Alix E. Seif
· Associate Professor of Pediatrics (Oncology) at the Children's Hospital of PhiladelphiaVerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2002–2026
About
Alix E. Seif, MD, MPH, is an Associate Professor of Pediatrics (Oncology) at the Children's Hospital of Philadelphia. She is a core faculty member at CHOP and a member of the Penn Center for Cancer Care Innovation (PC3I). Dr. Seif serves as the Director of Clinical Research at the Center for Childhood Cancer Research within the Division of Oncology at The Children's Hospital of Philadelphia. Her educational background includes a BA in Linguistics with Honours from McGill University, an MA in Linguistics from McGill University, an MPH in Epidemiology and Biostatistics, and an MD from Oregon Health Sciences University. She is also certified in Implementation Science from the University of Pennsylvania. Her research and clinical work focus on pediatric oncology, with contributions to understanding leukemia, lymphoma, and other childhood cancers, as well as developing evidence-based approaches to personalized care in pediatric oncology.
Research signals
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Research topics
- Biology
- Immunology
- Medicine
- Computer Science
- Internal medicine
- Pathology
- Genetics
- Computational biology
- Virology
- Bioinformatics
Selected publications
Transplantation and Cellular Therapy · 2026-02-01
articleSSRN Electronic Journal · 2026-01-01
preprintOpen accessTransplantation and Cellular Therapy · 2026-02-01
articleTransplantation and Cellular Therapy · 2026-02-01
articleOpen accessBK polyomavirus (BKPyV) reactivation is nearly universal after pediatric hematopoietic stem cell transplant (HSCT); yet, only a quarter of patients develop BKPyV cystitis. We hypothesize that BKPyV reactivation alone is not sufficient for cystitis and that differential host immune responses to BKPyV are major determinants of disease. We assessed differences in cellular and soluble host factors that contribute to BKPyV cystitis after HSCT. Plasma from 25 HSCT recipients underwent proteomics analysis (Somascan 7k platform) at 6 timepoints: baseline (pre-HSCT), day 7, 14, 30, 60 and 90. Paired immunoglobulin-like type 2 receptor alpha (PILRA) genotyping was performed on 112 consecutive patients at baseline. Single cell RNAseq was performed on day 60 peripheral blood mononuclear cells (PBMCs) from 12 HSCT recipients. We compared the plasma proteomes of patients with BKPyV viremia and cystitis (n=5) versus no cystitis (n=6). PILRA was a leading differentially expressed protein (DEP) at baseline (p=2.64e-2), day 7 (p=4.28e-2), day 14 (p=3e-3), day 30 (p=8.04e-3) and day 60 (p=5.09-3, Fig.1A). PILRA genotyping tested whether a known functional polymorphism (rs1859788) affects cystitis risk (Fig. 1B). Baseline heterozygotes (A/G, 12.5% cystitis rate) were significantly less likely to develop cystitis compared to homozygous (G/G, 39% cystitis rate; or A/A, 31% cystitis rate) patients (p=0.004). PBMC transcriptomes were compared between patients with BKPyV viremia and cystitis (n=3) versus BKPyV viremia and no cystitis (n=3). PILRA is predominantly expressed on monocytes and was a differentially expressed gene (DEG) in both CD16+ (q=4.6e-6) and CD14+ (q=2.6e-57) monocytes (Fig.2B). Pathway and upstream regulator analysis of CD14+ and CD16+ monocytes showed increased antiviral response (p=4.6e-19 and p=7.8e-23), interferon gamma (p=4e-17 and p=2.7e-12), and interferon alpha/beta (p=3.5e-15 and p=2.1e-11) enrichment in cystitis patients (Fig.2A). The interferon stimulated genes, interferon induced protein 44-like (IFI44L) and interferon induced protein 44 (IFI44), were leading DEGs in 9/11 cell types studied (Fig. 2C). PILRA is a negative regulator of inflammatory processes and exists both in a membrane bound and soluble form. Baseline PILRA genotype was associated with cystitis risk in this study and the significantly lower soluble PILRA levels coupled with increased cellular PILRA expression support an increase in cell surface PILRA in cystitis patients. We conclude that soluble and monocytic PILRA differences contribute to a heightened interferon response to BKPyV that may cause inflammation and cystitis through interferon stimulated genes such as IFI44L and IFI44. Ongoing work aims to identify the mechanisms of PILRA-associated interferon production, as well as multiomic data analysis from BKPyV negative patients.
Transplantation and Cellular Therapy · 2026-02-01
articleNature Communications · 2025-10-22 · 1 citations
articleOpen accessAbstract B-cell acute lymphoblastic leukemia (B-ALL) is the most common pediatric malignancy. Given racial/ethnic differences in incidence and outcomes, B-ALL genome-wide association studies among children of African ancestry are needed. Leveraging multi-institutional datasets with 840 African American children with B-ALL and 3360 controls, nine loci achieved genome-wide significance ( P < 5 × 10 −8 ) after meta-analysis. Two loci were established trans-ancestral susceptibility regions ( IKZF1 , ARID5B ), while the remaining novel loci were specific to African populations. Five-year overall survival among children carrying novel risk alleles was significantly worse (83% versus 96% in non-carriers, P = 4.8 × 10 −3 ). Novel risk variants were also associated with subtype-specific disease ( P < 0.05), including higher susceptibility for a subtype overrepresented in African American children ( TCF3-PBX1 ) and lower susceptibility for a subtype with excellent prognosis ( ETV6-RUNX1 ). Functional experiments revealed novel B-ALL risk variants had allele-specific differences in transcriptional activity ( P < 0.05) in B-cell and leukemia cell lines. These findings shed insights into ancestry-related differences in leukemogenesis and prognosis.
Bkpyv Replication Kinetics and Association with Hemorrhagic Cystitis in Pediatric HSCT Recipients
Transplantation and Cellular Therapy · 2025-02-01
articleMicrobiology Spectrum · 2025-06-24 · 4 citations
articleOpen accessfamily. The BKPyV genome is divided into three regions, including the non-coding control region (NCCR), the early region, and the late region. BKPyV has one of the highest mutation rates among DNA viruses, and four genotypes have been identified based on amino acid variation within the VP1 region. Mutations within the NCCR have been noted, and this region exhibits hypervariability. Here, we show that many of the point mutations observed within the NCCR are genotype-associated, termed genotype-associated polymorphisms (GAPs). These GAPs correlate with regions of hypervariability, are inherent to their genotype, and can be used to genotype clinical strains, separate from other genomic regions. We also show that these GAPs fall within predicted transcription factor binding sites and therefore provide targets for further functional studies.IMPORTANCEBK Polyomavirus (BKPyV) is the cause of hemorrhagic cystitis in hematopoietic cell transplant recipients and BKPyV-associated nephropathy in renal transplant recipients and thus is an important determinant of transplant outcome. The viral mechanisms leading to disease manifestation remain to be thoroughly explored, but viral genetic variation has emerged as an area of interest. Understanding genomic diversity between and within BKPyV genotypes can provide sites of interest that may ultimately improve screening strategies and provide insights into the viral factors that contribute to disease.
Leukemia Research · 2025-09-01
articleBK polyomavirus genotype IV isolates from virus-specific T-cell therapy recipients
Microbiology Resource Announcements · 2025-08-27
articleOpen accessBK polyomavirus (BKPyV) can cause disease in transplant recipients. Virus-specific T-cell (VST) therapy is effective in decreasing virus levels in many individuals. BKPyV genetic variation can impact replication kinetics and immune responses. Here, we present the near full-length BKPyV genome sequences from two VST recipients in which genotype IV was isolated.
Frequent coauthors
- 301 shared
Richard Aplenc
Hospital for Sick Children
- 248 shared
Brian T. Fisher
University of Pennsylvania
- 205 shared
Yimei Li
Children's Hospital of Philadelphia
- 176 shared
Stephan A. Grupp
Children's Hospital of Philadelphia
- 109 shared
Yuan‐Shung Huang
Children's Hospital of Philadelphia
- 105 shared
David T. Teachey
Children's Hospital of Philadelphia
- 96 shared
Rochelle Bagatell
Children's Hospital of Philadelphia
- 93 shared
Kelly Getz
University of Pennsylvania
Education
- 1992
B.A., Linguistics - Honours, First Class
McGill University
- 1995
M.A., Linguistics
McGill University
- 2002
M.D.
Oregon Health Sciences University
- 2002
Other, Epidemiology and Biostatistics
Oregon Health Sciences University
- 2025
Other, Implementation Science
University of Pennsylvania
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