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Pratt VM, Scott SA, Pirmohamed M, et al., editors. Medical Genetics Summaries [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2012-.

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Abacavir Therapy and HLA-B*57:01 Genotype

, MD.

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Created: ; Last Update: April 18, 2018.

Estimated reading time: 15 minutes


Abacavir (brand name Ziagen) is used in the treatment of human immunodeficiency virus (HIV) infection. Abacavir is a nucleoside (and nucleotide) reverse transcriptase inhibitor (NRTI), and is used in combination with other medications as part of highly active antiretroviral therapy (HAART) (1).

Hypersensitivity reactions associated with abacavir can be severe and potentially fatal. Symptoms include fever, rash, vomiting, and shortness of breath. They typically appear within the first 42 days of treatment (11 days median onset).

HLA-B*57:01 significantly increases the risk of hypersensitivity reactions when abacavir is administered. Approximately 6% of Caucasians and 2-3% of African Americans carry this allele in the human leukocyte antigen B (HLA-B) gene. The HLA-B gene plays an important role in how the immune system recognizes and responds to pathogens, and mediates hypersensitivity reactions. HLA-B*57:01 has been found to be associated with abacavir hypersensitivity across different ethnicities, including Caucasians, Hispanics, and individuals of African origin (2, 3).

Screening for the HLA-B*57:01 allele before starting abacavir therapy is recommended for all patients according to the FDA drug label for abacavir (Table 1). Even if previously tolerated, screening should happen before restarting abacavir therapy if HLA-B*57:01 status is unknown. Abacavir is contraindicated in HLA-B*5701-positive patients, and in patients with a prior hypersensitivity reaction to abacavir. Dosing guidelines from the professional societies, Clinical Pharmacogenetics Implementation Consortium (CPIC) and the Dutch Pharmacogenetics Working Group (DPWG) of the Royal Dutch Association for the Advancement of Pharmacy (KNMP), also recommend that HLA-B*57:01 screening should be performed prior to initiation of abacavir therapy and an alternate drug be administered for patients with the allele (Table 2, Table 3)(1, 3-5).

Table 1.

FDA (2017) Drug Label for Abacavir. Therapeutic Recommendations based on HLA-B*57:01 Genotype. Warnings and Precautions.

GenotypeHypersensitivity reactions
HLA-B*5701-positive patientsDue to the potential for severe, serious, and possibly fatal hypersensitivity reactions with abacavir sulfate:
All patients should be screened for the HLA-B*5701 allele prior to initiating therapy with abacavir tablets or reinitiation of therapy with abacavir tablets, unless patients have a previously documented HLA-B*5701 allele assessment.
Abacavir tablets are contraindicated in patients with a prior hypersensitivity reaction to abacavir and in HLA-B*5701-positive patients.

Please see 2017 Statement from the US Food and Drug Administration (FDA) for more information from the FDA. Table adapted from (1).

Table 3.

DPWG (2017) Recommendations for Abacavir based on HLA-B Genotype

HLA-B*57:01-positiveAbacavir is contraindicated for HLA-B*57:01-positive patients. Advise the prescriber to prescribe an alternative according to the current guidelines.

Please see 2017 Summary of recommendations from the Dutch Pharmacogenetics Working Group (DPWG) of the Royal Dutch Association for the Advancement of Pharmacy (KNMP) for more information from DPWG. Table adapted from (5).

Drug: Abacavir

Abacavir is an antiretroviral drug that belongs to the drug class of nucleoside (and nucleotide) reverse transcriptase inhibitors (NRTIs). The NRTIs, also known as nucleoside (or nucleotide) analogs, were the first type of drug available to treat HIV infection, and they remain effective today. In addition to abacavir, NRTIs include drugs such as AZT/zidovudine, emtricitabine, tenofovir, and lamivudine. Abacavir is always used in combination with other drugs.

Antiretroviral drugs, like abacavir, inhibit the activity of retroviruses, such as HIV. To replicate, retroviruses must convert their RNA genome into a DNA copy, which can then be inserted into the host cell’s genome. Abacavir inhibits the conversion of viral RNA to DNA, preventing viral replication.

Abacavir is a pro-drug and its antiviral activity is facilitated by the drug’s phosphorylation by intracellular enzymes to form carbovir triphosphate, a nucleoside analog. Carbovir triphosphate competes with the natural substrate of the HIV reverse transcriptase enzyme, to be incorporated into viral DNA. Once incorporated, the nucleoside analog terminates DNA chain elongation, preventing further synthesis of viral DNA (6).

Abacavir started to be used in the late 1990s, as part of a combination of therapies to treat HIV. However, the use of abacavir in the US was limited by a severe hypersensitivity reaction that occurred in approximately 5-8% of patients. Symptoms occurred during the first 6 weeks and included a constellation of symptoms presenting as rash, fever, fatigue, gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain), and acute respiratory symptoms (e.g., cough and dyspnea) (7). Life-threatening skin diseases, Stevens-Johnson syndrome and toxic-epidermal necrolysis, can occur in severe reactions.

Data from the PREDICT-1 study suggest that 100% of individuals with immunologically confirmed (abacavir patch test positive) abacavir hypersensitivity present within 3 weeks of initial dosing. The median onset of symptoms is 9-11 days (1, 7, 8).

Abacavir can trigger a hypersensitivity reaction in people who have the HLA-B*57:01 allele. The frequency of the HLA-B*57:01 allele varies by population; for example, approximately 6% of Caucasians, and 2-3% of African-American and admixed American populations carry at least one copy of this high-risk HLA-B allele (Table 4). HLA-B*57:01-postitive individuals have an increased risk of a hypersensitivity reaction to abacavir compared to HLA-B*57:01-negative individuals (8).

Table 4.

CPIC (2014) Assignment of likely HLA-B Phenotypes based on Genotype

Likely phenotypeGenotypeExamples of diplotype
Very low risk of hypersensitivity (constitutes ~94%a of patients)Absence of *57:01 alleles (reported as “negative” on a genotyping test)*X/*Xb
High risk of hypersensitivity (~6% of patients)Presence of at least one *57:01 allele (reported as “positive” on a genotyping test)*57:01/*Xb

HLA-B, human leukocyte antigen B.


See supplementary data online for estimates of genotype frequencies among different ethnic/geographic groups.


*X = any HLA-B genotype other than *57:01.

Table adapted from (3).

The FDA-approved label for abacavir states that all patients should be screened for the HLA-B*57:01 allele prior to initiating therapy with abacavir, or when reinitiating therapy with abacavir, unless patients have a previously documented HLA-B*57:01 allele assessment. The FDA also warns that abacavir must be discontinued immediately if a hypersensitivity reaction is suspected, regardless of HLA-B*57:01 status and even when other diagnoses are possible (1).

Several studies have shown that routine genetic screening for HLA-B*57:01 significantly reduces the incidence of abacavir-induced hypersensitivity, and is cost-effective. Because it is rare for individuals who do not carry the high-risk HLA variant to develop hypersensitivity, adhering to the screening guidelines can reduce the incidence of immunologically confirmed cases of abacavir hypersensitivity to nearly zero (9-12).

HLA Gene Family

The HLA genes are members of the major histocompatibility complex (MHC) gene family, which includes more than 200 genes. The MHC family has been subdivided into 3 subgroups based on the structure and function of the encoded proteins: class I, class II, and class III. The class I region contains the genes encoding the HLA molecules HLA-A, HLA-B, and HLA-C. These molecules are expressed on the surfaces of almost all cells and play an important role in antigen presentation. The HLA region also contains a variety of other genes, including genes involved in immunity and genes not known to be involved in immune function.

An important role of HLA class I molecules is to present peptides (processed fragments of antigens) to immune cells (CD8+ T cells). Most of these peptides originate from the breakdown of normal cellular proteins (“self”). However, if foreign peptide fragments are presented, e.g., from a pathogen, CD8+T cells will recognize the peptides as “non-self” and will be activated to release inflammatory cytokines and launch an immune response to dispose of the pathogen (or foreign body).

Because HLA molecules need to present such a wide variety of “self” and “non-self” peptides, the HLA genes are both numerous and highly polymorphic. More than 4,700 HLA-B alleles have been identified (6, 13).

HLA Allele Nomenclature

HLA allele nomenclature includes the HLA prefix, followed by the gene, an asterisk and a four (or six) digit number that corresponds to the assigned allele number (14). For example, the HLA-B*15:02: allele is composed of:

  • HLA: the HLA prefix (the HLA region on chromosome 6)
  • B: the B gene (a particular HLA gene in this region)
  • 15: the allele group (historically determined by serotyping, i.e., a group of alleles that share the same serotype)
  • 02: the specific HLA allele (a specific protein sequence; determined by genetic analysis).

Additional digits have been added to the nomenclature to discriminate between alleles that do not differ in the protein amino acid sequence but differ in their genetic sequence (i.e., due to synonymous and noncoding genetic variants).

Variation in HLA genes plays an important role in susceptibility to autoimmune disease and infections. These variations are also critical in the context of transplant surgery where better outcomes are observed if the donor and recipient are HLA-compatible.

HLA variants have also been associated with susceptibility to Type B adverse drug reactions. For example, as noted above, an HLA-B variant has been associated with severe hypersensitivity reactions to abacavir. Other HLA-B variants have been associated with severe reactions to allopurinol (used to treat gout), and carbamazepine and phenytoin (used to treat epilepsy).

Gene: HLA-B

The HLA-B*57:01 allele is associated with an increased risk of hypersensitivity reaction to abacavir. Studies across ethnicities have reported that in immunologically confirmed cases of abacavir hypersensitivity, 100% of cases occurred in patients who were carriers of this HLA variant (7).

Other immune factors are also involved, however. For example, not everyone who carries the high-risk HLA allele will develop abacavir hypersensitivity - approximately 39% of individuals who are positive for HLA-B*57:01 will tolerate abacavir treatment (8).

Cytotoxic (CD8+) T cells mediate the hypersensitivity reaction to abacavir. Abacavir is thought to form a non-covalent complex with HLA-B*57:01 (15-18). Several theories have been proposed for how this drug peptide-HLA complex activates the T cell receptor, which then releases inflammatory cytokines, signaling the start of the hypersensitivity response (19-23). More than one immune mechanism may be involved (7). It has been shown that abacavir occupies a space below the region of HLA that presents peptides. This leads to altered peptide presentation (including the presentation of self-peptides to which the host has not been tolerized) and triggers an autoimmune-like reaction (19, 24).

The hypersensitivity reaction to abacavir is thought to be maintained over the lifetime of an individual. The reintroduction of abacavir to a sensitized individual may be fatal, presumably due to a rapid activation of a memory T cell population. Therefore, abacavir is contraindicated in individuals with a prior hypersensitivity reaction to abacavir (1, 25).

HLA-B*57:01 also has an important role in HIV infection. In Caucasians with HIV, HLA-B*57:01 has been linked to a lower viral load set point (the amount of viral RNA detected in blood during the asymptomatic phase of HIV infection) (26). In addition, HLA-B*57:01 is overrepresented in a small group of individuals who have HIV which has not progressed to AIDs, despite lack of treatment with antiretroviral therapy. These individuals are known as “long-term non-progressors” (27).

The frequency of the HLA-B*57:01 allele varies significantly by population. The allele is most common in Northern Thai and Indian populations (up to 20%). It is relatively common in European populations (6–7%), and is present but less common in African Americans, admixed American populations, and Middle Eastern populations (2-3%). HLA-B*57:01 is uncommon in homogenous South-Asian and African populations, being mostly absent in the Japanese, and some African populations (2, 3, 28).

Genetic Testing

Pharmacogenetic testing is now routine in HIV clinical practice (28).The NIH’s Genetic Testing Registry (GTR) provides examples of the genetic tests that are currently available for abacavir hypersensitivity, and the HLA-B gene.

The genotype results for an HLA allele such as HLA-B*57:01 can either be “positive” or “negative”. There are no intermediate phenotypes because the HLA genes are expressed in a codominant manner.

Abacavir is contradicted in patients with a “positive” result, and only one copy of the *57:01 allele is required for a positive result. Therefore, the positive result is either “heterozygous” or “homozygous”, depending upon whether the patient is carrying one or 2 copies of the *57:01 allele, respectively.

A negative result indicates that the patient does not carry the HLA-B*57:01 allele. However, a negative result does not rule out the possibility of a patient developing abacavir hypersensitivity. Therefore, clinicians should carefully monitor all patients according to standard practices (3).

Therapeutic Recommendations based on Genotype

This section contains excerpted1 information on gene-based dosing recommendations. Neither this section nor other parts of this review contain the complete recommendations from the sources.

2017 Statement from the US Food and Drug Administration (FDA)

Serious and sometimes fatal hypersensitivity reactions have occurred with abacavir sulfate. These hypersensitivity reactions have included multi-organ failure and anaphylaxis and typically occurred within the first 6 weeks of treatment with abacavir sulfate (median time to onset was 9 days); although abacavir hypersensitivity reactions have occurred any time during treatment. Patients who carry the HLA-B*57:01 allele are at a higher risk of abacavir hypersensitivity reactions; although, patients who do not carry the HLA-B*57:01 allele have developed hypersensitivity reactions. Hypersensitivity to abacavir was reported in approximately 206 (8%) of 2,670 patients in 9 clinical trials with abacavir-containing products where HLA-B*57:01 screening was not performed. The incidence of suspected abacavir hypersensitivity reactions in clinical trials was 1% when subjects carrying the HLA-B*57:01 allele were excluded. In any patient treated with abacavir, the clinical diagnosis of hypersensitivity reaction must remain the basis of clinical decision making.

Due to the potential for severe, serious, and possibly fatal hypersensitivity reactions with abacavir sulfate:

  • All patients should be screened for the HLA-B*57:01 allele prior to initiating therapy with abacavir tablets or reinitiation of therapy with abacavir tablets, unless patients have a previously documented HLA-B*57:01 allele assessment.
  • Abacavir tablet is contraindicated in patients with a prior hypersensitivity reaction to abacavir and in HLA-B*57:01 -positive patients.
  • Before starting abacavir tablets, review medical history for prior exposure to any abacavir-containing product. NEVER restart abacavir tablets or any other abacavir-containing product following a hypersensitivity reaction to abacavir, regardless of HLA-B*57:01 status.
  • To reduce the risk of a life-threatening hypersensitivity reaction, regardless of HLA-B*57:01 status, discontinue abacavir tablets immediately if a hypersensitivity reaction is suspected, even when other diagnoses are possible (e.g., acute onset respiratory diseases such as pneumonia, bronchitis, pharyngitis, or influenza; gastroenteritis; or reactions to other medications).
  • If a hypersensitivity reaction cannot be ruled out, do not restart abacavir tablets or any other abacavir-containing products because more severe symptoms which may include life-threatening hypotension and death, can occur within hours.
  • If a hypersensitivity reaction is ruled out, patients may restart abacavir tablets. Rarely, patients who have stopped abacavir for reasons other than symptoms of hypersensitivity have also experienced life-threatening reactions within hours of reinitiating abacavir therapy. Therefore, reintroduction of abacavir tablets or any other abacavir-containing product is recommended only if medical care can be readily accessed.
  • A Medication Guide and Warning Card that provide information about recognition of hypersensitivity reactions should be dispensed with each new prescription and refill.

Please review the complete therapeutic recommendations that are located here: (1).

2014 Statement from the Clinical Pharmacogenetics Implementation Consortium (CPIC)

We agree with others that HLA-B*57:01 screening should be performed in all abacavir-naive individuals before initiation of abacavir-containing therapy (see Table 2); this is consistent with the recommendations of the FDA, the US Department of Health and Human Services, and the European Medicines Agency. In abacavir-naive individuals who are HLA-B*57:01-positive, abacavir is not recommended and should be considered only under exceptional circumstances when the potential benefit, based on resistance patterns and treatment history, outweighs the risk. HLA-B*57:01 genotyping is widely available in the developed world and is considered the standard of care prior to initiating abacavir. Where HLA-B*57:01 genotyping is not clinically available (such as in resource-limited settings), some have advocated initiating abacavir, provided there is appropriate clinical monitoring and patient counseling about the signs and symptoms of HSR [hypersensitivity reaction], although this remains at the clinician’s discretion.

Please review the complete therapeutic recommendations that are located here (3, 4).

2017 Summary of Recommendations from the Dutch Pharmacogenetics Working Group (DPWG) of the Royal Dutch Association for the Advancement of Pharmacy (KNMP)

HLA-B*57:01-positive patients have a strongly increased risk of a hypersensitivity reaction to abacavir.


Abacavir is contraindicated for HLA-B*57:01-positive patients.


Advise the prescriber to prescribe an alternative according to the current guidelines.

Background information


Although the mechanism of hypersensitivity reactions to abacavir is not fully known, experimental data suggest the following mechanism.

Abacavir metabolites (aldehydes and acids) form a covalent bond with cellular proteins. Peptides derived from these modified proteins bind to HLA-B*5701 and are recognised on the cell surface as foreign by the immune cells, which triggers an immune response against cells containing abacavir. For more information about the HLA-B*57:01 genotype: see the general background information about HLA on the KNMP Knowledge Bank or on http://www.knmp.nl/ (search for HLA).

Other considerations:

If tests are performed for HLA-B57 instead of HLA-B*57:01, some patients will incorrectly be denied treatment with abacavir. This is primarily the case in patients of African descent, where HLA-B*57:03 is the most common HLA-B57 sub-type and to a lesser extent for Caucasian patients, where HLA-B*57:01 is the most common HLA-B57 sub-type. If there are enough alternatives, it is not a problem that the patient is being denied abacavir incorrectly.

Clinical consequences:

HLA-B*5701-positive patients have a strongly increased risk of a hypersensitivity reaction to abacavir (OR [odds ratio] 7 to 960 for clinically diagnosed hypersensitivity reactions and 900 to 1945 for immunologically confirmed hypersensitivity reactions).

Exclusion of HLA-B*5701-positive patients from abacavir therapy reduced the number of clinically diagnosed hypersensitivity reactions in predominantly white populations by 56-96% and the number of immunologically confirmed hypersensitivity reactions by 100%.

Hypersensitivity reactions to abacavir generally disappear spontaneously after stopping abacavir, but can be fatal in severe cases.

Please review the complete therapeutic recommendations that are located here: ( 5 ).


Nomenclature of Selected HLA-B alleles

Allele namedbSNP reference identifier for allele location
HLA-B*57:01 rs2395029 is a tag SNP for HLA-B*57:01

For the MHC region, variations in genes such as HLA-B occur across the whole sequence of the gene, not a single locus. Therefore, the HLA-B*57:01 allele is defined by its sequence (GenBank: AF196183.1) rather than single coding or protein variants. If there is strong linkage disequilibrium between one or more SNPs, the presence of these SNPs (tag SNPs) may be used for HLA typing (29). In the case of HLA-B, the presence of the rs2395029 allele (a SNP in the HLA complex P5 gene) is 99.9% predictive of the presence of an HLA-B*57:01 allele (30).

Pharmacogenetic Allele Nomenclature: International Workgroup Recommendations for Test Result Reporting (4).

Guidelines on the naming of HLA genes are available from HLA Nomenclature.


The author would like to thank Inge Holsappel, Pharmacist at the Royal Dutch Pharmacists Association (KNMP), the Netherlands, for reviewing the information regarding the guidelines of the Dutch Pharmacogenetics Working Group (DPWG); David A. Ostrov, PhD, Associate Professor, Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine; Professor Anthony W. Purcell, Department of Biochemistry and Molecular Biology and Biomedicine Discovery Institute, Monash University, Australia; and Lisa Ross, Director, Clinical Sciences Group at ViiV Healthcare, Durham, North Carolina; for reviewing this summary.

2015 version:

The author would like to thank Elizabeth Phillips, MD, FIDSA, John A. Oates Chair in Clinical Research, Professor of Medicine and Pharmacology, Director of Personalized Immunology, Oates Institute for Experimental Therapeutics, Vanderbilt University Medical Center; and Professor Munir Pirmohamed, David Weatherall Chair of Medicine, University of Liverpool and Director of the MRC Centre for Drug Safety Sciences, for reviewing this summary.

Version History

To view the 2015 version of this summary (Created: September 1, 2015) please click here.


ABACAVIR- abacavir tablet, film coated [package insert]. Miami, FL; 2017 May. Available from: https://dailymed​.nlm​.nih.gov/dailymed/drugInfo​.cfm?setid=0d791375-e311-41f9-87b8-940657e6318c.
Sousa-Pinto B., Pinto-Ramos J., Correia C., Goncalves-Costa G., et al. Pharmacogenetics of abacavir hypersensitivity: A systematic review and meta-analysis of the association with HLA-B*57:01. J Allergy Clin Immunol. 2015;136(4):1092–4.e3. [PubMed: 25934581]
Martin M.A., Klein T.E., Dong B.J., Pirmohamed M., et al. Clinical pharmacogenetics implementation consortium guidelines for HLA-B genotype and abacavir dosing. Clinical pharmacology and therapeutics. 2012;91(4):734–8. [PMC free article: PMC3374459] [PubMed: 22378157]
Martin M.A., Hoffman J.M., Freimuth R.R., Klein T.E., et al. Clinical Pharmacogenetics Implementation Consortium Guidelines for HLA-B Genotype and Abacavir Dosing: 2014 update. Clin Pharmacol Ther. 2014;95(5):499–500. [PMC free article: PMC3994233] [PubMed: 24561393]
Royal Dutch Pharmacists Association (KNMP). Dutch Pharmacogenetics Working Group (DPWG). Pharmacogenetic Guidelines [Internet]. Netherlands. Abacavir – HLA-B*5701 [Cited July 2017]. Available from: http://kennisbank​.knmp.nl [Access is restricted to KNMP membership.]
HLA Nomenclature [Internet]. Royal Free Hospital, London, UK. HLA Nomenclature: HLA Alleles Numbers [Cited 2018 January 09]. Available from: http://hla​.alleles.org​/nomenclature/stats.html.
Illing P.T., Purcell A.W., McCluskey J. The role of HLA genes in pharmacogenomics: unravelling HLA associated adverse drug reactions. Immunogenetics. 2017;69(8-9):617–630. [PubMed: 28695285]
Mallal S., Phillips E., Carosi G., Molina J.M., et al. HLA-B*5701 screening for hypersensitivity to abacavir. N Engl J Med. 2008;358(6):568–79. [PubMed: 18256392]
Cargnin S., Jommi C., Canonico P.L., Genazzani A.A., et al. Diagnostic accuracy of HLA-B*57:01 screening for the prediction of abacavir hypersensitivity and clinical utility of the test: a meta-analytic review. Pharmacogenomics. 2014;15(7):963–76. [PubMed: 24956250]
Small C.B., Margolis D.A., Shaefer M.S., Ross L.L. HLA-B*57:01 allele prevalence in HIV-infected North American subjects and the impact of allele testing on the incidence of abacavir-associated hypersensitivity reaction in HLA-B*57:01-negative subjects. BMC Infect Dis. 2017;17(1):256. [PMC free article: PMC5387336] [PubMed: 28399804]
Ruiz-Iruela C., Padulles-Zamora N., Podzamczer-Palter D., Alonso-Pastor A., et al. HLA-B*57: 01 genotyping in the prevention of hypersensitivity to abacavir: 5 years of experience. Pharmacogenet Genomics. 2016;26(8):390–6. [PubMed: 27195528]
Sousa-Pinto B., Correia C., Gomes L., Gil-Mata S., et al. HLA and Delayed Drug-Induced Hypersensitivity. Int Arch Allergy Immunol. 2016;170(3):163–79. [PubMed: 27576480]
Nomenclature for Factors of the HLA System: HLA Alleles [Cited 23 June 2016]. Available from: http://hla​.alleles.org/alleles/index​.html.
Choo S.Y. The HLA system: genetics, immunology, clinical testing, and clinical implications. Yonsei Med J. 2007;48(1):11–23. [PMC free article: PMC2628004] [PubMed: 17326240]
Almeida C.A., Martin A.M., Nolan D., Lucas A., et al. Cytokine profiling in abacavir hypersensitivity patients. Antiviral therapy. 2008;13(2):281–8. [PubMed: 18505179]
Chessman D., Kostenko L., Lethborg T., Purcell A.W., et al. Human leukocyte antigen class I-restricted activation of CD8+ T cells provides the immunogenetic basis of a systemic drug hypersensitivity. Immunity. 2008;28(6):822–32. [PubMed: 18549801]
Lucas A., Lucas M., Strhyn A., Keane N.M., et al. Abacavir-reactive memory T cells are present in drug naive individuals. PLoS One. 2015;10(2):e0117160. [PMC free article: PMC4326126] [PubMed: 25674793]
Metushi I.G., Wriston A., Banerjee P., Gohlke B.O., et al. Acyclovir Has Low but Detectable Influence on HLA-B*57:01 Specificity without Inducing Hypersensitivity. PLoS One. 2015;10(5):e0124878. [PMC free article: PMC4449000] [PubMed: 26024233]
Ostrov D.A., Grant B.J., Pompeu Y.A., Sidney J., et al. Drug hypersensitivity caused by alteration of the MHC-presented self-peptide repertoire. Proc Natl Acad Sci U S A. 2012;109(25):9959–64. [PMC free article: PMC3382472] [PubMed: 22645359]
Norcross M.A., Luo S., Lu L., Boyne M.T., et al. Abacavir induces loading of novel self-peptides into HLA-B*57: 01: an autoimmune model for HLA-associated drug hypersensitivity. AIDS. 2012;26(11):F21–9. [PMC free article: PMC4155923] [PubMed: 22617051]
Illing P.T., Vivian J.P., Dudek N.L., Kostenko L., et al. Immune self-reactivity triggered by drug-modified HLA-peptide repertoire. Nature. 2012;486(7404):554–8. [PubMed: 22722860]
White, K., S. Gaudieri, and E. Phillips, HLA and the pharmacogenomics of drug hypersensitivity, in Handbook of Pharmacogenomics and Stratified Medicine. 2014, Elsevier. p. 437-465.
White K.D., Chung W.H., Hung S.I., Mallal S., et al. Evolving models of the immunopathogenesis of T cell–mediated drug allergy: The role of host, pathogens, and drug response. J. Allergy Clin. Immunol. 2015;136(2):219–34. [PMC free article: PMC4577472] [PubMed: 26254049]
Pirmohamed M., Ostrov D.A., Park B.K. New genetic findings lead the way to a better understanding of fundamental mechanisms of drug hypersensitivity. J Allergy Clin Immunol. 2015;136(2):236–44. [PMC free article: PMC4534769] [PubMed: 26254050]
Rodríguez-Nóvoa S., Barreiro P., Jimenez-Nacher I., Soriano V. Overview of the pharmacogenetics of HIV therapy. The pharmacogenomics journal. 2006;6(4):234–45. [PubMed: 16462814]
Fellay J., Shianna K.V., Ge D., Colombo S., et al. A whole-genome association study of major determinants for host control of HIV-1. Science. 2007;317(5840):944–7. [PMC free article: PMC1991296] [PubMed: 17641165]
Migueles S.A., Sabbaghian M.S., Shupert W.L., Bettinotti M.P., et al. HLA B*5701 is highly associated with restriction of virus replication in a subgroup of HIV-infected long term nonprogressors. Proceedings of the National Academy of Sciences of the United States of America. 2000;97(6):2709–14. [PMC free article: PMC15994] [PubMed: 10694578]
Michels A.W., Ostrov D.A. New approaches for predicting T cell-mediated drug reactions: A role for inducible and potentially preventable autoimmunity. J Allergy Clin Immunol. 2015;136(2):252–7. [PMC free article: PMC4529959] [PubMed: 26254052]
de Bakker P.I., McVean G., Sabeti P.C., Miretti M.M., et al. A high-resolution HLA and SNP haplotype map for disease association studies in the extended human MHC. Nature genetics. 2006;38(10):1166–72. [PMC free article: PMC2670196] [PubMed: 16998491]
Colombo S., Rauch A., Rotger M., Fellay J., et al. The HCP5 single-nucleotide polymorphism: a simple screening tool for prediction of hypersensitivity reaction to abacavir. The Journal of infectious diseases. 2008;198(6):864–7. [PubMed: 18684101]



The FDA labels specific drug formulations. We have substituted the generic names for any drug labels in this excerpt. The FDA may not have labeled all formulations containing the generic drug. Certain terms, genes and genetic variants may be corrected in accordance to nomenclature standards, where necessary. We have given the full name of abbreviations, shown in square brackets, where necessary.

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