Evidence map›Paper›PMID 39567865›Full record

ArticleGut microbes

Rotavirus rewires host cell metabolic pathways toward glutamine catabolism for effective virus infection.

Suvrotoa Mitra, Ratul Datta Chaudhuri, Rakesh Sarkar, Shreya Banerjee, Arpita Mukherjee, Ranjana Sharma, Animesh Gope, Kei Kitahara, Shin-Ichi Miyoshi, Mamta Chawla-Sarkar

Abstract read
In one paragraph

Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Suvrotoa MitraDivision of Virology, ICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Kolkata, West Bengal, India.ORCID 0000-0003-0651-5884
Ratul Datta ChaudhuriDivision of Virology, ICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Kolkata, West Bengal, India.
Rakesh SarkarDepartment of Plant and Microbial Biology, University of California, Berkeley, USA.
Shreya BanerjeeDivision of Virology, ICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Kolkata, West Bengal, India.
Arpita MukherjeeDivision of Virology, ICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Kolkata, West Bengal, India.
Ranjana SharmaDivision of Virology, ICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Kolkata, West Bengal, India.
Animesh GopeDivision of Virology, ICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Kolkata, West Bengal, India.
Kei KitaharaICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Collaborative Research Center of Okayama University for Infectious Diseases in India, Kolkata, India.
Shin-Ichi MiyoshiICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Collaborative Research Center of Okayama University for Infectious Diseases in India, Kolkata, India.
Mamta Chawla-SarkarDivision of Virology, ICMR-National Institute of Cholera and Enteric Diseases (presently ICMR-NIRBI), Kolkata, West Bengal, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rotavirus (RV) accounts for 19.11% of global diarrheal deaths. Though GAVI assisted vaccine introduction has curtailed RV induced mortality, factors like RV strain diversity, differential infantile gut microbiome, malnutrition, interference from maternal antibodies and other administered vaccines, etc. often compromise vaccine efficacy. Herein emerges the need of antivirals which can be administered adjunct to vaccination to curb the socio-economic burden stemming from frequent RV infection. Cognisance of pathogen-perturbed host cellular physiology has revolutionized translational research and aided precision-based therapy, particularly for viruses, with no metabolic machinery of their own. To date there has been limited exploration of the host cellular metabolome in context of RV infection. In this study, we explored the endometabolomic landscape of human intestinal epithelial cells (HT-29) on RV-SA11 infection. Significant alteration of host cellular metabolic pathways like the nucleotide biosynthesis pathway, alanine, aspartate and glutamate metabolism pathway, the host citric acid cycle was observed in RV-SA11 infection scenario. Detailed study further revealed that RV replication is exclusively dependent on glutamine metabolism for their propagation in host cells. Glutamine metabolism generates glutamate, aspartate, and asparagine which facilitates virus infection. Abrogation of aspartate biogenesis from glutamine by use of Aminooxyacetic acid (AOAA), significantly curbed RV-SA11 infection in-vitro and in-vivo. Overall, the study improves our understanding of host-rotavirus interactome and recognizes host glutamine metabolism pathway as a suitable target for effective therapeutic intervention against RV infection.

Indexed as

GlutamineMetabolic Networks and PathwaysRotavirusRotavirus InfectionsVirus ReplicationAnimalsEpithelial CellsGastrointestinal MicrobiomeHost-Pathogen InteractionsHT29 CellsHumansMiceGlutamineantiviralaspartate aminotransferaseglutamine metabolismmetabolomicsRotavirus

Identifiers

PMID39567865
PMCPMC11583611

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.