Evidence map›Paper›PMID 37115804›Full record

ArticlePLoS pathogens2023

Genomic analysis unveils genome degradation events and gene flux in the emergence and persistence of S. Paratyphi A lineages.

Jobin John Jacob, Agila K Pragasam, Karthick Vasudevan, Aravind Velmurugan, Monisha Priya Teekaraman, Tharani Priya Thirumoorthy, Pallab Ray, Madhu Gupta, Arti Kapil, Sulochana Putil Bai and 20 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 27% of its field
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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Comparative genomics ofVirulence · 2025
    Article
  2. Article
  3. Review
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

30 authors at 14 institutions in 2 countries.

Jobin John JacobChristian Medical College, Vellore, India.
Agila K PragasamChristian Medical College, Vellore, India.
Karthick VasudevanChristian Medical College, Vellore, India.
Aravind VelmuruganChristian Medical College, Vellore, India.
Monisha Priya TeekaramanChristian Medical College, Vellore, India.
Tharani Priya ThirumoorthyChristian Medical College, Vellore, India.
Pallab RayPost Graduate Institute of Medical & Educational Research, Chandigarh, India.
Madhu GuptaPost Graduate Institute of Medical & Educational Research, Chandigarh, India.
Arti KapilAll India Institute of Medical Sciences, New Delhi, India.
Sulochana Putil BaiKanchi Kamakoti Childs Trust Hospital, Chennai, India.
Savitha NagarajSt. John's Medical College, Bengaluru, India.
Karnika SaigalChacha Nehru Bal Chikitsalaya, Delhi, India.
Temsunaro Rongsen ChandolaCentre for Health Research & Development-Society for Applied Studies, New Delhi, India.
Maria ThomasChristian Medical College, Ludhiana, India.
Ashish BavdekarKEM Hospital & Research Centre, Pune, India.
Sheena Evelyn EbenezerThe Duncan Hospital, Raxaul, India.
Jayanthi ShastriTopiwala National Medical College & BYL Nair Charitable Hospital, Mumbai, India.
Anuradha DeTopiwala National Medical College & BYL Nair Charitable Hospital, Mumbai, India.
Shantha DuttaICMR-National Institute of Cholera and Enteric Diseases, Kolkata, India.
Anna P AlexanderLady Willingdon Hospital, Manali, India.
Roshine Mary KoshyMakunda Christian Leprosy & General Hospital, Karimjang, India.
Dasaratha R JinkaRural Development Trust Hospital, Bathalapalli, Andhra Pradesh, India.
Ashita SinghChinchpada Christian Hospital, Nandurbar, India.
Sunil Kumar SrivastavaDepartment of Microbiology, SSN College, University of Delhi, Delhi, India.
Shalini AnandanChristian Medical College, Vellore, India.
Gordon DouganCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Department of Medicine, University of Cambridge, Cambridge, United Kingdom.
Jacob JohnChristian Medical College, Vellore, India.
Gagandeep KangChristian Medical College, Vellore, India.
Balaji VeeraraghavanChristian Medical College, Vellore, India.
Ankur MutrejaCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Department of Medicine, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0002-1118-8075
Christian Medical College, Vellore · INPost Graduate Institute of Medical Education and Research · INTopiwala National Medical College & BYL Nair Charitable Hospital · INUniversity of Cambridge · GBAll India Institute of Medical Sciences · INAtal Bihari Vajpayee Institute of Medical Sciences and Dr. Ram Manohar Lohia Hospital · INChacha Nehru Bal Chikitsalaya · INChristian Medical College · INKanchi Kamakoti CHILDS Trust Hospital · INMedical Trust Hospital · INNational Institute of Cholera and Enteric Diseases · INSociety for Applied Studies · INSt.John's Medical College Hospital · INUniversity of Delhi · IN

Funding

Wellcome Trust
6 · The paper itself

Abstract

Paratyphoid fever caused by S. Paratyphi A is endemic in parts of South Asia and Southeast Asia. The proportion of enteric fever cases caused by S. Paratyphi A has substantially increased, yet only limited data is available on the population structure and genetic diversity of this serovar. We examined the phylogenetic distribution and evolutionary trajectory of S. Paratyphi A isolates collected as part of the Indian enteric fever surveillance study "Surveillance of Enteric Fever in India (SEFI)." In the study period (2017-2020), S. Paratyphi A comprised 17.6% (441/2503) of total enteric fever cases in India, with the isolates highly susceptible to all the major antibiotics used for treatment except fluoroquinolones. Phylogenetic analysis clustered the global S. Paratyphi A collection into seven lineages (A-G), and the present study isolates were distributed in lineages A, C and F. Our analysis highlights that the genome degradation events and gene acquisitions or losses are key molecular events in the evolution of new S. Paratyphi A lineages/sub-lineages. A total of 10 hypothetically disrupted coding sequences (HDCS) or pseudogenes-forming mutations possibly associated with the emergence of lineages were identified. The pan-genome analysis identified the insertion of P2/PSP3 phage and acquisition of IncX1 plasmid during the selection in 2.3.2/2.3.3 and 1.2.2 genotypes, respectively. We have identified six characteristic missense mutations associated with lipopolysaccharide (LPS) biosynthesis genes of S. Paratyphi A, however, these mutations confer only a low structural impact and possibly have minimal impact on vaccine effectiveness. Since S. Paratyphi A is human-restricted, high levels of genetic drift are not expected unless these bacteria transmit to naive hosts. However, public-health investigation and monitoring by means of genomic surveillance would be constantly needed to avoid S. Paratyphi A serovar becoming a public health threat similar to the S. Typhi of today.

Indexed as

Typhoid FeverAnti-Bacterial AgentsGenomicsHumansPhylogenySalmonella paratyphi ASalmonella typhiAnti-Bacterial Agents

Identifiers

PMID37115804
PMCPMC10171690
OpenAlexW4367309190

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.