# Impact of memory T cells on SARS-CoV-2 vaccine response in hematopoietic stem cell transplant

**Authors:** Jennifer VanOudenhove, Yuxin Liu, Raman Nelakanti, Dongjoo Kim, Emma Busarello, Natalia Tijaro Ovalle, Zhihong Qi, Padmavathi Mamillapalli, Alexa Siddon, Zhiliang Bai, Alfredo Axtmayer, Cheryl Corso, Shalin Kothari, Francine Foss, Iris Isufi, Toma Tebaldi, Lohith Gowda, Rong Fan, Stuart Seropian, Stephanie Halene

PMC · DOI: 10.1371/journal.pone.0320744 · PLOS One · 2025-04-28

## TL;DR

HSCT recipients show strong antibody responses to SARS-CoV-2 vaccines but often lack memory T cell activity, which may affect protection against infection.

## Contribution

Identifies a defect in memory T cells post-HSCT that correlates with poor cellular immune response despite strong humoral immunity.

## Key findings

- Memory T cell defects were observed in HSCT recipients after vaccination.
- Most patients had strong antibody responses but some still developed mild infections.
- No severe disease or deaths occurred among vaccinated HSCT recipients.

## Abstract

During the COVID-19 pandemic, hematopoietic stem cell transplant (HSCT) recipients had elevated mortality rates from SARS-CoV-2 infection, ranging between 10–40%. SARS-CoV-2 mRNA vaccines are important tools in preventing severe disease, yet their efficacy post-transplant remains unclear, especially in patients subjected to myeloablative chemotherapy and immunosuppression. We evaluated humoral and adaptive immune responses to the SARS-CoV-2 mRNA vaccination series in 42 HSCT recipients and 5 healthy controls. Post-vaccination responses were assessed by anti-spike IgG and nucleocapsid levels, and antigen specific T cell activity. Immune profiling was performed using clinical flow and mass cytometry. Patients were selected based on humoral and cellular responses for single-cell RNA with TCR and BCR sequencing. Our studies revealed defects in memory T cells that correlated with an absence of cellular response despite nearly universal humoral response. Several patients with a robust antibody response developed COVID-19 infection, but none developed severe disease or died from the infection.

## Linked entities

- **Diseases:** COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** TRBV20OR9-2 (T cell receptor beta variable 20/OR9-2 (non-functional)) [NCBI Gene 6962] {aka CDR3, TCRBV20S2, TCRBV2O, TCRBV2S2O}, S (surface glycoprotein) [NCBI Gene 43740568] {aka spike glycoprotein}, N (nucleocapsid phosphoprotein) [NCBI Gene 43740575], BCR (BCR activator of RhoGEF and GTPase) [NCBI Gene 613] {aka ALL, BCR1, CML, D22S11, D22S662, PHL}
- **Diseases:** infection (MESH:D007239), COVID-19 (MESH:D000086382)
- **Species:** Homo sapiens (human, species) [taxon 9606], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12036906/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12036906/full.md

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Source: https://tomesphere.com/paper/PMC12036906