ArticlemBio2026
Tight junction protein claudin-1 is a novel internalization factor for swine enteric coronaviruses infection.
Article in mBio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Swine enteric coronaviruses (SeCoVs), including transmissible gastroenteritis virus (TGEV), porcine epidemic diarrhea virus (PEDV), and porcine deltacoronavirus (PDCoV), have been reported to use aminopeptidase N (APN) as a cellular receptor. However, APN alone cannot effectively explain the infection of both APN-positive and APN-negative enterocytes by PEDV and TGEV, nor the wide host range of PDCoV, suggesting the involvement of other host factors. In this study, we demonstrate that TGEV infection in piglets upregulates claudin-1 expression not only in infected cells but also in uninfected cells. Claudin-1 levels correlated strongly with TGEV N protein levels in the jejunum of infected piglets. Functional studies revealed that claudin-1 overexpression enhanced cellular susceptibility to TGEV, PEDV, and PDCoV, whereas its knockout significantly attenuated infection. Mechanistically, claudin-1 specifically interacts with the S1 or receptor-binding domain (RBD) of SeCoVs and promotes viral internalization. Furthermore, induction of claudin-1 in piglets promotes PDCoV infection in the intestine. Notably, claudin-1 also binds to the S1 protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Collectively, our results identify claudin-1 as a novel internalization factor for porcine enteric coronaviruses, playing a critical role in facilitating infection within the digestive tract, and highlight its potential as a target for future clinical interventions. IMPORTANCE: We observed a downregulation in the expression of the majority of tight junction proteins in intestinal tissues infected with transmissible gastroenteritis virus (TGEV). However, unexpectedly, claudin-1 exhibited a significant upregulation in intestinal epithelial cells. This intriguing finding prompted us to delve deeper into the potential role of claudin-1 in facilitating virus invasion of epithelial cells. Utilizing overexpression and knockout cell lines, we demonstrate that claudin-1 is an internalization factor for swine enteric coronaviruses (SeCoVs), including TGEV, porcine epidemic diarrhea virus (PEDV), and porcine deltacoronavirus (PDCoV). Notably, claudin-1 interacts with the S1 protein of TGEV, PEDV, PDCoV, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), spanning across alpha, beta, and delta coronaviruses. Our findings provide deeper insights into the infection mechanisms and pathogenesis of SeCoVs and SARS-CoV-2.
Indexed as
Identifiers
What OpenQuestion holds
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.