ArticleNpj viruses2025
Gut infection and dysbiosis are hallmarks of severe SARS-CoV-2 variants.
Article in Npj viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Gut Microbiota from Patients with Long COVID Persisting for 2 Years Result in Alterations in Mice that Resemble Post-COVID Symptoms.Probiotics and antimicrobial proteins · 2026Article
- Oral and plasma microbiome in the context of acute febrile illness.medRxiv : the preprint server for health sciences · 2026Article
- Dual role of ACE2 in regulating inflammation triggered by Omicron S1 and other SARS-CoV-2 Spike variants.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2, the virus behind the COVID-19 pandemic, is primarily a respiratory pathogen, with host entry mediated by the ACE2 receptor that determines viral tropism. Notably, in humans, ACE2 is highly expressed in the gastrointestinal (GI) tract, particularly the small intestine (SI), prompting us to examine GI infectivity of SARS-CoV-2 variants of concern (VOCs). We found that ACE2 expression in Syrian hamsters closely resembles humans, supporting their use in studying GI tropism. Using this model, we compared infection and pathology of the ancestral Wuhan-like strain (Hong Kong), Delta, and Omicron variants. Despite high ACE2 expression, GI infection and pathology were generally low relative to the respiratory tract. However, the Delta variant showed markedly enhanced GI infectivity and pathology, especially in the SI, and caused the greatest disruption of the gut microbiome. These findings link SARS-CoV-2 virulence with GI infection and microbiome disturbance, establishing Syrian hamsters as a relevant model.
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.