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Record W4414168979 · doi:10.1128/jvi.00823-25

Human guanylate-binding protein (GBP) 1 inhibits replication of severe acute respiratory syndrome coronavirus 2

2025· article· en· W4414168979 on OpenAlexaff
Rubaiyea Farrukee, Francesca L. Mordant, Charley Mackenzie-Kludas, Dejan Mesner, Masahiro Yamomoto, Clare Jolly, Andrëw G. Brööks, Kanta Subbarao, Sarah L. Londrigan, Patrick C. Reading

Bibliographic record

VenueJournal of Virology · 2025
Typearticle
Languageen
FieldMedicine
TopicSARS-CoV-2 and COVID-19 Research
Canadian institutionsUniversité LavalInstitute of Infection and Immunity
FundersDepartment of Health and Aged Care, Australian GovernmentUniversity of MelbourneWellcome Trust
KeywordsInfectivityViral replicationVirusAntiviral drugCoronavirusImmune systemIntracellularEpitopeGene

Abstract

fetched live from OpenAlex

ABSTRACT Severe respiratory syndrome coronavirus 2 (SARS-CoV-2) infections are associated with significant morbidity and mortality worldwide. Identification and characterization of intracellular proteins with antiviral activity (known as restriction factors) is a key first step towards the future development of novel host-directed antiviral therapies. In this study, we investigated the antiviral activity of 14 different interferon-stimulated gene (ISG) proteins against SARS-CoV-2. Overexpression of human guanylate binding protein (GBP) 1 resulted in potent inhibition of the ancestral SARS-CoV-2 strain, as well as against Alpha, Beta, Delta, Omicron BA.1, and Omicron BA.2 variants of concern (VOCs). Moreover, knockdown or knockout of endogenous human GBP1 resulted in enhanced titers of SARS-CoV-2. While hGBP1 can restrict some viruses via actin remodeling, our data indicate that this is not the mechanism here. Moreover, we show that unlike GBP2 and GBP5, which impair spike protein processing, GBP1 did not reduce infectivity of spike-pseudotyped viruses following titration on Caco-2 cells. Multiple human GBPs have been reported to inhibit SARS-CoV-2 in vitro ; however, we report no significant differences in virus titers recovered from the upper or lower airways of SARS-CoV-2-infected wild-type mice compared to from mice lacking the chromosome 3 cluster of mouse GBPs (GBP1/2/3/5/7). Together, our studies describe the ability of human GBP1 to inhibit SARS-CoV-2 replication, highlighting this host protein as a potential target for the development of host-directed antiviral therapies against this virus. IMPORTANCE Viruses like SARS-CoV-2 can cause widespread illness and death. While currently licensed antiviral drugs are critical tools, drug resistance can develop. Our immune system produces intracellular proteins called “restriction factors” that can limit virus replication within cells. These proteins are promising targets for developing new antiviral therapies. In this study, we identified one such protein, human GBP1, which inhibited a range of SARS-CoV-2 variants in vitro , including Delta and Omicron. Interestingly, GBP1 inhibited SARS-CoV-2 through a different mechanism to that of other human GBPs as it did not interfere with prosessing of the viral spike protein. Of interest, a cluster of mouse GBPs, including GBP1, did not demontrate significant antiviral activity in a mouse model of infection. Overall, our findings suggest that human GBP1 could be a valuable target for host-directed antiviral strategies and highlight the limitations of using mouse models to study certain aspects of human innate immunity.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.002

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.056
GPT teacher head0.399
Teacher spread0.343 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2025
Admission routes1
Has abstractyes

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