ArticlemBio2026
Human alphacoronavirus replication and innate immune induction in airway culture systems.
Article in mBio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Coronavirus Nsp15 endoribonuclease: linking viral RNA regulation to immune evasion and viral fitness.Journal of virology · 2026Review
- PKR condensation at viral replication complexes initiates its activation.Cell reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Compared with lethal betacoronaviruses, there is limited knowledge of how human alphacoronaviruses HCoV-NL63 (NL63) and HCoV-229E (229E) interact with host innate immune responses. We compared NL63 and 229E infections in human lung-derived cell lines, A549 IMPORTANCE: Seasonal human coronaviruses (HCoVs) are the causative agents of more than 15% of common cold cases each year. However, compared with more virulent HCoVs such as SARS-CoV-2, there has been limited research on these viruses. We compared the replication of HCoV-NL63 (NL63) and HCoV-229E (229E). Additionally, we examined their interactions with interferon signaling and related innate immune pathways in lung-derived cell lines and primary nasal epithelial cultures. 229E replicates efficiently in each of these culture systems, with significant dsRNA-induced pathway induction only in nasal cells. In contrast, NL63 replicates efficiently only in nasal cell cultures but induces innate immune pathways in all three culture systems. Moreover, the conserved CoV innate immune antagonist endoribonuclease U aids in evading these responses in 229E infection. This study expands our understanding of common-cold HCoV-host interactions and provides insight into differences between seasonal and lethal HCoVs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.