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  • 1. Abi-Rached, Laurent
    et al.
    Jobin, Matthew J.
    Kulkarni, Subhash
    McWhinnie, Alasdair
    Dalva, Klara
    Gragert, Loren
    Babrzadeh, Farbod
    Stanford University, United States .
    Gharizadeh, Baback
    Luo, Ma
    Plummer, Francis A.
    Kimani, Joshua
    Carrington, Mary
    Middleton, Derek
    Rajalingam, Raja
    Beksac, Meral
    Marsh, Steven G. E.
    Maiers, Martin
    Guethlein, Lisbeth A.
    Tavoularis, Sofia
    Little, Ann-Margaret
    Green, Richard E.
    Norman, Paul J.
    Parham, Peter
    The Shaping of Modern Human Immune Systems by Multiregional Admixture with Archaic Humans2011Inngår i: Science, ISSN 0036-8075, E-ISSN 1095-9203, Vol. 334, nr 6052, s. 89-94Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Whole genome comparisons identified introgression from archaic to modern humans. Our analysis of highly polymorphic human leukocyte antigen (HLA) class I, vital immune system components subject to strong balancing selection, shows how modern humans acquired the HLA-B*73 allele in west Asia through admixture with archaic humans called Denisovans, a likely sister group to the Neandertals. Virtual genotyping of Denisovan and Neandertal genomes identified archaic HLA haplotypes carrying functionally distinctive alleles that have introgressed into modern Eurasian and Oceanian populations. These alleles, of which several encode unique or strong ligands for natural killer cell receptors, now represent more than half the HLA alleles of modern Eurasians and also appear to have been later introduced into Africans. Thus, adaptive introgression of archaic alleles has significantly shaped modern human immune systems.

  • 2. Gottlieb, Bruce
    et al.
    Alvarado, Carlos
    Wang, Chunlin
    Gharizadeh, Baback
    Babrzadeh, Farbod
    Stanford Genome Technology Center, Stanford University, Palo Alto, CA, United States .
    Richards, Brent
    Batist, Gerald
    Basik, Mark
    Beitel, Lenore K.
    Trifiro, Mark
    Making Sense of Intratumor Genetic Heterogeneity: Altered Frequency of Androgen Receptor CAG Repeat Length Variants in Breast Cancer Tissues2013Inngår i: Human Mutation, ISSN 1059-7794, E-ISSN 1098-1004, Vol. 34, nr 4, s. 610-618Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    To examine the significance of intratumor genetic heterogeneity (ITGH) of the androgen receptor (AR) gene in breast cancer, patient-matched samples of laser capture microdissected breast tumor cells, adjacent normal breast epithelia cells, and peripheral blood leukocytes were sequenced using a novel next generation sequencing protocol. This protocol measured the frequency of distribution of a variable AR CAG repeat length, a functional polymorphism associated with breast cancer risk. All samples exhibited some degree of ITGH with up to 30 CAG repeat length variants identified. Each type of tissue exhibited a different distribution profile of CAG repeat lengths with substantial differences in the frequencies of zero and 1825 CAG AR variants. Tissue differences in the frequency of ARs with each of these CAG repeat lengths were significant as measured by paired, twin t-tests. These results suggest that preferential selection of 1825 CAG repeat length variants in breast tumors may be associated with breast cancer, and support the observation that shorter CAG repeats may protect against breast cancer. They also suggest that merely identifying variant genes will be insufficient to determine the critical mutational events of oncogenesis, which will require measuring the frequency of distribution of mutations within cancerous and matching normal tissues.

  • 3. Javanmard, M.
    et al.
    Babrzadeh, Farbod
    Davis, R. W.
    Stanford Genome Technology Center, Stanford University, United States.
    Microfluidic force spectroscopy for characterization of biomolecular interactions with piconewton resolution2010Inngår i: Applied Physics Letters, ISSN 0003-6951, E-ISSN 1077-3118, Vol. 97, nr 17, s. 173704-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    In this paper we present a scalable method based on the use of microfluidics and shear force spectroscopy which can be used for determining the affinity between molecules. Our method involves the use of functionalization of the surface of microfluidic channels with ligand molecules, and the surface of microspheres with receptor molecules. Bound beads are detached from the surface of the microchannels using pressure driven flow. The drag force required to detach the beads is used to determine the affinity of the bond holding the two molecules together. The minimum force we are able to detect is 5 pN. We have used this method to determine the binding force between protein-protein interactions and DNA base-pair interactions. We also have shown the ability of this technique to distinguish between strong and weak protein-protein interactions. Using this approach, it may be possible to multiplex an array of these functionalized channels onto a chip and probe the interactions between large varieties of biomolecules.

  • 4. Javanmard, Mehdi
    et al.
    Babrzadeh, Farbod
    KTH, Skolan för bioteknologi (BIO), Biokemi.
    Nyrén, Pål
    KTH, Skolan för bioteknologi (BIO), Biokemi.
    Davis, Ronald W.
    Improvement in cell capture throughput using parallel bioactivated microfluidic channels2012Inngår i: Biomedical microdevices (Print), ISSN 1387-2176, E-ISSN 1572-8781, Vol. 14, nr 4, s. 625-629Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Optimization of targeted cell capture with microfluidic devices continues to be a challenge. On the one hand, microfluidics allow working with microliter volumes of liquids, whereas various applications in the real world require detection of target analyte in large volumes, such as capture of rare cell types in several ml of blood. This contrast of volumes (microliter vs. ml) has prevented the emergence of microfluidic cell capture sensors in the clinical setting. Here, we study the improvement in cell capture and throughput achieved using parallel bioactivated microfluidic channels. The device consists of channels in parallel with each other tied to a single channel. We discuss fabrication and testing of our devices, and show the ability for an improvement in throughput detection of target cells.

  • 5. Li, Linlin
    et al.
    Victoria, Joseph
    Kapoor, Amit
    Blinkova, Olga
    Wang, Chunlin
    Babrzadeh, Farbod
    Stanford Genome Technology Center, Stanford University, United States .
    Mason, Carl J.
    Pandey, Prativa
    Triki, Hinda
    Bahri, Olfa
    Oderinde, Bamidele Soji
    Baba, Marycelin Mandu
    Bukbuk, David Nadeba
    Besser, John M.
    Bartkus, Joanne M.
    Delwart, Eric L.
    A Novel Picornavirus Associated with Gastroenteritis2009Inngår i: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 83, nr 22, s. 12002-12006Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    A novel picornavirus genome was sequenced, showing 42.6%, 35.2%, and 44.6% of deduced amino acid identities corresponding to the P1, P2, and P3 regions, respectively, of the Aichi virus. Divergent strains of this new virus, which we named salivirus, were detected in 18 stool samples from Nigeria, Tunisia, Nepal, and the United States. A statistical association was seen between virus shedding and unexplained cases of gastroenteritis in Nepal (P = 0.0056). Viruses with approximately 90% nucleotide similarity, named klassevirus, were also recently reported in three cases of unexplained diarrhea from the United States and Australia and in sewage from Spain, reflecting a global distribution and supporting a pathogenic role for this new group of picornaviruses.

  • 6. Margeridon-Thermet, S
    et al.
    Shulman, NS
    Ahmed, A
    Shahriar, R
    Liu, T
    Wang, C
    Holmes, SP
    Babrzadeh, Farbod
    Stanford Genome Technology Centre, USA.
    Gharizadeh, B
    Hanczaruk, B
    Simen, BB
    Egholm, M
    Shafer, RW
    Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients2009Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 199, nr 9, s. 1275-1285Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The dynamics of emerging nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI) resistance in hepatitis B virus (HBV) are not well understood because standard dideoxynucleotide direct polymerase chain reaction (PCR) sequencing assays detect drug-resistance mutations only after they have become dominant. To obtain insight into NRTI resistance, we used a new sequencing technology to characterize the spectrum of low-prevalence NRTI-resistance mutations in HBV obtained from 20 plasma samples from 11 NRTI-treated patients and 17 plasma samples from 17 NRTI-naive patients, by using standard direct PCR sequencing and ultra-deep pyrosequencing (UDPS). UDPS detected drug-resistance mutations that were not detected by PCR in 10 samples from 5 NRTI-treated patients, including the lamivudine-resistance mutation V173L (in 5 samples), the entecavir-resistance mutations T184S (in 2 samples) and S202G (in 1 sample), the adefovir-resistance mutation N236T (in 1 sample), and the lamivudine and adefovir-resistance mutations V173L, L180M, A181T, and M204V (in 1 sample). G-to-A hypermutation mediated by the apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like family of cytidine deaminases was estimated to be present in 0.6% of reverse-transcriptase genes. Genotype A coinfection was detected by UDPS in each of 3 patients in whom genotype G virus was detected by direct PCR sequencing. UDPS detected low-prevalence HBV variants with NRTI-resistance mutations, G-to-A hypermutation, and low-level dual genotype infection with a sensitivity not previously possible.

  • 7. Margeridon-Thermet, Severine
    et al.
    Svarovskaia, Evguenia S.
    Babrzadeh, Farbod
    Stanford Genome Technology Center, Stanford University, Stanford, CA, United States .
    Martin, Ross
    Liu, Tommy F.
    Pacold, Mary
    Reuman, Elizabeth C.
    Holmes, Susan P.
    Borroto-Esoda, Katyna
    Shafer, Robert W.
    Low-Level Persistence of Drug Resistance Mutations in Hepatitis B Virus-Infected Subjects with a Past History of Lamivudine Treatment2013Inngår i: Antimicrobial Agents and Chemotherapy, ISSN 0066-4804, E-ISSN 1098-6596, Vol. 57, nr 1, s. 343-349Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We sought to determine the prevalence of hepatitis B virus (HBV) lamivudine (LAM)-resistant minority variants in subjects who once received LAM but had discontinued it prior to virus sampling. We performed direct PCR Sanger sequencing and ultradeep pyrosequencing (UDPS) of HBV reverse transcriptase (RT) of plasma viruses from 45 LAM-naive subjects and 46 LAM-experienced subjects who had discontinued LAM a median of 24 months earlier. UDPS was performed to a depth of similar to 3,000 reads per nucleotide. Minority variants were defined as differences from the Sanger sequence present in >= 0.5% of UDPS reads in a sample. Sanger sequencing identified >= 1 LAM resistance mutations (rtL80I/V, rtM204I, and rtA181T) in samples from 5 (11%) of 46 LAM-experienced and none of 45 LAM-naive subjects (0%; P = 0.06). UDPS detected >= 1 LAM resistance mutations (rtL80I/V, rtV173L, rtL180M, rtA181T, and rtM204I/V) in 10 (22%) of the 46 LAM-experienced subjects, including 5 in whom LAM resistance mutations were not identified by Sanger sequencing. Overall, LAM resistance mutations were more likely to be present in LAM-experienced (10/46, 22%) than LAM-naive subjects (0/45, 0%; P = 0.001). The median time since LAM discontinuation was 12.8 months in the 10 subjects with a LAM resistance mutation compared to 30.5 months in the 36 LAM-experienced subjects without a LAM resistance mutation (P < 0.001). The likelihood of detecting a LAM resistance mutation was significantly increased using UDPS compared to Sanger sequencing and was inversely associated with the time since LAM discontinuation.

  • 8. Narooie-Nejad, Mehrnaz
    et al.
    Paylakhi, Seyed Hassan
    Shojaee, Seyedmehdi
    Fazlali, Zeinab
    Kanavi, Mozhgan Rezaei
    Nilforushan, Naveed
    Yazdani, Shahin
    Babrzadeh, Farbod
    National Institute of Genetic Engineering and Biotechnology, Tehran, Iran .
    Suri, Fatemeh
    Ronaghi, Mostafa
    Elahi, Elahe
    Paisan-Ruiz, Coro
    Loss of function mutations in the gene encoding latent transforming growth factor beta binding protein 2, LTBP2, cause primary congenital glaucoma2009Inngår i: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 18, nr 20, s. 3969-3977Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Glaucoma is a heterogeneous group of optic neuropathies that manifests by optic nerve head cupping or degeneration of the optic nerve, resulting in a specific pattern of visual field loss. Glaucoma leads to blindness if left untreated, and is considered the second leading cause of blindness worldwide. The subgroup primary congenital glaucoma (PCG) is characterized by an anatomical defect in the trabecular meshwork, and age at onset in the neonatal or infantile period. It is the most severe form of glaucoma. CYP1B1 was the first gene genetically linked to PCG, and CYP1B1 mutations are the cause of disease in 20-100% of patients in different populations. Here, we report that LTBP2 encoding latent transforming growth factor beta binding protein 2 is a PCG causing gene, confirming results recently reported. A disease-associated locus on chromosome 14 was identified by performing whole genome autozygosity mapping in Iranian PCG families using high density single nucleotide polymorphism chips, and two disease-segregating loss of function mutations in LTBP2, p.Ser472fsX3 and p.Tyr1793fsX55, were observed in two families while sequencing candidate genes in the locus. The p.Tyr1793fsX55 mutation affects an amino acid close to the C-terminal of the encoded protein. Subsequently, LTBP2 expression was shown in human eyes, including the trabecular meshwork and ciliary processes that are thought to be relevant to the etiology of PCG.

  • 9. Parameswaran, Poornima
    et al.
    Sklan, Ella
    Wilkins, Courtney
    Burgon, Trever
    Samuel, Melanie A.
    Lu, Rui
    Ansel, K. Mark
    Heissmeyer, Vigo
    Einav, Shirit
    Jackson, William
    Doukas, Tammy
    Paranjape, Suman
    Polacek, Charlotta
    dos Santos, Flavia Barreto
    Jalili, Roxana
    Babrzadeh, Farbod
    Stanford Genome Technology Center, Stanford University School of Medicine, United States .
    Gharizadeh, Baback
    Grimm, Dirk
    Kay, Mark
    Koike, Satoshi
    Sarnow, Peter
    Ronaghi, Mostafa
    Ding, Shou-Wei
    Harris, Eva
    Chow, Marie
    Diamond, Michael S.
    Kirkegaard, Karla
    Glenn, Jeffrey S.
    Fire, Andrew Z.
    Six RNA Viruses and Forty-One Hosts: Viral Small RNAs and Modulation of Small RNA Repertoires in Vertebrate and Invertebrate Systems2010Inngår i: PLoS Pathogens, ISSN 1553-7366, E-ISSN 1553-7374, Vol. 6, nr 2, s. e1000764-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We have used multiplexed high-throughput sequencing to characterize changes in small RNA populations that occur during viral infection in animal cells. Small RNA-based mechanisms such as RNA interference (RNAi) have been shown in plant and invertebrate systems to play a key role in host responses to viral infection. Although homologs of the key RNAi effector pathways are present in mammalian cells, and can launch an RNAi-mediated degradation of experimentally targeted mRNAs, any role for such responses in mammalian host-virus interactions remains to be characterized. Six different viruses were examined in 41 experimentally susceptible and resistant host systems. We identified virus-derived small RNAs (vsRNAs) from all six viruses, with total abundance varying from "vanishingly rare'' (less than 0.1% of cellular small RNA) to highly abundant (comparable to abundant micro-RNAs "miRNAs''). In addition to the appearance of vsRNAs during infection, we saw a number of specific changes in host miRNA profiles. For several infection models investigated in more detail, the RNAi and Interferon pathways modulated the abundance of vsRNAs. We also found evidence for populations of vsRNAs that exist as duplexed siRNAs with zero to three nucleotide 39 overhangs. Using populations of cells carrying a Hepatitis C replicon, we observed strand-selective loading of siRNAs onto Argonaute complexes. These experiments define vsRNAs as one possible component of the interplay between animal viruses and their hosts.

  • 10. Toh, Soo Ting
    et al.
    Jin, Yu
    Liu, Lizhen
    Wang, Jingbo
    Babrzadeh, Farbod
    Department of Biochemistry, Stanford Genome Technology Centre, Stanford University, Palo Alto, United States.
    Gharizadeh, Baback
    Ronaghi, Mostafa
    Toh, Han Chong
    Chow, Pierce Kah-Hoe
    Chung, Alexander Y-F.
    Ooi, London L-P-J.
    Lee, Caroline G-L.
    Deep sequencing of the hepatitis B virus in hepatocellular carcinoma patients reveals enriched integration events, structural alterations and sequence variations2013Inngår i: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 34, nr 4, s. 787-798Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Chronic hepatitis B virus (HBV) infection is epidemiologically associated with hepatocellular carcinoma (HCC), but its role in HCC remains poorly understood due to technological limitations. In this study, we systematically characterize HBV in HCC patients. HBV sequences were enriched from 48 HCC patients using an oligo-bead-based strategy, pooled together and sequenced using the FLX-Genome-Sequencer. In the tumors, preferential integration of HBV into promoters of genes (P < 0.001) and significant enrichment of integration into chromosome 10 (P < 0.01) were observed. Integration into chromosome 10 was significantly associated with poorly differentiated tumors (P < 0.05). Notably, in the tumors, recurrent integration into the promoter of the human telomerase reverse transcriptase (TERT) gene was found to correlate with increased TERT expression. The preferred region within the HBV genome involved in integration and viral structural alteration is at the 3'-end of hepatitis B virus X protein (HBx), where viral replication/transcription initiates. Upon integration, the 3'-end of the HBx is often deleted. HBxhuman chimeric transcripts, the most common type of chimeric transcripts, can be expressed as chimeric proteins. Sequence variation resulting in non-conservative amino acid substitutions are commonly observed in HBV genome. This study highlights HBV as highly mutable in HCC patients with preferential regions within the host and virus genome for HBV integration/structural alterations.

  • 11. Varghese, Vici
    et al.
    Shahriar, Rajin
    Rhee, Soo-Yon
    Liu, Tommy
    Simen, Birgitte B.
    Egholm, Michael
    Hanczaruk, Bozena
    Blake, Lisbeth A.
    Gharizadeh, Baback
    Babrzadeh, Farbod
    Stanford Genome Technology Center, Stanford University, School of Medicine, United States .
    Bachmann, Michael H.
    Fessel, W. Jeffrey
    Shafer, Robert W.
    Minority Variants Associated with Transmitted and Acquired HIV-1 Nonnucleoside Reverse Transcriptase Inhibitor Resistance: Implications for the Use of Second-Generation Nonnucleoside Reverse Transcriptase Inhibitors2009Inngår i: Journal of Acquired Immune Deficiency Syndromes, ISSN 1525-4135, E-ISSN 1944-7884, Vol. 52, nr 3, s. 309-315Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: K103N, the most common nonnucleoside reverse transcriptase inhibitor (NNRTI)-resistant mutation in patients with transmitted resistance and in patients receiving a failing NNRTI-containing regimen, is fully susceptible to the new NNRTI, etravirine. Therefore, we sought to determine how often NNRTI-resistant Mutations other than K103N occur as minority variants in plasma samples for which standard genotypic resistance testing detects K103N alone. Methods: We performed ultradeep pyrosequencing (UDPS; 454 Life Sciences a Roche Company, Branford, CT) of plasma virus samples from 13 treatment-naive and 20 NNRTI-experienced patients in whom standard genotypic resistance testing revealed K103N but no other major NNRTI-resistance mutations. Results: Samples from 0 of 13 treatment-naive patients vs. 7 of 20 patients failing an NNRTI-containing regimen had minority variants with major etravirine-associated NNRTI-resistant mutations (P = 0.03, Fisher exact test): Y181C (7.0%), Y181C (3.6%) + G190A (3.2%), L1001 (14%), L100I (32%) + 190A (5.4%), K101E (3.8%) + G190A (4.9%), K101E (4.0%) + G190S (4.8%), and G190S (3.1%). Conclusions: In treatment-naive patients, UDPS did not detect additional major NNRTI-resistant mutations suggesting that etravirine may be effective in patients with transmitted K103N. In NNRTI-experienced patients, UDPS often detected additional major NNRTI-resistant mutations suggesting that etravirine may not be fully active in patients with acquired K103N.

  • 12. Varghese, Vici
    et al.
    Wang, Elijah
    Babrzadeh, Farbod
    Stanford Genome Technology Center, Stanford University, School of Medicine, United States .
    Bachmann, Michael H.
    Shahriar, Rajin
    Liu, Tommy
    Mappala, Svetlana Jean M.
    Gharizadeh, Baback
    Fessel, W. Jeffrey
    Katzenstein, David
    Kassaye, Seble
    Shafer, Robert W.
    Nucleic Acid Template and the Risk of a PCR-Induced HIV-1 Drug Resistance Mutation2010Inngår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 5, nr 6, s. e10992-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The HIV-1 nucleoside RT inhibitor (NRTI)-resistance mutation, K65R confers intermediate to high-level resistance to the NRTIs abacavir, didanosine, emtricitabine, lamivudine, and tenofovir; and low-level resistance to stavudine. Several lines of evidence suggest that K65R is more common in HIV-1 subtype C than subtype B viruses. Methods and Findings: We performed ultra-deep pyrosequencing (UDPS) and clonal dideoxynucleotide sequencing of plasma virus samples to assess the prevalence of minority K65R variants in subtype B and C viruses from untreated individuals. Although UDPS of plasma samples from 18 subtype C and 27 subtype B viruses showed that a higher proportion of subtype C viruses contain K65R (1.04% vs. 0.25%; p < 0.001), limiting dilution clonal sequencing failed to corroborate its presence in two of the samples in which K65R was present in >1.5% of UDPS reads. We therefore performed UDPS on clones and site-directed mutants containing subtype B- and C-specific patterns of silent mutations in the conserved KKK motif encompassing RT codons 64 to 66 and found that subtype-specific nucleotide differences were responsible for increased PCR-induced K65R mutation in subtype C viruses. Conclusions: This study shows that the RT KKK nucleotide template in subtype C viruses can lead to the spurious detection of K65R by highly sensitive PCR-dependent sequencing techniques. However, the study is also consistent with the subtype C nucleotide template being inherently responsible for increased polymerization-induced K65R mutations in vivo.

  • 13. Wang, Chunlin
    et al.
    Krishnakumar, Sujatha
    Wilhelmy, Julie
    Babrzadeh, Farbod
    Stanford Univ, Stanford Genome Technol Ctr, Palo Alto, CA.
    Stepanyan, Lilit
    Su, Laura F.
    Levinson, Douglas
    Fernandez-Vina, Marcelo A.
    Davis, Ronald W.
    Davis, Mark M.
    Mindrinos, Michael
    High-throughput, high-fidelity HLA genotyping with deep sequencing2012Inngår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 109, nr 22, s. 8676-8681Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Human leukocyte antigen (HLA) genes are the most polymorphic in the human genome. They play a pivotal role in the immune response and have been implicated in numerous human pathologies, especially autoimmunity and infectious diseases. Despite their importance, however, they are rarely characterized comprehensively because of the prohibitive cost of standard technologies and the technical challenges of accurately discriminating between these highly related genes and their many allelles. Here we demonstrate a high-resolution, and cost-effective methodology to type HLA genes by sequencing, which combines the advantage of long-range amplification, the power of high-throughput sequencing platforms, and a unique genotyping algorithm. We calibrated our method for HLA-A, -B, -C, and -DRB1 genes with both reference cell lines and clinical samples and identified several previously undescribed alleles with mismatches, insertions, and deletions. We have further demonstrated the utility of this method in a clinical setting by typing five clinical samples in an Illumina MiSeq instrument with a 5-d turnaround. Overall, this technology has the capacity to deliver low-cost, high-throughput, and accurate HLA typing by multi-plexing thousands of samples in a single sequencing run, which will enable comprehensive disease-association studies with large cohorts. Furthermore, this approach can also be extended to include other polymorphic genes.

  • 14. Wang, Chunlin
    et al.
    Sanders, Catherine M.
    Yang, Qunying
    Schroeder, Harry W., Jr.
    Wang, Elijah
    Babrzadeh, Farbod
    Stanford Genome Technology Center, United States .
    Gharizadeh, Baback
    Myers, Richard M.
    Hudson, James R., Jr.
    Davis, Ronald W.
    Han, Jian
    High throughput sequencing reveals a complex pattern of dynamic interrelationships among human T cell subsets2010Inngår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 107, nr 4, s. 1518-1523Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Developing T cells face a series of cell fate choices in the thymus and in the periphery. The role of the individual T cell receptor (TCR) in determining decisions of cell fate remains unresolved. The stochastic/selection model postulates that the initial fate of the cell is independent of TCR specificity, with survival dependent on additional TCR/coreceptor "rescue" signals. The "instructive" model holds that cell fate is initiated by the interaction of the TCR with a cognate peptide-MHC complex. T cells are then segregated on the basis of TCR specificity with the aid of critical coreceptors and signal modulators [Chan S, Correia-Neves M, Benoist C, Mathis (1998) Immunol Rev 165: 195-207]. The former would predict a random representation of individual TCR across divergent T cell lineages whereas the latter would predict minimal overlap between divergent T cell subsets. To address this issue, we have used high-throughput sequencing to evaluate the TCR distribution among key T cell developmental and effector subsets from a single donor. We found numerous examples of individual subsets sharing identical TCR sequence, supporting a model of a stochastic process of cell fate determination coupled with dynamic patterns of clonal expansion of T cells bearing the same TCR sequence among both CD4(+) and CD8+ populations.

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