Evidence map›Paper›PMID 38501831›Full record

ArticlemSphere2024

Structural implications of BK polyomavirus sequence variations in the major viral capsid protein Vp1 and large T-antigen: a computational study.

Janani Durairaj, Océane M Follonier, Karoline Leuzinger, Leila T Alexander, Maud Wilhelm, Joana Pereira, Caroline A Hillenbrand, Fabian H Weissbach, Torsten Schwede, Hans H Hirsch

Open access · goldAbstract read
In one paragraph

Article in mSphere, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Janani DurairajBiozentrum, University of Basel, Basel, Switzerland.ORCID 0000-0002-1698-4556
Océane M FollonierBiozentrum, University of Basel, Basel, Switzerland.ORCID 0009-0002-2577-1808
Karoline LeuzingerTransplantation & Clinical Virology, Department of Biomedicine, Medical Faculty, University of Basel, Basel, Switzerland.ORCID 0000-0002-5654-9356
Leila T AlexanderBiozentrum, University of Basel, Basel, Switzerland.
Maud WilhelmTransplantation & Clinical Virology, Department of Biomedicine, Medical Faculty, University of Basel, Basel, Switzerland.ORCID 0000-0003-4081-9398
Joana PereiraBiozentrum, University of Basel, Basel, Switzerland.
Caroline A HillenbrandTransplantation & Clinical Virology, Department of Biomedicine, Medical Faculty, University of Basel, Basel, Switzerland.ORCID 0009-0008-5393-4807
Fabian H WeissbachTransplantation & Clinical Virology, Department of Biomedicine, Medical Faculty, University of Basel, Basel, Switzerland.ORCID 0000-0003-0969-8153
Torsten SchwedeBiozentrum, University of Basel, Basel, Switzerland.ORCID 0000-0003-2715-335X
Hans H HirschTransplantation & Clinical Virology, Department of Biomedicine, Medical Faculty, University of Basel, Basel, Switzerland.ORCID 0000-0003-0883-0423
SIB Swiss Institute of Bioinformatics · CHUniversity of Basel · CH

Funding

Swiss National Science Foundation 310030_212589
6 · The paper itself

Abstract

BK polyomavirus (BKPyV) is a double-stranded DNA virus causing nephropathy, hemorrhagic cystitis, and urothelial cancer in transplant patients. The BKPyV-encoded capsid protein Vp1 and large T-antigen (LTag) are key targets of neutralizing antibodies and cytotoxic T-cells, respectively. Our single-center data suggested that variability in Vp1 and LTag may contribute to failing BKPyV-specific immune control and impact vaccine design. We, therefore, analyzed all available entries in GenBank (1516 IMPORTANCE: Type and rate of amino acid variations in BKPyV may provide important insights into BKPyV diversity in human populations and an important step toward defining determinants of BKPyV-specific immunity needed to protect vulnerable patients from BKPyV diseases. Our analysis of BKPyV sequences obtained from human specimens reveals an unexpectedly high genetic variability for this double-stranded DNA virus that strongly relies on host cell DNA replication machinery with its proof reading and error correction mechanisms. BKPyV variability and immune escape should be taken into account when designing further approaches to antivirals, monoclonal antibodies, and vaccines for patients at risk of BKPyV diseases.

Indexed as

Antigens, Viral, TumorBK VirusCapsid ProteinsGenetic VariationComputational BiologyGenotypeHumansMutationPolyomavirus InfectionsAntigens, Viral, TumorCapsid ProteinsVP1 protein, polyomavirusBK virusgenotypeimmune escapemutantpolyomaviruspredictionserotypestructurevaccinevariantVp1, large T antigen

Identifiers

PMID38501831
PMCPMC11036806
OpenAlexW4392953852

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.