in America, but in a completely different locale.
– Murphy on the series' anthology format[9]

tag: div

text: Creators Murphy and Falchuk began working on American Horror Story before their Fox series Glee began production. Murphy wanted to do the opposite of what he had done previously and thus began his work on the series. He stated: "I went from Nip/Tuck to Glee, so it made sense that I wanted to do something challenging and dark. And I always had loved, as Brad had, the horror genre. So it just was a natural for me."[10] Falchuk was intrigued by the idea of putting a different angle on the horror genre, stating that their main goal in creating the series was to scare viewers. "You want people to be a little bit off balance afterwards," he said.[11]

text: In February 2011, FX officially announced that it had ordered a pilot for a possible series from Ryan Murphy and Brad Falchuk, with both Murphy and Falchuk writing and Murphy directing. Dante Di Loreto was announced as executive producer. Production on the series began in April 2011.[12] In July 2011, FX officially announced the project had been picked up to series.[13]

text: From the beginning, Murphy and Falchuk planned that each season of the series would tell a different story.[9] After the first season finale aired, Murphy spoke of his plans to change the cast and location for the second season.[14] He did say, however, that some actors who starred in the first season would be returning. "The people that are coming back will be playing completely different characters, creatures, monsters, etc. [The Harmons'] stories are done. People who are coming back will be playing entirely new characters," he announced.[9] In November 2012, FX chief executive, John Landgraf, described the unique format of the series stating: "[T]he notion of doing an anthological series of miniseries with a repertory cast – has proven groundbreaking, wildly successful and will prove to be trendsetting."[15]

text: At the 2013 PaleyFest, Falchuk compared the series to horror films: "It does demand a little bit of compassion at the end because you fall in love with these characters in a different way than you would in a movie," he said. "If you want to kill everybody in a movie except one person, you can kind of get away with that, but if you're looking to do a horror TV show, you have a different responsibility to the characters because the audience has a different affection for them."[16]

text: Murphy then explained the process of planning a series' season takes about a year. "We come up with story first and then we come up with the characters," he said. "It is a repertory company, so we'll move people around and sometimes there won't yet be a role for somebody. Like when we started [the second season], I really had no idea that Dylan [McDermott] would be the person to play Sarah's son, but the deeper we got, I thought, that would work great."[16]

text: In an August 2015 article for Entertainment Weekly, Murphy revealed that the show is mulling producing two seasons a year. The first being broadcast in the spring and the second in the fall. He explained, "We're doing something that we've never done before on the show where we're doing two different groups of writers rooms. Some of our writers will be bouncing around but a whole different group coming in late August. The next thing we’re crafting up is very, very different than [Hotel]. Not smaller. But just not opulent. More rogue and more dark."[17]

text: Casting[edit]

text: Connie Britton was first to be cast in the series, portraying female lead Vivien Harmon on Murder House.[18] Denis O'Hare joined second as Larry Harvey.[19] Jessica Lange soon followed as Constance, her first regular role on television.[20] Dylan McDermott joined the cast soon after Lange as the male lead Ben Harmon.[21] Taissa Farmiga and Evan Peters were the last actors to be added to the main cast, portraying Violet Harmon and Tate Langdon, respectively.[22]

text: In March 2012, Murphy revealed that the second season had been planned around Jessica Lange, who portrays Sister Jude, a sadistic nun who runs the asylum.[23] Evan Peters, Sarah Paulson, Lily Rabe and Zachary Quinto also return, with the latter three joining the main cast.[24] Peters portrays Kit Walker, an inmate accused of murdering his wife.[25] Paulson portrays Lana, a lesbian reporter who gets committed to the asylum because of her sexuality and intent to snoop around the sanitarium.[26] Rabe's character is Sister Mary Eunice, clumsy second-in-charge to Sister Jude.[27] Quinto portrays Dr. Thredson, a psychiatrist at the asylum.[28][29] Lizzie Brocheré stars as Grace Bertrand, a character described originally as "a fierce, ferocious, extremely sexual, and dangerous wild-child sexpot", but the role was later heavily revamped.[30][31] James Cromwell co-stars as Dr. Arthur Arden, who proclaims to be in charge of the asylum and performs dark experiments on its patients.[32][33][34] Joseph Fiennes starred as Monsignor Timothy Howard, a possible love interest for Sister Jude.[34][35][36]

text: For the third season, series executive producers and co-creators Ryan Murphy and Brad Falchuk stated that, as with the second season, "many actors" would return in different roles, beginning with Jessica Lange.[37] Evan Peters and Sarah Paulson were confirmed to return, portraying Kyle Spencer and Cordelia Foxx, respectively. Murphy added that Lange would portray a "real glamour-cat lady", later revealed to be named Fiona Goode.[38] Taissa Farmiga, Violet in the first season, starred as Zoe Benson, a character that is involved in a prominent romance during the season.[39] Lily Rabe co-starred as Misty Day.[40] Recurring cast member Frances Conroy joined as a main cast member, playing the character of Myrtle Snow.[39] Oscar-winning actress Kathy Bates was confirmed to co-star. It was first reported that she would portray "a woman who, at the start, is Lange's character's best friend, but will become her worst enemy", but this was altered.[41] Murphy stated that Bates' character will be "five times worse than [her] Misery character" and is also inspired by a "true event". She portrayed Madame Delphine LaLaurie, an immortal racist.[42] It was announced in May 2013 that Emma Roberts had been added to the cast. Roberts played Madison Montgomery, a "self-involved party girl".[43] In July 2013, season one alum Denis O'Hare also joined the cast in an unknown role,[44] later revealed as Spalding.

text: In November 2013, Ryan Murphy confirmed that Jessica Lange would be returning for a fourth season, although in a reduced capacity. It was later revealed she would be playing Freak Show owner Elsa Mars.[45] Kathy Bates returned in a main role, portraying bearded lady Ethel Darling.[46] On March 29, 2014, Murphy announced that Sarah Paulson, Evan Peters, Frances Conroy, Emma Roberts, Denis O'Hare, and Angela Bassett would all return for the fourth season.[47] Paulson portrayed conjoined sisters Bette and Dot Tattler; Peters portrayed "Lobster Boy" Jimmy Darling; Conroy played the well-off Gloria Mott; Bassett portrayed three-breasted hermaphrodite Desiree Dupree; and O'Hare played Stanley, a conman working with Roberts' Maggie Esmerelda. At PaleyFest 2014, it was revealed that Michael Chiklis would be joining the cast as Dell Toledo, the father of Jimmy, ex-husband of Ethel, and current husband of Desiree.[48] Finn Wittrock later joined the main cast as Gloria's spoiled son, Dandy Mott.

text: For the series' fifth cycle, singer-songwriter Lady Gaga was announced as the first and newest main cast member on February 25, 2015.[49] After a special guest appearance on the previous season, Matt Bomer joined the fifth season's cast along with series newcomer Cheyenne Jackson during PaleyFest 2015.[50] Chloë Sevigny and Wes Bentley were promoted as main cast members, after they appear as recurring special guests in Asylum and Freak Show respectively.[51] Murphy later announced the returns of Kathy Bates, Sarah Paulson, Evan Peters and Angela Bassett.[52] In June 2015, it was announced Denis O'Hare would also return for the fifth season.[53] In August 2015, Murphy announced the character roles for the cast: Gaga's Elizabeth Johnson also known as "The Countess", a fashionista vampire who owns the Hotel Cortez; Jackson's Will Drake, a desperate fashion designer; O'Hare's Liz Taylor, a transgender bartender who works at the hotel's Blue Parrot Lounge bar; Sevigny's Alex Lowe, a pediatrician who was the wife of Bentley's John Lowe, a detective who investigates the murders inside the hotel; Bomer's Donovan, the lover to the Countess whom often had conflict with his mother and hotel manager, Bates' Iris; Bassett's Ramona Royale, a former actress who was the former lover of Elizabeth; Paulson's Sally, a drug addict who had a rivalry with Iris and forms a bond with John since his visit in the hotel.[54] Peters co-starred as serial killer James Patrick March and the original hotelier of the Hotel Cortez.

text: In February 2016, Angela Bassett confirmed she would return to join the main cast of the sixth season during an interview with Larry King.[55] Denis O'Hare announced that he will also appear in the season in a May 2016 interview.[56] In June 2016, Cheyenne Jackson, Evan Peters, Wes Bentley, and Kathy Bates announced their returns for the sixth season.[57][58][59] In August 2016, Sarah Paulson announced that she would return to the series in the sixth season and Ryan Murphy announced that Oscar winner Cuba Gooding Jr. had joined the main cast.[60][61] In September 2016, the full main cast was announced after the first episode with the inclusion of André Holland and returning series veteran Lily Rabe.[62] On Halloween 2016, Murphy announced that Paulson's Asylum character, Lana Winters would also appear in the series after the recent appearance of the actress' first role Billie Dean Howard from Murder House in the final episode of the fifth season.[63][64]

text: For the seventh season, Paulson and Peters were set to return to the series, as announced during the Winter 2017 TCA Press Tour.[65] Billie Lourd, who made her breakout appearance with Murphy in 2015, was confirmed to join the main cast in April, while Jackson was the next series regular to return in the next month.[66][67][68] In June, Alison Pill was announced to co-star in the season, portraying the partner of Paulson's character.[69]

text: On October 2017, Paulson announced that she'll return for the series' eighth cycle. [70] The next year, Peters was announced to appear in the main cast while Bates returned to the series after Roanoke, leading the season with Paulson.[71] Jackson confirmed he will return while Adina Porter was promoted to the series' main cast after her first appearance in Murder House as well as Leslie Grossman since Cult.[72] Lourd later returned to the main cast the next month. [73] On June, Roberts announced that she'll reprise her Coven character Madison Montgomery in the eighth season.[74] The next month, Australian actor Cody Fern was cast as the adult Michael Langdon who was last seen at the first series' final episode.[75]

text: Filming[edit]

text: The pilot episode was shot on location in a house in Country Club Park, Los Angeles, California, which serves as the haunted house and crime scene in the series. Designed and built in 1908 by Alfred Rosenheim, the president of the American Institute of Architects' Los Angeles chapter, the Tudor or Collegiate Gothic-style single family home was previously used as a convent.[76][77] The first season was filmed on sets which are an exact replica of the house.[78] Details such as Louis Comfort Tiffany stained glass windows and hammered bronze light fixtures were re-created to preserve the look of the house.[76]

text: Production and shooting for the second season began in late July 2012 for a scheduled premiere in mid October.[79] The exteriors for the second season were filmed in Hidden Valley, Ventura County, California, a rural area outside Los Angeles, although the season took place in Massachusetts.[80]

text: Principal photography for the third season began on July 23, 2013,[81] in New Orleans, Louisiana.[82][83] It was first reported that the season would film in multiple locations, but filming primarily took place in New Orleans.[84]

text: Principal photography for the fourth season began on July 15, 2014, in New Orleans, though the story takes place in Jupiter, Florida.

text: Principal photography for the fifth season began on July 14, 2015, in Los Angeles, California, where the story also takes place.[85] Murphy revealed a six-story hotel set was being built on the Fox lot. A dummy set of the hotel was built at the 2015 San Diego Comic-Con, showing an Art Deco style building from the 1920s, inspired by the old Hollywood era.[86]

text: Filming for the sixth season began on July 6, 2016 at Santa Clarita, California.[87] Set constructions include a colonial settler home to speculate the disappearance of the Roanoke Colony.[88]

text: Filming for the seventh season was originally planned to begin in Orange, California on June 2017 before it was moved to May instead.[89][90]

text: Filming for the eighth season is set to begin on June 16, 2018.[91]

text: Title sequences[edit]

text: American Horror Story's title screens offer vague hints to important plot elements and events that compose each season. For Murder House, Murphy described the sequence as a mini-mystery and stated that: "By the time you see the ninth episode of this season, every image in that title sequence will be explained," establishing the purpose of the title sequence for future seasons.[92]

text: The opening title sequence was created by Kyle Cooper and his company Prologue. He also created the title sequence for the AMC series The Walking Dead and the 1995 film Seven. The theme music was composed by sound designer Cesar Davila-Irizarry and musician Charlie Clouser.[93] The cinematography was done by Juan Ruiz Anchía and the editing by Gabriel J. Diaz.

text: For Murder House, the sequence is set in the Harmons' basement and includes images of postmortem young children, fetuses in jars, skulls, a christening dress, a nurse's uniform, and a figure holding a pair of bloody hedge clippers. A photo of alleged axe murderer Lizzie Borden is also shown.

text: Asylum's opening sequence is done by the same creative team. "We are shooting a new title sequence with the same team that did last year's," series creator Ryan Murphy said. "The song may stay... not sure."[94] The music was kept, and the new title sequence was set around the Asylum, using shots of inmates raving and surgeons operating on patients with bandages obscuring their faces. Elements include a young girl walking backwards on her hands and feet up a staircase and a shot of the Virgin Mary's smile changing from one of benevolence to one of spite.

text: Coven's opening sequence keeps the same music, and this sequence is the first one to be filmed primarily outside and not in an enclosed location. Shots include figures wearing black robes and capirotes, a bony-skeleton creature with wings and shots of dead goats, the Minotaur from the season also appears. For the first time, there are actual backgrounds that appear with the actor names instead of an all-black background, some of these images include witches hanging and Santa Muerte. Other elements include a black man with piercing eyes and a disturbing smile as well as voodoo dolls. The final shot continues after the figures in black capirotes seize one of their own who is later seen burning at a stake where young, dress-clad witches dance around.

text: Freak Show's opening sequence changed things up, the series theme music remains intact albeit with an added carnival-like soundscape. The sequence is composed of both CGI and stop-motion animation and features strange characters such as a skeleton chimera of a human being and an elephant riding a bicycle, a skeleton of what appears to be a single head but two bodies, a devil-like man, a boy in a wheel chair with deformed legs, a character with severe syndactyly of the hands and feet, a clown who can twist his head around, a woman with a third leg where her genitalia should be, and a demonic cymbal-banging monkey toy. There are also shots of side show attractions like the Human Blockhead, knife throwing and sword swallowing. The main recurring element features a balloon twister popping balloons with a knife.

text: Hotel's opening sequence also was very different from previous seasons', taking a more biblical approach. The font, while remaining the same as the first four seasons, glow in red against a hotel wallpaper. The Ten Commandments are also shown throughout the video. The intro returns to live-action like the first three seasons. Visuals include many people scrubbing blood all over the walls and the floor, strange things shown through peepholes, people being victims to the hotel, little kids running around the hotel, as well as many different creatures.[95]

text: Roanoke featured no title sequence or opening credits, instead opting for a simple title card from the first season, Murder House, while the series theme music plays over the end credits. At the end of the finale's credits, the title of the season "American Horror Story: Roanoke" was revealed.

text: In the development of Cult, Murphy confirmed that the opening sequence will return. Cult's opening sequence features the series theme music played by a marching band. The sequence is live-action. Visuals include: a gang of clowns rises from a casket, Donald Trump and Hillary Clinton masks, a George Washington statue, a dead dog killed by toxic gas, a Merry Go Round, bloody hands that cannot be washed, beehive, toxic smoke released from a grenade, holes in several forms, bloody US flag with sound of a xylophone playing The Star-Spangled Banner, blood covered couple having sex and a handcuffed pinky promise. Clowns also appear throughout the sequence.

text: Apocalypse's opening sequence features the original theme music from the first three seasons. Red and white are the main colors, visually representing Murder House and Coven. The sequence includes images of nuclear disaster and sketches of demons fusing together. Others visuals include candles burning, snakes, skulls of both humans and goats, a scorpion, a blooming flower, and photos of nuclear-testing documents. Visuals from the title sequences of both season 1 and season 3 are also included with slight alterations, including the skeletal winged creature in the forest (Coven), the nurse's blouse (Murder House), a picture of a baby that has been set on fire (Murder House), and the goat skulls (Coven). It is notable that many images are shown in reverse.

text: The title sequence for all seasons of the show use a variation of the Willow typeface that very closely resembles a style for which Scottish designer Charles Rennie Mackintosh was known.[96]

text: Promotion[edit]

text: As part of the promotion for the series, FX launched a "House Call" campaign, in which viewers at home could sign up and come face-to-face with a character from the series.[97] Prior to the series premiere, FX released several clues to shine light on the series. They were offered on the show's official YouTube channel. Ten clues were released.[98] In September 2011, FX launched a website which allows visitors to tour the Murder House throughout the decades and look for clues.[99]

text: In August 2012, the first promo for the second season was released on the American Horror Story Facebook page entitled "Special Delivery", in which a nun carries a couple of buckets filled with body parts through a field. As a church bell rings, the nun empties one bucket's bloody contents, leaving the empty bucket behind, and resumes her trek.[100] Over 20 subsequent teasers were released.[101] Four photos were also released on EW.com.[102] Two televised teasers, titled "Meet the Residents", were released on August 31, 2012. They feature the patients and some staff (such as Dr. Thredson, played by Zachary Quinto, and Sister Mary Eunice, played by Lily Rabe) lying in twin beds and dealing with their individual issues as the heads of the asylum (Jessica Lange, Joseph Fiennes and James Cromwell) look on. The song "Que Sera, Sera", mixed with the show's theme music, plays.[103] To promote Cult, a competition was set up where fans who donated to the Children's Hospital Los Angeles could get a chance to get a walk-on role in an episode, and lunch with Evan Peters.[104]

text: Universal's Halloween Horror Nights[edit]

text: On August 16, 2016, FX announced a deal had been struck to feature an American Horror Story exhibit at Universal Studios Hollywood and Universal Orlando for their Halloween Horror Nights. The maze will feature sets and themes from Murder House, Freak Show, and Hotel. Universal said of the experience, "Twisted scenes from Murder House will unleash the evil spirits that possess the Harmon estate, spiraling guests through decades of the tortured dead who previously resided there. In Freak Show, guests will join a troupe of biological misfits in a sinister sideshow where they'll be stalked by the murderous and deformed Twisty the Clown. Finally, guests will succumb to the warped desires of The Countess after checking into the haunted Hotel Cortez, conceived from the beginning as a torture chamber for its customers."[105]

text: In 2017, the show returned as haunted attractions to both parks, with Universal Orlando having an attraction based on Asylum, Coven, and Roanoke, and Universal Studios Hollywood basing their attraction solely on Roanoke.

text: Broadcast[edit]

text: The series premiered on October 5, 2011, and is broadcast on the cable television channel FX in the United States. In November 2011, it premiered internationally on the respective countries' Fox Networks Group. The first season premiered on October 5, 2011, and concluded on December 21, 2011. The second season premiered on October 17, 2012, and concluded on January 23, 2013. The third season premiered on October 9, 2013, and concluded on January 29, 2014. The fourth season premiered on October 8, 2014, and concluded on January 21, 2015. The fifth season premiered on October 7, 2015, and concluded on January 13, 2016. The sixth season premiered on September 14, 2016, and concluded on November 16, 2016. The seventh season premiered on September 5, 2017, and concluded on November 14, 2017. The latter three seasons premiered on the same day and same time with the American broadcasts on FX in Canada, though the first season followed a slightly different schedule as that network launched on October 31, 2011. The series is aired in India on STAR World Premiere HD shortly after its U.S. airing. Along with it, it airs on FX India on standard definition.

text: Reception[edit]

text: Critical response[edit]

text:
Season

Critical response

Rotten Tomatoes

Metacritic

Murder House

73% (39 reviews)

62 (30 reviews)

Asylum

84% (44 reviews)

65 (23 reviews)

Coven

84% (35 reviews)

71 (24 reviews)

Freak Show

79% (34 reviews)

69 (19 reviews)

Hotel

64% (48 reviews)

60 (24 reviews)

Roanoke

76% (14 reviews)

72 (9 reviews)

Cult

73% (46 reviews)

66 (24 reviews)

Apocalypse

93% (62 reviews)

63 (6 reviews)

text: The first season of American Horror Story: Murder House received generally positive reviews from critics. Review aggregator Rotten Tomatoes reported that 74% of 38 critics gave the first season a positive review. The site's consensus stated: "Convoluted yet effective, American Horror Story is strange, gory, and twisted enough to keep viewers hooked."[106] The first season scored 62 out of 100 on Metacritic based on 30 reviews.[107] Ken Tucker from Entertainment Weekly awarded the pilot episode a B+, stating: "AHS is pretty much all scare, all the time: a whole lotta screams, sex, jolts, mashed faces, psychotic behavior, and dead babies."[108] Hank Stuever from The Washington Post said in his review that: "Overdoing things is one of Murphy's trademark flaws, but this show has a captivating style and giddy gross-outs."[109] Not all reviews were favorable: Alan Sepinwall of HitFix gave the series a D−, saying: "It is so far over the top that the top is a microscopic speck in its rearview mirror, and so full of strange sounds, sights and characters that you likely won't forget it – even though many of you will wish you could."[110] Sepinwall would later go on to call it one of the worst TV shows of 2011.[111] The Los Angeles Times' Mary McNamara gave it a mixed review, stating that it "collapses into camp... upon more than one occasion" but also noting that it is "hard to look away."[112]

text: The second season, American Horror Story: Asylum, received mostly positive reviews from critics. Review aggregator Rotten Tomatoes reported that 84% of 43 critics gave the season a positive review. The site's consensus is: "American Horror Story: Asylum crosses boundaries to shock and scare with sexy subplots and some innovative takes on current social issues."[113] It scored 65 out of 100 on Metacritic based on 23 reviews.[114] James Poniewozik from Time stated: "AHS: Asylum feels like a more focused, if equally frenetic, screamfest. It's also gorgeously realized, with a vision of its '60s institution setting so detailed you can smell the stale air and incense."[115] Maureen Ryan of The Huffington Post said: "It's to the credit of Asylum's writers, directors and cast that the emotional pain of the characters often feels as real as their uncertainty and terror."[116] Verne Gay from Newsday gave the season a C grade, stating it "has some good special effects, just not much of a story to hang them on."[117] Linda Stasi of the New York Post thought the season was "over the top," adding: "I need to enter [an asylum] myself after two hours of this craziness."[118]

text: The third season, American Horror Story: Coven, received positive reviews. Review aggregator Rotten Tomatoes reported that 84% of 34 critics gave the season a positive review. The site's consensus reads: "A noteworthy ensemble cast combined with creepy storytelling and campy, outrageous thrills make American Horror Story: Coven a potently structured fright-fest."[119] It scored 71 out of 100 on Metacritic based on 24 reviews, the highest score for the show to that point. Not all reviews were positive, however, with criticism focused mainly in regards to the progression of both the story and certain character arcs in the second half of the season. The A.V. Club gave this season the low rating of a D+, with critic Todd Van DerWerff remarking: "It lurched drunkenly from idea to idea, never settling on one long enough to build anything of worth."[120]

text: The fourth season, American Horror Story: Freak Show, received mostly positive reviews. Review aggregator Rotten Tomatoes reports that 79% of 32 critics gave the season a positive review. The site's consensus is: "Though it may turn off new viewers unaccustomed to its unabashed weirdness, Freak Show still brings the thrills, thanks to its reliably stylish presentation and game cast."[121] It scored 69 out of 100 on Metacritic based on 19 "generally favorable" reviews.[122]

text: The fifth season, American Horror Story: Hotel, received mixed to positive reviews from critics. Rotten Tomatoes reports that 63% of 43 critics gave the season a positive review. The site's consensus is: "Favoring garish style over effective storytelling, the fifth American Horror Story strands a talented cast at Ryan Murphy's Hotel." Audience reception on the same website was also mixed, with 57% of viewers giving the show a favorable review.[123] Hotel scored a 60 out of 100 on Metacritic based on 24 "mixed or average" reviews.[124]

text: The sixth season, American Horror Story: Roanoke, received positive reviews from critics. Rotten Tomatoes reports that 78% of 13 critics gave the season a positive review. The site's consensus is: "American Horror Story: My Roanoke Nightmare takes a surprising turn away from prior AHS formats, revisiting the deliberate pace of earlier seasons on a spookier, smaller scale, even if the true-crime format feels overdone."[125] It scored a 72 on Metacritic based on six reviews.[126]

text: The seventh season, American Horror Story: Cult, received generally positive reviews from critics. Rotten Tomatoes reports that 73% of 47 critics gave the season a positive review. The site's consensus is: "American Horror Story: Cult intrigues with timely, over-the-top creepiness – and lots of clowns – despite being hampered by broad political generalizations and occasional holes in the narrative's logic."[127] It scored a 66 on Metacritic based on 24 "generally favorable" reviews.[128]

text: The eighth season, American Horror Story: Apocalypse, received positive reviews from critics. Rotten Tomatoes reports that 93% of 105 critics gave the season a positive review.[129] It scored a 63 on Metacritic based on 6 "generally favorable" reviews.[130]

text: Ryan Murphy and Brad Falchuk have been credited with creating a series that increases both the LGBT creators and storylines in the industry. Harriet Earle has stated that they utilize "the formal structure of the serialized anthology...to present serial narratives made by and about 'queers,' openly subverting gender and sexual norms that define the majority of television".[131]

text: Ratings[edit]

text: The pilot episode of American Horror Story was watched by 3.2 million viewers and averaged a 1.6 rating in the 18–49 years adult demographic, the most sought after by advertisers.[132] These were the best numbers FX had ever received for a series premiere.[133] The episode was seen by 3.2 million total viewers in 59 countries.[134] Ratings increased as the season progressed, with the season finale being watched by 3.22 million viewers and receiving a 1.7 ratings share in the 18–49 years adult demographic.[135] The series premiere aired in November 2011 across Europe and Latin America on Fox International Channels, and ranked as first or second most watched telecast in its timeslot among all paid television in most metered markets.[134] "Numbers so strong, it's scary. American Horror Story has brought droves of new viewers to a killer global lineup", said Hernan Lopez, the president of Fox International Channels.[134]

text: The second season's premiere gained a 2.2 18–49 ratings share and gathered 3.85 million viewers,[136] marking the highest numbers for the series.[137] By the season's sixth episode, the numbers dropped to a series-low 0.9 18–49 ratings share and 1.89 million viewers;[138] however, they rebounded to above two million viewers for the subsequent episodes,[139][140] and reached 2.29 million viewers for the season's finale.[141] The premiere of the fifth season of the series became the second most-watched telecast in the network's history, only behind the premiere episode of the previous season, which was watched by 6.13 million viewers.[142] The show was subsequently renewed for another season; John Landgraf, the CEO of the network, commented on the show's success by saying that American Horror Story, the network's highest rated series, "has unquestionably joined the ranks of television's landmark series."[143] In 2016, a New York Times study of the 50 TV shows with the most Facebook Likes found that "unlike a lot of shows about the supernatural", American Horror Story was "more popular in cities, but also throughout parts of the Southwest".[144]

text:
Season
Timeslot (ET)

Episodes

First aired

Last aired
TV season
Avg. viewers(millions)

Date

Viewers(millions)

Date

Viewers(millions)

1
Wednesday 10:00 p.m.

12

October 5, 2011

3.18

December 21, 2011

3.22
2011–12
2.82

2

13

October 17, 2012

3.85

January 23, 2013

2.29
2012–13
2.53

3

13

October 9, 2013

5.54

January 29, 2014

4.24
2013–14
4.00

4

13

October 8, 2014

6.13

January 21, 2015

3.27
2014–15
3.85

5

12

October 7, 2015

5.81

January 13, 2016

2.24
2015–16
2.89

6

10

September 14, 2016

5.14

November 16, 2016

2.45
2016–17
2.93

7
Tuesday 10:00 p.m.

11

September 5, 2017

3.93

November 14, 2017

1.97
2017–18
2.22

8
Wednesday 10:00 p.m.

TBA

September 12, 2018

3.08

TBA

TBD
2018–19
TBA

text: Accolades[edit]

text: American Horror Story has won 73 of its 303 award nominations. The franchise has garnered 28 Primetime Emmy Award nominations, with Jessica Lange winning for Outstanding Supporting Actress in a Miniseries or a Movie and for Outstanding Lead Actress in a Miniseries or a Movie, James Cromwell winning for Outstanding Supporting Actor in a Miniseries or a Movie, and Kathy Bates winning for Outstanding Supporting Actress in a Miniseries or a Movie. It received an additional 50 Creative Arts Emmy Award nominations, winning eleven times, including Outstanding Hairstyling for a Miniseries or a Movie, Outstanding Costumes for a Miniseries, Movie, or Special, Outstanding Sound Editing for a Miniseries, Movie, or Special, and Outstanding Prosthetic Makeup for a Series, Limited Series, Movie or a Special.[145] It has received nine Golden Globe Award nominations, with Lange winning for Best Supporting Actress in a Series, Miniseries or Television Film,[146] and Lady Gaga winning for Best Actress in a Miniseries or Television Film.[147] The series has also received three Screen Actors Guild Award nominations, with Lange winning for Outstanding Performance by a Female Actor in a Drama Series.[148] Additional accolades include eighteen Critics' Choice Television Awards nominations, with four wins,[149] the GLAAD Media Award for Outstanding TV Miniseries,[150] four Costume Designers Guild Awards nominations, winning three times,[151] eight wins out of ten nominations at the Make-Up Artists and Hair Stylists Guild,[152] five People's Choice Awards nominations, winning once,[153] and eleven Satellite Awards nomination, with three wins.[154]

text: Spin-off[edit]

text: On October 7, 2014, it was announced that FX had ordered a 10-episode spin-off[155] titled American Crime Story, developed by Scott Alexander and Larry Karaszewski.[156] While each season of American Horror Story focuses on a new horror theme, each season of American Crime Story focuses on a new true crime story. The series features American Horror Story cast members Sarah Paulson, Connie Britton, Cuba Gooding Jr., Finn Wittrock and Cody Fern.