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482 results on '"Naranbhai, Vivek"'

1. Altered IL-6 signalling and risk of tuberculosis: a multi-ancestry mendelian randomisation study

Author

Akhtar, Shaheen, Anwar, Mohammad, Asgar, Omar, Ashraf, Samina, Bidi, Saeed, Breen, Gerome, Broster, James, Chung, Raymond, Collier, David, Curtis, Charles J, Chaudhary, Shabana, Colligan, Grainne, Deloukas, Panos, Durham, Ceri, Durrani, Faiza, Eto, Fabiola, Finer, Sarah, Gafton, Joseph, Angel, Ana, Griffiths, Chris, Harvey, Joanne, Heng, Teng, Hodgson, Sam, Huang, Qin Qin, Hurles, Matt, Hunt, Karen A, Hussain, Shapna, Islam, Kamrul, Iyer, Vivek, Jacobs, Benjamin M, Kalantzis, Georgios, Khan, Ahsan, Langenberg, Claudia, Lavery, Cath, Lee, Sang Hyuck, MacArthur, Daniel, Malik, Sidra, Malawsky, Daniel, Martin, Hilary, Mason, Dan, Mathur, Rohini, Mazid, Mohammed Bodrul, McDermott, John, Morton, Caroline, Newman, Bill, Owor, Elizabeth, Qureshi, Asma, Ramachandrappa, Shwetha, Raza, Mehru, Russell, Jessry, Safa, Nishat, Samuel, Miriam, Siddiqui, Moneeza, Simpson, Michael, Solly, John, Spreckley, Marie, Stow, Daniel, Taylor, Michael, Trembath, Richard C, Tricker, Karen, van Heel, David A, Walter, Klaudia, Winckley, Caroline, Wood, Suzanne, Wright, John, Zengeya, Ishevanhu, Zöllner, Julia, Schurz, Haiko, Naranbhai, Vivek, Yates, Tom A, Gilchrist, James J, Parks, Tom, Dodd, Peter J, Möller, Marlo, Hoal, Eileen G, Morris, Andrew P, Hill, Adrian V S, van Crevel, Reinout, van Laarhoven, Arjan, Ottenhoff, Tom H M, Metspalu, Andres, Magi, Reedik, Meyer, Christian G, Ellis, Magda, Thye, Thorsten, Mahasirimongkol, Surakameth, Pasomsub, Ekawat, Tokunaga, Katsushi, Omae, Yosuke, Yanai, Hideki, Mushiroda, Taisei, Kubo, Michiaki, Takahashi, Atsushi, Kamatani, Yoichiro, Alisjahbana, Bachti, Liu, Wei, Sheng, A-dong, Yang, Yurong, Hamilton, Fergus, Ghazal, Peter, Timpson, Nicholas J, and Pollara, Gabriele

Published
2025
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2. Genetic variation that determines TAPBP expression levels associates with the course of malaria in an HLA allotype-dependent manner

Author

Walker-Sperling, Victoria, Digitale, Jean C, Viard, Mathias, Martin, Maureen P, Bashirova, Arman, Yuki, Yuko, Ramsuran, Veron, Kulkarni, Smita, Naranbhai, Vivek, Li, Hongchuan, Anderson, Stephen K, Yum, Lauren, Clifford, Robert, Kibuuka, Hannah, Ake, Julie, Thomas, Rasmi, Rowland-Jones, Sarah, Rek, John, Arinaitwe, Emmanuel, Kamya, Moses, Rodriguez-Barraquer, Isabel, Feeney, Margaret E, and Carrington, Mary

Subjects
Malaria, Biotechnology, Vector-Borne Diseases, Rare Diseases, Vaccine Related, Genetics, Immunization, Aetiology, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Binding Sites, Genetic Variation, Histocompatibility Antigens Class I, Humans, Malaria, Falciparum, Membrane Transport Proteins, MicroRNAs, Peptides, Plasmodium falciparum, RNA, Messenger, Transcription Factor AP-2, malaria, tapasin, HLA
Abstract

HLA class I (HLA-I) allotypes vary widely in their dependence on tapasin (TAPBP), an integral component of the peptide-loading complex, to present peptides on the cell surface. We identified two single-nucleotide polymorphisms that regulate TAPBP messenger RNA (mRNA) expression in Africans, rs111686073 (G/C) and rs59097151 (A/G), located in an AP-2α transcription factor binding site and a microRNA (miR)-4486 binding site, respectively. rs111686073G and rs59097151A induced significantly higher TAPBP mRNA expression relative to the alternative alleles due to higher affinity for AP-2α and abrogation of miR-4486 binding, respectively. These variants associated with lower Plasmodium falciparum parasite prevalence and lower incidence of clinical malaria specifically among individuals carrying tapasin-dependent HLA-I allotypes, presumably by augmenting peptide loading, whereas tapasin-independent allotypes associated with relative protection, regardless of imputed TAPBP mRNA expression levels. Thus, an attenuated course of malaria may occur through enhanced breadth and/or magnitude of antigen presentation, an important consideration when evaluating vaccine efficacy.

Published
2022

4. HLA class I signal peptide polymorphism determines the level of CD94/NKG2–HLA-E-mediated regulation of effector cell responses

Author

Lin, Zhansong, Bashirova, Arman A., Viard, Mathias, Garner, Lee, Quastel, Max, Beiersdorfer, Maya, Kasprzak, Wojciech K., Akdag, Marjan, Yuki, Yuko, Ojeda, Pedro, Das, Sudipto, Andresson, Thorkell, Naranbhai, Vivek, Horowitz, Amir, McMichael, Andrew J., Hoelzemer, Angelique, Gillespie, Geraldine M., Garcia-Beltran, Wilfredo F., and Carrington, Mary

Published
2023
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5. Genomic and transcriptomic analysis of checkpoint blockade response in advanced non-small cell lung cancer

Author

Ravi, Arvind, Hellmann, Matthew D., Arniella, Monica B., Holton, Mark, Freeman, Samuel S., Naranbhai, Vivek, Stewart, Chip, Leshchiner, Ignaty, Kim, Jaegil, Akiyama, Yo, Griffin, Aaron T., Vokes, Natalie I., Sakhi, Mustafa, Kamesan, Vashine, Rizvi, Hira, Ricciuti, Biagio, Forde, Patrick M., Anagnostou, Valsamo, Riess, Jonathan W., Gibbons, Don L., Pennell, Nathan A., Velcheti, Vamsidhar, Digumarthy, Subba R., Mino-Kenudson, Mari, Califano, Andrea, Heymach, John V., Herbst, Roy S., Brahmer, Julie R., Schalper, Kurt A., Velculescu, Victor E., Henick, Brian S., Rizvi, Naiyer, Jänne, Pasi A., Awad, Mark M., Chow, Andrew, Greenbaum, Benjamin D., Luksza, Marta, Shaw, Alice T., Wolchok, Jedd, Hacohen, Nir, Getz, Gad, and Gainor, Justin F.

Published
2023
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6. IL7 genetic variation and toxicity to immune checkpoint blockade in patients with melanoma

Author

Taylor, Chelsea A., Watson, Robert A., Tong, Orion, Ye, Weiyu, Nassiri, Isar, Gilchrist, James J., de los Aires, Alba Verge, Sharma, Piyush Kumar, Koturan, Surya, Cooper, Rosalin A., Woodcock, Victoria K., Jungkurth, Elsita, Shine, Brian, Coupe, Nicholas, Payne, Miranda J., Church, David N., Naranbhai, Vivek, Groha, Stefan, Emery, Paul, Mankia, Kulveer, Freedman, Matthew L., Choueiri, Toni K., Middleton, Mark R., Gusev, Alexander, and Fairfax, Benjamin P.

Published
2022
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7. Germline variants associated with toxicity to immune checkpoint blockade

Author

Groha, Stefan, Alaiwi, Sarah Abou, Xu, Wenxin, Naranbhai, Vivek, Nassar, Amin H., Bakouny, Ziad, El Zarif, Talal, Saliby, Renee Maria, Wan, Guihong, Rajeh, Ahmad, Adib, Elio, Nuzzo, Pier V., Schmidt, Andrew L., Labaki, Chris, Ricciuti, Biagio, Alessi, Joao Victor, Braun, David A., Shukla, Sachet A., Keenan, Tanya E., Van Allen, Eliezer, Awad, Mark M., Manos, Michael, Rahma, Osama, Zubiri, Leyre, Villani, Alexandra-Chloe, Fairfax, Benjamin, Hammer, Christian, Khan, Zia, Reynolds, Kerry, Semenov, Yevgeniy, Schrag, Deborah, Kehl, Kenneth L., Freedman, Matthew L., Choueiri, Toni K., and Gusev, Alexander

Published
2022
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8. CCR5AS lncRNA variation differentially regulates CCR5, influencing HIV disease outcome

Author

Kulkarni, Smita, Lied, Alexandra, Kulkarni, Viraj, Rucevic, Marijana, Martin, Maureen P, Walker-Sperling, Victoria, Anderson, Stephen K, Ewy, Rodger, Singh, Sukhvinder, Nguyen, Hoang, McLaren, Paul J, Viard, Mathias, Naranbhai, Vivek, Zou, Chengcheng, Lin, Zhansong, Gatanaga, Hiroyuki, Oka, Shinichi, Takiguchi, Masafumi, Thio, Chloe L, Margolick, Joseph, Kirk, Gregory D, Goedert, James J, Hoots, W Keith, Deeks, Steven G, Haas, David W, Michael, Nelson, Walker, Bruce, Le Gall, Sylvie, Chowdhury, Fatema Z, Yu, Xu G, and Carrington, Mary

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Human Genome, HIV/AIDS, Sexually Transmitted Infections, Infectious Diseases, Genetics, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, 3' Untranslated Regions, Alleles, Biomarkers, CD4-Positive T-Lymphocytes, Cell Membrane, Gene Expression Regulation, Genes, Reporter, Genetic Variation, Genotype, HIV Infections, HIV-1, Humans, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Population Groups, Prognosis, RNA Stability, RNA, Antisense, RNA, Long Noncoding, RNA, Messenger, Receptors, CCR5, Viral Load, Biochemistry and cell biology
Abstract

Multiple genome-wide studies have identified associations between outcome of human immunodeficiency virus (HIV) infection and polymorphisms in and around the gene encoding the HIV co-receptor CCR5, but the functional basis for the strongest of these associations, rs1015164A/G, is unknown. We found that rs1015164 marks variation in an activating transcription factor 1 binding site that controls expression of the antisense long noncoding RNA (lncRNA) CCR5AS. Knockdown or enhancement of CCR5AS expression resulted in a corresponding change in CCR5 expression on CD4+ T cells. CCR5AS interfered with interactions between the RNA-binding protein Raly and the CCR5 3' untranslated region, protecting CCR5 messenger RNA from Raly-mediated degradation. Reduction in CCR5 expression through inhibition of CCR5AS diminished infection of CD4+ T cells with CCR5-tropic HIV in vitro. These data represent a rare determination of the functional importance of a genome-wide disease association where expression of a lncRNA affects HIV infection and disease progression.

Published
2019

9. Cutaneous Toxicities Associated with Immune Checkpoint Inhibitors: An Observational, Pharmacovigilance Study

Author

Le, Thomas K., Brown, Isabelle, Goldberg, Rebecca, Taylor, Matthew T., Deng, Junwen, Parthasarathy, Varsha, Bordeaux, Zachary A., Alphonse, Martin Prince, Kwatra, Madan M., Naranbhai, Vivek, Gusev, Alexander, Alhariri, Jihad, LeBoeuf, Nicole R., Reynolds, Kerry L., Cappelli, Laura C., Naidoo, Jarushka, Brahmer, Julie R., Kang, Sewon, Semenov, Yevgeniy R., and Kwatra, Shawn G.

Published
2022
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10. Response to Severe Acute Respiratory Syndrome Coronavirus 2 Initial Series and Additional Dose Vaccine in Patients With Predominant Antibody Deficiency

Author

Barmettler, Sara, DiGiacomo, Daniel V., Yang, Nancy J., Lam, Tiffany, Naranbhai, Vivek, Dighe, Anand S., Burke, Kristin E., Blumenthal, Kimberly G., Ling, Morris, Hesterberg, Paul E., Saff, Rebecca R., MacLean, James, Ofoman, Onosereme, Berrios, Cristhian, St Denis, Kerri J., Lam, Evan C., Gregory, David, Iafrate, Anthony John, Poznansky, Mark, Lee, Hang, Balazs, Alejandro, Pillai, Shiv, and Farmer, Jocelyn R.

Published
2022
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11. Variation in cell-associated unspliced HIV RNA on antiretroviral therapy is associated with the circadian regulator brain-and-muscle-ARNT-like-1

Author

Chang, Christina C, Naranbhai, Vivek, Stern, Jared, Roche, Michael, Dantanarayana, Ashanti, Ke, Ruian, Tennakoon, Surekha, Solomon, Ajantha, Hoh, Rebecca, Hartogensis, Wendy, Hecht, Frederick M, Sikaris, Ken, Price, David J, Elliott, Julian H, Deeks, Steven G, Churchill, Melissa, Cameron, Paul U, Hengartner, Nicolas, Perelson, Alan S, and Lewin, Sharon R

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Sexually Transmitted Infections, Infectious Diseases, Neurosciences, HIV/AIDS, Genetics, 1.1 Normal biological development and functioning, ARNTL Transcription Factors, Anti-Retroviral Agents, Blood Cells, Cells, Cultured, Female, Gene Expression Profiling, HIV, HIV Infections, Host-Pathogen Interactions, Humans, Male, Middle Aged, RNA, Viral, Real-Time Polymerase Chain Reaction, Transcription, Genetic, brain-and-muscle-ARNT-like-1, circadian rhythm, HIV latency, HIV transcription, stress, unspliced RNA, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Virology, Biomedical and clinical sciences, Health sciences
Abstract

Objective(s)To determine whether variation in cell-associated unspliced (CA-US) HIV RNA in HIV-infected individuals on antiretroviral therapy (ART) has a circadian basis.MethodsProspective observational study of HIV-infected individuals on ART. Blood was collected on three occasions and CA-US HIV RNA and mRNA of the circadian-locomotor-output-cycles-kaput (CLOCK)-associated genes quantified by real time PCR. CLOCK-associated proteins were over-expressed in a cell line stably transfected with an HIV long-terminal repeat (LTR) luciferase reporter.ResultsUsing a mixed effects model, there was a significant increase in log-CA-US RNA at the third visit compared with the first visit (effect size of 0.619 with standard error (SE) of 0.098, P

Published
2018

12. Killer cell immunoglobulin-like receptor 3DL1 variation modifies HLA-B*57 protection against HIV-1

Author

Martin, Maureen P, Naranbhai, Vivek, Shea, Patrick R, Qi, Ying, Ramsuran, Veron, Vince, Nicolas, Gao, Xiaojiang, Thomas, Rasmi, Brumme, Zabrina L, Carlson, Jonathan M, Wolinsky, Steven M, Goedert, James J, Walker, Bruce D, Segal, Florencia P, Deeks, Steven G, Haas, David W, Migueles, Stephen A, Connors, Mark, Michael, Nelson, Fellay, Jacques, Gostick, Emma, Llewellyn-Lacey, Sian, Price, David A, Lafont, Bernard A, Pymm, Phillip, Saunders, Philippa M, Widjaja, Jacqueline, Wong, Shu Cheng, Vivian, Julian P, Rossjohn, Jamie, Brooks, Andrew G, and Carrington, Mary

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Human Genome, Sexually Transmitted Infections, Genetics, Clinical Research, HIV/AIDS, Infectious Diseases, 2.1 Biological and endogenous factors, Good Health and Well Being, Adult, Cohort Studies, Female, Genetic Variation, HIV Infections, HIV-1, HLA-B Antigens, Humans, Male, Middle Aged, Receptors, KIR3DL1, AIDS/HIV, Innate immunity, MHC class 1, NK cells, Medical and Health Sciences, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

HLA-B*57 control of HIV involves enhanced CD8+ T cell responses against infected cells, but extensive heterogeneity exists in the level of HIV control among B*57+ individuals. Using whole-genome sequencing of untreated B*57+ HIV-1-infected controllers and noncontrollers, we identified a single variant (rs643347A/G) encoding an isoleucine-to-valine substitution at position 47 (I47V) of the inhibitory killer cell immunoglobulin-like receptor KIR3DL1 as the only significant modifier of B*57 protection. The association was replicated in an independent cohort and across multiple outcomes. The modifying effect of I47V was confined to B*57:01 and was not observed for the closely related B*57:03. Positions 2, 47, and 54 tracked one another nearly perfectly, and 2 KIR3DL1 allotypes differing only at these 3 positions showed significant differences in binding B*57:01 tetramers, whereas the protective allotype showed lower binding. Thus, variation in an immune NK cell receptor that binds B*57:01 modifies its protection. These data highlight the exquisite specificity of KIR-HLA interactions in human health and disease.

Published
2018

13. T cell reactivity to the SARS-CoV-2 Omicron variant is preserved in most but not all individuals

Author

Naranbhai, Vivek, Nathan, Anusha, Kaseke, Clarety, Berrios, Cristhian, Khatri, Ashok, Choi, Shawn, Getz, Matthew A., Tano-Menka, Rhoda, Ofoman, Onosereme, Gayton, Alton, Senjobe, Fernando, Zhao, Zezhou, St Denis, Kerri J., Lam, Evan C., Carrington, Mary, Garcia-Beltran, Wilfredo F., Balazs, Alejandro B., Walker, Bruce D., Iafrate, A. John, and Gaiha, Gaurav D.

Published
2022
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14. mRNA-based COVID-19 vaccine boosters induce neutralizing immunity against SARS-CoV-2 Omicron variant

Author

Garcia-Beltran, Wilfredo F., St. Denis, Kerri J., Hoelzemer, Angelique, Lam, Evan C., Nitido, Adam D., Sheehan, Maegan L., Berrios, Cristhian, Ofoman, Onosereme, Chang, Christina C., Hauser, Blake M., Feldman, Jared, Roederer, Alex L., Gregory, David J., Poznansky, Mark C., Schmidt, Aaron G., Iafrate, A. John, Naranbhai, Vivek, and Balazs, Alejandro B.

Published
2022
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16. HLA tapasin independence : broader peptide repertoire and HIV control

Author

Bashirova, Arman A., Viard, Mathias, Naranbhai, Vivek, Grifoni, Alba, Garcia-Beltran, Wilfredo, Akdag, Marjan, Yuki, Yuko, Gao, Xiaojiang, O’hUigin, Colm, Raghavan, Malini, Wolinsky, Steven, Bream, Jay H., Duggal, Priya, Martinson, Jeremy, Michael, Nelson L., Kirk, Gregory D., Buchbinder, Susan P., Haas, David, Goedert, James J., Deeks, Steven G., Fellay, Jacques, Walker, Bruce, Goulder, Philip, Cresswell, Peter, Elliott, Tim, Sette, Alessandro, Carlson, Jonathan, and Carrington, Mary

Published
2020

18. Elevated HLA-A expression impairs HIV control through inhibition of NKG2A-expressing cells

Author

Ramsuran, Veron, Naranbhai, Vivek, Horowitz, Amir, Qi, Ying, Martin, Maureen P, Yuki, Yuko, Gao, Xiaojiang, Walker-Sperling, Victoria, Del Prete, Gregory Q, Schneider, Douglas K, Lifson, Jeffrey D, Fellay, Jacques, Deeks, Steven G, Martin, Jeffrey N, Goedert, James J, Wolinsky, Steven M, Michael, Nelson L, Kirk, Gregory D, Buchbinder, Susan, Haas, David, Ndung’u, Thumbi, Goulder, Philip, Parham, Peter, Walker, Bruce D, Carlson, Jonathan M, and Carrington, Mary

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Infectious Diseases, Sexually Transmitted Infections, Women's Health, HIV/AIDS, 2.1 Biological and endogenous factors, Inflammatory and immune system, Infection, Alleles, CD4 Lymphocyte Count, Cohort Studies, HIV, HIV Infections, HLA Antigens, Humans, Killer Cells, Natural, Ligands, NK Cell Lectin-Like Receptor Subfamily C, Protein Sorting Signals, Viremia, General Science & Technology
Abstract

The highly polymorphic human leukocyte antigen (HLA) locus encodes cell surface proteins that are critical for immunity. HLA-A expression levels vary in an allele-dependent manner, diversifying allele-specific effects beyond peptide-binding preference. Analysis of 9763 HIV-infected individuals from 21 cohorts shows that higher HLA-A levels confer poorer control of HIV. Elevated HLA-A expression provides enhanced levels of an HLA-A-derived signal peptide that specifically binds and determines expression levels of HLA-E, the ligand for the inhibitory NKG2A natural killer (NK) cell receptor. HLA-B haplotypes that favor NKG2A-mediated NK cell licensing (i.e., education) exacerbate the deleterious effect of high HLA-A on HIV control, consistent with NKG2A-mediated inhibition impairing NK cell clearance of HIV-infected targets. Therapeutic blockade of HLA-E:NKG2A interaction may yield benefit in HIV disease.

Published
2018

19. Natural Killer cells demonstrate distinct eQTL and transcriptome-wide disease associations, highlighting their role in autoimmunity

Author

Gilchrist, James J., Makino, Seiko, Naranbhai, Vivek, Sharma, Piyush K., Koturan, Surya, Tong, Orion, Taylor, Chelsea A., Watson, Robert A., de los Aires, Alba Verge, Cooper, Rosalin, Lau, Evelyn, Danielli, Sara, Hameiri-Bowen, Dan, Lee, Wanseon, Ng, Esther, Whalley, Justin, Knight, Julian C., and Fairfax, Benjamin P.

Published
2022
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20. Structure-guided T cell vaccine design for SARS-CoV-2 variants and sarbecoviruses

Author

Nathan, Anusha, Rossin, Elizabeth J., Kaseke, Clarety, Park, Ryan J., Khatri, Ashok, Koundakjian, Dylan, Urbach, Jonathan M., Singh, Nishant K., Bashirova, Arman, Tano-Menka, Rhoda, Senjobe, Fernando, Waring, Michael T., Piechocka-Trocha, Alicja, Garcia-Beltran, Wilfredo F., Iafrate, A. John, Naranbhai, Vivek, Carrington, Mary, Walker, Bruce D., and Gaiha, Gaurav D.

Published
2021
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22. Remote Fingerstick Blood Collection for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Antibody Testing

Author

Garcia-Beltran, Wilfredo F., Miller, Tyler E., Kirkpatrick, Grace, Nixon, Andrea, Astudillo, Michael G., Yang, Diane, Mahanta, Lisa M., Murali, Mandakolathur, Dighe, Anand S., Lennerz, Jochen, Thierauf, Julia, Naranbhai, Vivek, and Iafrate, A. John

Subjects
Control, Diagnosis, Usage, Methods, Epidemics -- Control -- United States, Blood tests -- Methods, Home medical tests -- Usage, Serologic tests -- Methods, COVID-19 -- Diagnosis -- Control, Blood -- Medical examination, Serodiagnosis -- Methods
Abstract

The ongoing pandemic of coronavirus disease 2019 (COVID-19), caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has continued to ignite the rapid development of diagnostic tests that [...], The rapid worldwide spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has propelled the rapid development of serologic tests that can detect anti-SARS-CoV-2 antibodies. These have been used for studying the prevalence and spread of infection in different populations, and helping establish a recent diagnosis of coronavirus disease 2019 (COVID-19), and will likely be used to confirm humoral immunity after infection or vaccination. However, nearly all lab-based high-throughput SARS-CoV-2 serologic assays require a serum sample from venous blood draw, limiting their applications and scalability. Here, we present a method that enables large-scale SARS-CoV-2 serologic studies by combining self or office collection of fingerprick blood with a volumetric absorptive microsampling device (Mitra, Neoteryx LLC) with a high-throughput electrochemiluminescence-based SARS-CoV-2 total antibody assay (Roche Elecsys, Roche Diagnostics Inc) that is emergency use authorization approved for use on serum samples and widely used by clinical laboratories around the world. We found that the Roche Elecsys assay has a high dynamic range that allows for accurate detection of SARS-CoV-2 antibodies in serum samples diluted 1:20 as well as contrived dried blood extracts. Extracts of dried blood from Mitra devices acquired in a community seroprevalence study showed near identical sensitivity and specificity in detection of SARS-CoV-2 antibodies compared with neat sera using predefined thresholds for each specimen type. Overall, this study affirms the use of Mitra dried blood collection device with the Roche Elecsys SARS-CoV-2 total antibody assay for remote or at-home testing as well as large-scale community seroprevalence studies. doi: 10.5858/arpa.2020-0713-SA

Published
2021
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23. 8th IAS Conference on HIV Pathogenesis, Treatment & Prevention 19–22 July 2015, Vancouver, Canada

Author

Pate, Kelly Metcalf, Pohlmeyer, Chris, Walker‐Sperling, Victoria, Foote, Jeremy, Najarro, Kevin, Cryer, Catherine, Salgado, Maria, Gama, Lucio, Engle, Elizabeth, Shirk, Erin, Queen, Suzanne, Chioma, Stanley, Vermillion, Meghan, Bullock, Brandon, Li, Ming, Lyons, Claire, Adams, Robert, Zink, Chris, Clements, Janice, Mankowski, Joseph, Blankson, Joel, Micci, Luca, Ryan, Emily, Fromentin, Rémi, Benne, Clarisse, Chomont, Nicolas, Lifson, Jeffrey, Paiardini, Mirko, Lee, Sulggi, Fromentin, Remi, Silicano, Robert, Silicano, Janet, Richman, Douglas, O'Doherty, Una, Palmer, Sarah, Burbelo, Peter, Deeks, Steven, Ghneim, Khader, Ahlers, Jeff, Fourati, Slim, Shive, Carey, Cameron, Mark, Mukerjee, Pranab, Ghannoum, Mahmoud, Rodriguez, Benigno, Lederman, Michael, Sekaly, Rafick, Frange, Pierre, Faye, Albert, Avettand‐Fenoel, Veronique, Bellaton, Erainna, Deschamps, Diane, Angin, Mathieu, Caillat‐Zucman, Sophie, Peytavin, Gilles, Le Chenadec, Jerome, Warszawski, Josiane, Rouzioux, Christine, Saez‐Cirion, Asier, Cohort, ANRS Epf‐Co10 Pediatric, Chang, Christina, Cameron, Paul, Elliott, Julian, Perelson, Alan, Roche, Michael, Dantanarayana, Ashanti, Solomon, Ajantha, Naranbhai, Vivek, Tenakoon, Surekha, Hoh, Rebecca, McMahon, James, Sikaris, Ken, Hartogensis, Wendy, Bacchetti, Peter, Hecht, Frederick, Deeks, Steve, Lewin, Sharon, Byrareddy, Siddappa, Arthos, James, Cicala, Claudia, Reimann, Keith, Parslow, Tristram, Santangelo, Philip, Villinger, Francois, Fauci, Anthony, Ansari, Aftab, George, Michael, Weiser, Barbara, Burger, Harold, Lewy, Tyler, Anastos, Kathryn, Asmuth, David, Somsouk, Ma, Hunt, Peter, Min, Zhong, Miller, Christopher, and Li, Xiao Dong

Subjects
Mental Health, Digestive Diseases, Infectious Diseases, Pediatric AIDS, Bioengineering, Prevention, Clinical Research, Genetics, Health Services, Pediatric, Behavioral and Social Science, HIV/AIDS, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Infection, Reproductive health and childbirth, Good Health and Well Being, Clinical Sciences, Public Health and Health Services, Other Medical and Health Sciences
Published
2015

24. Genetic basis of immune-mediated susceptibility to infectious disease

Author

Naranbhai, Vivek, Hill, Adrian V. S., McShane, Helen, and Morris, Andrew

Subjects
genomics, infectious diseases
Abstract

Infectious diseases remain a major driver of morbidity and mortality globally. For example, Mycobacterium tuberculosis causes about 10 million cases of tuberculosis (TB) and 1.5 million deaths. In a series of studies I demonstrate that discovering the genetic underpinnings of how immune factors affect susceptibility to diseases such as TB reveal new insights into disease susceptibility. Previous transcriptome-wide studies suggested that the ratio of myeloid:lymphoid transcripts was elevated in infants who subsequently developed TB. These data were reminiscent of observations made 80 years ago where the ratio of monocytes:lymphocytes (ML) at time of challenge with mycobacteria, was predictive of survival in animal models. To establish the peripheral blood ML ratio as a novel intermediate phenotype for TB susceptibility, I demonstrated that the ML ratio predicts TB disease in three independent cohorts of adults (n=2207), infants (n=1336) and pregnant women (n=1202). Moreover, in collaboration with others, these findings were extended to other diseases including malaria. Turning attention to the pathophysiologic basis of this association, I found qualitative differences in monocytes according to ML ratio even amongst healthy individuals (n=136), both in functional response to mycobacteria and in transcriptomic profile at rest. Next, I found that the ML and neutrophil:lymphocyte (NL) ratio are highly phenotypically and genetically correlated, suggesting the presence of pleiotropic genetic regulators. I present formal estimates of heritability based on concordance and structural equation modeling of data from twin studies (1664 twin pairs), and amongst unrelated adults (n=5034). A meta-analysis of four genome-wide association studies (total n=5768) was performed as a resource to understand how the ML and NL ratios may be regulated, and to facilitate Mendelian randomization studies. Finally, in a more generalised approach I identified genetic regulators of gene expression in monocytes and neutrophils from healthy adults (n=101) and demonstrated how these give fundamental new insights into a wide array of infectious and non-infectious diseases. Taken together, these studies offer original contributions to the understanding of how genetic factors give rise to immune-mediated susceptibility to infectious disease.

Published
2015

25. 8th IAS Conference on HIV Pathogenesis, Treatment and Prevention (IAS 2015).

Author

Pate, Kelly Metcalf, Pohlmeyer, Chris, Walker-Sperling, Victoria, Foote, Jeremy, Najarro, Kevin, Cryer, Catherine, Salgado, Maria, Gama, Lucio, Engle, Elizabeth, Shirk, Erin, Queen, Suzanne, Chioma, Stanley, Vermillion, Meghan, Bullock, Brandon, Li, Ming, Lyons, Claire, Adams, Robert, Zink, Chris, Clements, Janice, Mankowski, Joseph, Blankson, Joel, Micci, Luca, Ryan, Emily, Fromentin, Rémi, Benne, Clarisse, Chomont, Nicolas, Lifson, Jeffrey, Paiardini, Mirko, Lee, Sulggi, Fromentin, Remi, Silicano, Robert, Silicano, Janet, Richman, Douglas, O'Doherty, Una, Palmer, Sarah, Burbelo, Peter, Deeks, Steven, Ghneim, Khader, Ahlers, Jeff, Fourati, Slim, Shive, Carey, Cameron, Mark, Mukerjee, Pranab, Ghannoum, Mahmoud, Rodriguez, Benigno, Lederman, Michael, Sekaly, Rafick, Frange, Pierre, Faye, Albert, Avettand-Fenoel, Veronique, Bellaton, Erainna, Deschamps, Diane, Angin, Mathieu, Caillat-Zucman, Sophie, Peytavin, Gilles, Le Chenadec, Jerome, Warszawski, Josiane, Rouzioux, Christine, Saez-Cirion, Asier, Chang, Christina, Cameron, Paul, Elliott, Julian, Perelson, Alan, Roche, Michael, Dantanarayana, Ashanti, Solomon, Ajantha, Naranbhai, Vivek, Tenakoon, Surekha, Hoh, Rebecca, McMahon, James, Sikaris, Ken, Hartogensis, Wendy, Bacchetti, Peter, Hecht, Frederick, Deeks, Steve, Lewin, Sharon, Byrareddy, Siddappa, Arthos, James, Cicala, Claudia, Reimann, Keith, Parslow, Tristram, Santangelo, Philip, Villinger, Francois, Fauci, Anthony, Ansari, Aftab, George, Michael, Weiser, Barbara, Burger, Harold, Lewy, Tyler, Anastos, Kathryn, Asmuth, David, Somsouk, Ma, Hunt, Peter, Min, Zhong, Miller, Christopher, Li, Xiao Dong, and Hinkle, John

Subjects
Clinical Sciences, Public Health and Health Services, Other Medical and Health Sciences
Published
2015

26. Immunophenotypic Risk Factors for Low SARS-CoV-2 Immunization Response in Adults with Predominantly Antibody Deficiency over Five Total Vaccine Doses

Author

Zhang, Anna, primary, ELMOURSI, AHMED, additional, Digiacomo, Daniel, additional, Zhou, Baijun, additional, Tandon, Megha, additional, Hong, Joseph, additional, Yang, Nancy, additional, Ong, Mei-Sing, additional, Dighe, Anand, additional, Berrios, Cristhian, additional, Poznansky, Mark, additional, Iafrate, Anthony, additional, Naranbhai, Vivek, additional, Balazs, Alejandro, additional, Pillai, Shiv, additional, Barmettler, Sara, additional, and Farmer, Jocelyn, additional

Published
2024
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27. SARS-CoV-2 Vaccine Response Following Five Total Vaccine Doses in Adult Patients with Predominantly Antibody Deficiency (PAD)

Author

ELMOURSI, AHMED, primary, Zhang, Anna, additional, Digiacomo, Daniel, additional, Zhou, Baijun, additional, Tandon, Megha, additional, Hong, Joseph, additional, Yang, Nancy, additional, Ong, Mei-Sing, additional, Dighe, Anand, additional, Berrios, Cristhian, additional, Poznansky, Mark, additional, Iafrate, Anthony John, additional, Naranbhai, Vivek, additional, Balazs, Alejandro, additional, Pillai, Shiv, additional, Farmer, Jocelyn, additional, and Barmettler, Sara, additional

Published
2024
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28. A systematic review of definitions of extreme phenotypes of HIV control and progression.

Author

Gurdasani, Deepti, Iles, Louise, Dillon, David, Young, Elizabeth, Olson, Ashley, Naranbhai, Vivek, Fidler, Sarah, Gkrania-Klotsas, Effrossyni, Post, Frank, Kellam, Paul, Porter, Kholoud, and Sandhu, Manjinder

Subjects
Disease Progression, HIV Infections, HIV Long-Term Survivors, Humans, Phenotype, Terminology as Topic
Abstract

The study of individuals at opposite ends of the HIV clinical spectrum can provide invaluable insights into HIV biology. Heterogeneity in criteria used to define these individuals can introduce inconsistencies in results from research and make it difficult to identify biological mechanisms underlying these phenotypes. In this systematic review, we formally quantified the heterogeneity in definitions used for terms referring to extreme phenotypes in the literature, and identified common definitions and components used to describe these phenotypes. We assessed 714 definitions of HIV extreme phenotypes in 501 eligible studies published between 1 January 2000 and 15 March 2012, and identified substantial variation among these. This heterogeneity in definitions may represent important differences in biological endophenotypes and clinical progression profiles of individuals selected by these, suggesting the need for harmonized definitions. In this context, we were able to identify common components in existing definitions that may provide a framework for developing consensus definitions for these phenotypes in HIV infection.

Published
2014

29. T cell responses to SARS-CoV-2 infection and vaccination are elevated in B cell deficiency and reduce risk of severe COVID-19

Author

Zonozi, Reza, primary, Walters, Lucy C., additional, Shulkin, Aaron, additional, Naranbhai, Vivek, additional, Nithagon, Pravarut, additional, Sauvage, Gabriel, additional, Kaeske, Clarety, additional, Cosgrove, Katherine, additional, Nathan, Anusha, additional, Tano-Menka, Rhoda, additional, Gayton, Alton C., additional, Getz, Matthew A., additional, Senjobe, Fernando, additional, Worrall, Daniel, additional, Iafrate, A. John, additional, Fromson, Caroline, additional, Montesi, Sydney B., additional, Rao, Deepak A., additional, Sparks, Jeffrey A., additional, Wallace, Zachary S., additional, Farmer, Jocelyn R., additional, Walker, Bruce D., additional, Charles, Richelle C., additional, Laliberte, Karen, additional, Niles, John L., additional, and Gaiha, Gaurav D., additional

Published
2023
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31. Dynamic heterogeneity in COVID-19: Insights from a mathematical model.

Author

Voutouri, Chrysovalantis, Hardin, C. Corey, Naranbhai, Vivek, Nikmaneshi, Mohammad R., Khandekar, Melin J., Gainor, Justin F., Munn, Lance L., Jain, Rakesh K., and Stylianopoulos, Triantafyllos

Subjects
COVID-19, MATHEMATICAL models, VIRAL load, VIRUS diseases, TREATMENT effectiveness, HETEROGENEITY
Abstract

Critical illness, such as severe COVID-19, is heterogenous in presentation and treatment response. However, it remains possible that clinical course may be influenced by dynamic and/or random events such that similar patients subject to similar injuries may yet follow different trajectories. We deployed a mechanistic mathematical model of COVID-19 to determine the range of possible clinical courses after SARS-CoV-2 infection, which may follow from specific changes in viral properties, immune properties, treatment modality and random external factors such as initial viral load. We find that treatment efficacy and baseline patient or viral features are not the sole determinant of outcome. We found patients with enhanced innate or adaptive immune responses can experience poor viral control, resolution of infection or non-infectious inflammatory injury depending on treatment efficacy and initial viral load. Hypoxemia may result from poor viral control or ongoing inflammation despite effective viral control. Adaptive immune responses may be inhibited by very early effective therapy, resulting in viral load rebound after cessation of therapy. Our model suggests individual disease course may be influenced by the interaction between external and patient-intrinsic factors. These data have implications for the reproducibility of clinical trial cohorts and timing of optimal treatment. [ABSTRACT FROM AUTHOR]

Published
2024
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32. Polymorphism in a lincRNA Associates with a Doubled Risk of Pneumococcal Bacteremia in Kenyan Children

Author

Rautanen, Anna, Pirinen, Matti, Mills, Tara C., Rockett, Kirk A., Strange, Amy, Ndungu, Anne W., Naranbhai, Vivek, Gilchrist, James J., Bellenguez, Céline, Freeman, Colin, Band, Gavin, Bumpstead, Suzannah J., Edkins, Sarah, Giannoulatou, Eleni, Gray, Emma, Dronov, Serge, Hunt, Sarah E., Langford, Cordelia, Pearson, Richard D., Su, Zhan, Vukcevic, Damjan, Macharia, Alex W., Uyoga, Sophie, Ndila, Carolyne, Mturi, Neema, Njuguna, Patricia, Mohammed, Shebe, Berkley, James A., Mwangi, Isaiah, Mwarumba, Salim, Kitsao, Barnes S., Lowe, Brett S., Morpeth, Susan C., Khandwalla, Iqbal, Blackwell, Jenefer M., Bramon, Elvira, Brown, Matthew A., Casas, Juan P., Corvin, Aiden, Duncanson, Audrey, Jankowski, Janusz, Markus, Hugh S., Mathew, Christopher G., Palmer, Colin N.A., Plomin, Robert, Sawcer, Stephen J., Trembath, Richard C., Viswanathan, Ananth C., Wood, Nicholas W., Deloukas, Panos, Peltonen, Leena, Williams, Thomas N., Scott, J. Anthony G., Chapman, Stephen J., Donnelly, Peter, Hill, Adrian V.S., and Spencer, Chris C.A.

Published
2016
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35. Multi-ancestry meta-analysis of host genetic susceptibility to tuberculosis identifies shared genetic architecture.

Author

Schurz, Haiko, Naranbhai, Vivek, Yates, Tom A., Gilchrist, James J., Parks, Tom, Dodd, Peter J., Möller, Marlo, Hoal, Eileen G., Morris, Andrew P., and Hill, Adrian V. S.

Subjects
*HERITABILITY, *HLA histocompatibility antigens, *GENOME-wide association studies, *TUBERCULOSIS, *GENETIC disorders
Abstract

The heritability of susceptibility to tuberculosis (TB) disease has been well recognized. Over 100 genes have been studied as candidates for TB susceptibility, and several variants were identified by genome-wide association studies (GWAS), but few replicate. We established the International Tuberculosis Host Genetics Consortium to perform a multi-ancestry meta-analysis of GWAS, including 14,153 cases and 19,536 controls of African, Asian, and European ancestry. Our analyses demonstrate a substantial degree of heritability (pooled polygenic h2 = 26.3%, 95% CI 23.7-29.0%) for susceptibility to TB that is shared across ancestries, highlighting an important host genetic influence on disease. We identified one global host genetic correlate for TB at genome-wide significance (p<5 × 10-8) in the human leukocyte antigen (HLA)-II region (rs28383206, p-value= 5.2 × 10-9) but failed to replicate variants previously associated with TB susceptibility. These data demonstrate the complex shared genetic architecture of susceptibility to TB and the importance of large-scale GWAS analysis across multiple ancestries experiencing different levels of infection pressure. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Abstract 3468: Immunoproteasome expression and checkpoint blockade response in advanced non-small cell lung cancer

Author

Naranbhai, Vivek, primary, Ravi, Arvind, additional, Hellmann, Matthew, additional, Arniella, Monica, additional, Holton, Mark, additional, Freeman, Samuel, additional, Stewart, Chip, additional, Leshchiner, Ignaty, additional, Kim, Jaegil, additional, Akiyama, Yo, additional, Griffin, Aaron, additional, Vokes, Natalie, additional, Sakhi, Mustafa, additional, Kamesan, Vashine, additional, Rizvi, Hira, additional, Ricciuti, Biagio, additional, Forde, Patrick, additional, Anagnostou, Valsamo, additional, Riess, Jonathan, additional, Gibbons, Don, additional, Pennell, Nathan, additional, Velcheti, Vamsidhar, additional, Digumarthy, Subba, additional, Mino-Kenudson, Mari, additional, Califano, Andrea, additional, Heymach, John, additional, Herbst, Roy, additional, Brahmer, Julie, additional, Schalper, Kurt, additional, Velculescu, Victor, additional, Henick, Brian, additional, Rizvi, Naiyer, additional, Janne, Pasi, additional, Awad, Mark, additional, Chow, Andrew, additional, Greenbaum, Benjamin, additional, Luksza, Marta, additional, Shaw, Alice, additional, Wolchok, Jedd, additional, Hacohen, Nir, additional, Getz, Gad, additional, and Gainor, Justin, additional

Published
2023
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40. Commentary - Setting up data science research in Africa and engagement of stakeholders

Author

Murtala-Ibrahim, Fati, Jumare, Jibreel, Charurat, Manhattan, Xiong, Chenfeng, Naranbhai, Vivek, Dakum, Patrick, Collie, Shirley, Jassat, Waasila, Aliyu, Gambo, Ifedayo, Adetifa, and Abimiku, Alash’le

Abstract

Significance:Data science explores the use of big data to gain deeper insights and generate new knowledge and innovations which can lead to economic growth and sustainable development. However, setting up data science research comes with challenges. How we engage stakeholders is a major factor that determines success. This Commentary highlights important considerations for stakeholder engagement based on the experiences of investigators in a data science for health discovery project underway in Nigeria and South Africa. The perspectives presented will guide implementation in this relatively new but rapidly growing research domain.

Published
2023

43. Genital Inflammation and the Risk of HIV Acquisition in Women

Author

Masson, Lindi, Passmore, Jo-Ann S., Liebenberg, Lenine J., Werner, Lise, Baxter, Cheryl, Arnold, Kelly B., Wiliamson, Carolyn, Little, Francesca, Mansoor, Leila E., Naranbhai, Vivek, Lauffenburger, Douglas A., Ronacher, Katharina, Walzi, Gerhard, Garrett, Nigel J., Williams, Brent L., Couto-Rodriguez, Mara, Hornig, Mady, Lipkin, W. Ian, Grobler, Anneke, Karim, Quarraisha Abdool, and Karim, Salim S. Abdool

Published
2015

44. Altered IL-6 signalling and risk of tuberculosis disease: a meta-analysis and Mendelian randomisation study

Author

Hamilton, Fergus, Schurz, Haiko, Yates, Tom A., Gilchrist, James J., Möller, Marlo, Naranbhai, Vivek, Ghazal, Peter, Timpson, Nicholas J, Parks, Tom, and Pollara, Gabriele

Subjects
Article
Abstract

SummaryIL-6 responses are ubiquitous inMycobacterium tuberculosis (Mtb)infections, but their role in determining human tuberculosis (TB) disease risk is unknown. We used single nucleotide polymorphisms (SNPs) in and near the IL-6 receptor(IL6R)gene, focusing on the non-synonymous variant, rs2228145, associated with reduced classical IL-6 signalling, to assess the effect of altered IL-6 activity on TB disease risk. We identified 16 genome wide association studies (GWAS) of TB disease collating 17,982 cases of TB disease and 972,389 controls across 4 continents. Meta-analyses and Mendelian randomisation analyses revealed that reduced classical IL-6 signalling was associated with lower odds of TB disease, a finding replicated using multiple, independent SNP instruments and 2 separate exposure variables. Our findings establish a causal relationship between IL-6 signalling and the outcome ofMtbinfection, suggesting IL-6 antagonists do not increase the risk of TB disease and should be investigated as adjuncts in treatment.

Published
2023

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