ArticlePLoS pathogens2026
Limited protection against early-life lung murine cytomegalovirus infection results from deficiency of cytotoxic CD8 T cells.
Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Susceptibility of Mouse Brain to MCMV Infection and Neuroinflammation During Ontogeny.Pathogens (Basel, Switzerland) · 2024Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differential antiviral T cell immunity in early life impacts the clinical outcome of Cytomegalovirus (CMV) infection, but the underlying mechanisms are not well understood. T cells are known to be involved in protection from CMV disease. To further elucidate these mechanisms, we used a model of respiratory murine CMV (MCMV) infection and adoptive T cell transfers to characterize MCMV-specific T cell responses in early life. We analyzed the effector T cell differentiation using single-cell RNA sequencing and assessed the local pulmonary cytokine milieu. We found delayed enrichment of early-life murine MCMV-specific CD8 T cells due to a general deficiency of αβ T cells. Adoptive transfer of naïve adult T cells into neonates did not protect from lung MCMV infection due to generation of non-cytotoxic CD8 effector T cells. Furthermore, key cytokines required for effective CD8 T cell priming were absent in early life. Supplementation with these cytokines enhanced infection control by transferred adult T cells. The effector function of adult-primed T cells was not disrupted in neonates. Together, this study suggests defective CD8 T cell priming in neonates as a factor explaining the higher risk for MCMV lung disease in the early-life phase.
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Registered trials
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