# Lymphopenia in Bacterial Sepsis and SARS-CoV-2 Infection

**Authors:** Raluca Terteşş, Lucian Cristian Petcu, Bogdan Florentin Niţu, Mihaela Mariana Mavrodin, Elena Cucli, Elena Andreea Topa, Constantin Ionescu, Nicolae Cârciumaru, Simona Claudia Cambrea

PMC · DOI: 10.3390/biomedicines14020438 · Biomedicines · 2026-02-15

## TL;DR

The study compares lymphopenia and neutrophil-to-lymphocyte ratio in bacterial sepsis and SARS-CoV-2 infection, finding worse outcomes linked to lower lymphocyte counts and higher NLR in non-survivors.

## Contribution

The study uniquely evaluates longitudinal trends of lymphopenia and NLR in bacterial and viral sepsis, linking them to in-hospital mortality.

## Key findings

- Viral sepsis (e.g., COVID-19) causes a sustained decrease in lymphocyte counts and increased NLR compared to bacterial sepsis.
- Non-survivors had significantly lower lymphocyte counts from Day 3 and higher NLR on Day 7, regardless of infection type.
- Longitudinal trends in lymphocyte counts and NLR are more predictive of poor outcomes than early measurements.

## Abstract

Background: Sepsis is a life-threatening organ dysfunction that results from an exaggerated host immune response to disseminated infection. The relationship between lymphopenia and sepsis has been extensively studied, and in particular, sepsis-induced lymphopenia is gradually being recognized as an essential factor in the prognosis of sepsis. Notably, sepsis-induced lymphopenia has been associated with worse outcomes, including increased risk of secondary infections, multiple organ failure, and death. Few studies have directly compared the dynamic evolution of lymphocyte counts between different etiologies of sepsis or evaluated their prognostic value using serial measurements. This study aims to explore the temporal dynamics of lymphopenia, but also of neutrophil-to-lymphocyte (NLR) ratio in patients with severe systemic infections and to assess their relationship with in-hospital mortality. Methods: A prospective cohort of 95 adult patients was analyzed. Absolute lymphocyte counts (ALCs) and neutrophil-to-lymphocyte (NLR) ratio values were recorded on Days 1, 3, 5, and 7. Comparisons were made between different infectious etiologies and outcomes, and ROC analysis assessed predictive performance. Results and Conclusions: Patients with viral sepsis (“COVID-19”) showed a significant and sustained decrease in lymphocyte counts (p < 0.001) and a progressive increase in NLR (p < 0.001), unlike patients with bacterial sepsis. In correlation with outcome, regardless of etiology, lymphocyte counts were significantly lower in non-survivors from Day 3 onward, while NLR was significantly higher on Day 7 (p = 0.002). Early NLR and ALC had limited predictive value, but longitudinal trends were associated with poor prognosis.

## Linked entities

- **Diseases:** SARS-CoV-2 (MONDO:0100096), 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}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** Lymphopenia (MESH:D008231), critically ill (MESH:D016638), NLR (MESH:D015467), inflammation (MESH:D007249), systemic infections (MESH:D012141), circulatory failure (MESH:D012769), injury to (MESH:D014947), hematologic malignancy (MESH:D019337), paralysis (MESH:D010243), autoimmune disorders (MESH:D001327), multiple organ failure (MESH:D009102), bloodstream and urinary tract infections (MESH:D014552), immune dysfunction (MESH:D007154), COVID-19 (MESH:D000086382), infected (MESH:D007239), Viral sepsis (MESH:D014777), Mortality (MESH:D003643), Infectious Diseases (MESH:D003141), Sepsis (MESH:D018805), septic (MESH:D001170), Septic Shock (MESH:D012772), HIV infection (MESH:D015658), immune dysregulation (OMIM:614878), Bacterial (MESH:D001424), ALC (MESH:D009845)
- **Chemicals:** ROS (MESH:D017382)
- **Species:** Klebsiella pneumoniae (species) [taxon 573], Pseudomonas aeruginosa (species) [taxon 287], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606], Clostridioides difficile (species) [taxon 1496], Staphylococcus aureus (species) [taxon 1280], Stenotrophomonas maltophilia (species) [taxon 40324]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12938629/full.md

## References

29 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938629/full.md

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Source: https://tomesphere.com/paper/PMC12938629