
Benjamin Pinsky
· Associate ProfessorVerifiedStanford University · African Studies
Active 1998–2026
About
Joel Cabrita is the Susan Ford Dorsey Director of the Center for African Studies at Stanford University. His research interests include Eswatini, history, postcolonial theory, religion, media, and marginality in Africa. His work focuses on understanding the social and political dynamics within African contexts, particularly in relation to postcolonial developments and cultural expressions.
Research topics
- Medicine
- Virology
- Biology
- Internal medicine
- Computer Science
- Pathology
- Immunology
- Genetics
- Microbiology
- Computational biology
- Physical therapy
- Bioinformatics
- Materials science
- Nanotechnology
- Endocrinology
- Geography
- Emergency medicine
- Statistics
- Intensive care medicine
Selected publications
Adapting Clinical Chemistry Plasma as a Source for Liquid Biopsies
Zenodo (CERN European Organization for Nuclear Research) · 2026-02-23
datasetOpen accessThis dataset contains outputs from several analyses performed on plasma cell-free DNA samples, including viral read statistics, CpG methylation calls, genome-wide copy number profiles, and fragment length frequencies. These files are processed results from different computational workflows and support downstream exploratory and visualization tasks.
HIV-1 subtype diversity trends in a Northern California cohort
AIDS · 2026-02-25
articleOpen accessBetween 2000 and 2019, the Stanford Healthcare Clinical Virology Laboratory performed HIV-1 resistance testing for 9199 individuals in Northern California. Nonsubtype B viruses were identified in 3.5%, most often CRF01_AE (1.0%), subtype C (1.0%), CRF02_AG (0.46%), and subtype A (0.45%). Non-B viruses, particularly CRF01_AE and CRF02_AG, increased significantly over time. Although subtype B remained dominant, the rising presence of non-B subtypes reflects growing viral diversity within the U.S. epidemic.
PubMed · 2026-03-01
articleOpen access. 2026;116(3):307-311. https://doi.org/10.2105/AJPH.2025.308309).
Organoid modeling of lung-resident immune responses to SARS-CoV-2 infection
Research Square · 2026-02-12
preprintOpen accessImmunity · 2026-04-01 · 1 citations
articleOpen accessThe cellular, immunogenetic, and antigenic factors affecting the breadth of viral antigen variants recognized by human antibody responses are poorly defined. We developed highly multiplexed panels of DNA-tagged SARS-CoV-2 antigens from up to 20 viral variants to label and sort 6,262 antigen-binding circulating B cells from previously naive mRNA vaccinees or infected patients, and from deceased organ donor lymphoid tissues, to enable antigen receptor and transcriptome sequencing. Atypical B cells and a subset of class-switched memory cells with evidence of recent germinal center exposure were enriched for antigen binding. In contrast to atypical B cells, post-germinal center B cells showed progressively increasing variant binding breadth and somatic hypermutation over time. Vaccination, compared with infection, preferentially stimulated B cells expressing antibodies with inherently high antigen-binding breadth. This large-scale analysis reveals key determinants of antigen-binding breadth, critical for understanding responses to viral infection and guiding vaccine development against rapidly mutating viruses.
Sensors and Actuators B Chemical · 2025-04-03 · 2 citations
articleDrivers of differential antibody breadth in SARS-CoV-2 mRNA vaccination and infection 4823
The Journal of Immunology · 2025-11-01
articleOpen accessAbstract Description mRNA vaccination for SARS-CoV-2 (CoV-2) results in initial polyclonal antibodies of greater breadth compared to those stimulated by viral infection. Cellular, immunogenetic and antigenic factors leading to human antibody responses with broad viral variant recognition are poorly defined. Existing databases of CoV-2 binding antibodies have limited data about patient and B cell subset origins of the antibodies and their antigen variant binding. We used highly multiplexed panels of DNA-tagged CoV-2 antigens including Spike receptor binding domains from up to 20 viral variants to label and sort 6,262 antigen-binding B cells from peripheral blood of mRNA vaccinees, infected patients and the spleen and lymph nodes of deceased organ donors. Single-cell transcriptome and antigen DNA-tag data showed antigen-specific B cells enriched in a circulating class-switched memory subset with evidence of recent germinal center exposure, and in CD11c+ atypical B cells. Surprisingly, mRNA vaccination preferentially stimulates a subset of B cell receptor (BCR)-defined clonotypes, resulting in greater initial antigen binding breadth. Spleens show greater variant binding breadth than blood B cells from the initial months post-vaccination or infection. Together, these results systematically define the influence of CoV-2 mRNA vaccination and infection on particular B cell receptors and clonotypes, a topic of increasing importance as mRNA vaccination is evaluated for other pathogens. Funding Sources Supported by NIH/NIAID R01AI127877, NIH/NIAID R01AI130398, NIH 1U54CA260517, David Crown Foundation endowment/COVID-19 gift funds, NIH HIPC U19AI090023, U19AI057266, Sean N Parker Foundation/Sunshine Foundation, Early Postdoc.Mobility Fellowship Stipend (SNSF), Fulbright Fellowship, NHMRC Investigator grant, NSFC32270937/NSFC82341068 (Chinese NSF), Coulter COVID-19 Rapid Response Award, MSD kits. Topic Categories Viral Immunology (VIR)
2025-03-03
preprintOpen access<p>Supplement Figure 2</p>
UNC Libraries · 2025-05-06
articleOpen access2025-03-03
preprintOpen access<div>AbstractPurpose:<p>A first-in-human phase I study was conducted in patients with nasopharyngeal carcinoma to assess the safety and tolerability of VK-2019, a small-molecule selective inhibitor of Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1).</p>Patients and Methods:<p>Pharmacokinetic and pharmacodynamic studies were performed, including the measurement of EBV DNA plasma levels. Twenty-three patients received VK-2019 orally once daily at doses ranging from 60 to 1,800 mg using an accelerated titration design, with cohort expansion at 1,800 mg. EBV genome copy number and spatial transcriptomic analyses were conducted on biopsies collected from three patients at baseline and after treatment.</p>Results:<p>VK-2019 was well tolerated. One patient achieved a partial response. Pharmacokinetic results demonstrated good systemic exposure, with high intersubject variability. Decreases in EBV DNA plasma levels were observed in some patients. VK-2019 reduced EBV genome copy number and viral gene expression in patient tumor samples and induced changes in immune cell markers.</p>Conclusions:<p>VK-2019 at dosages up to 1,800 mg daily demonstrated an acceptable safety profile, achieved micromolar plasma concentrations, and showed on-target biological activity in tumors from patients with advanced EBV-positive nasopharyngeal carcinoma.</p></div>
Recent grants
NIH · $462k · 2017
Frequent coauthors
- 270 shared
Malaya K. Sahoo
Stanford University
- 139 shared
ChunHong Huang
Stanford University
- 123 shared
Catherine A. Hogan
- 110 shared
Quynh‐Thu Le
Stanford University
- 92 shared
Jesse J. Waggoner
Emory University
- 87 shared
Niaz Banaei
Stanford University
- 83 shared
James L. Zehnder
Stanford University
- 69 shared
K.C. Allen Chan
Chinese University of Hong Kong
Labs
Education
M.D.
University of Washington School of Medicine
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