Evidence map›Paper›PMID 26784284›Full record

ArticleJournal of virological methods2016

Full coding hepatitis E virus genotype 3 genome amplification method.

M Muñoz-Chimeno, J E Forero, J M Echevarría, J L Muñoz-Bellido, L Vázquez-López, L Morago, M C García-Galera, A Avellón

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In one paragraph

Article in Journal of virological methods, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  3. Hepatitis E virus genotype 3 microbiological surveillance by the Spanish Reference Laboratory: geographic distribution and phylogenetic analysis of subtypes from 2009 to 2019.Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2022
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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

8 authors at 3 institutions in 2 countries.

M Muñoz-ChimenoHepatitis Unit, National Center of Microbiology, Instituto de Salud Carlos III, Madrid Spain. Electronic address: milagrosmch@hotmail.com.
J E ForeroUniversidad Nacional de Colombia, Facultad de Ciencias Agrarias, Medellín Colombia. Electronic address: jforeroduarte@gmail.com.
J M EchevarríaHepatitis Unit, National Center of Microbiology, Instituto de Salud Carlos III, Madrid Spain. Electronic address: jmecheva@isciii.es.
J L Muñoz-BellidoMicrobiology Unit, Salamanca University Hospital, Salamanca Spain. Electronic address: jlmubel@usal.es.
L Vázquez-LópezHematology Unit, Salamanca University Hospital, Salamanca Spain. Electronic address: lvazlo@usal.es.
L MoragoHepatitis Unit, National Center of Microbiology, Instituto de Salud Carlos III, Madrid Spain. Electronic address: lmorago@isciii.es.
M C García-GaleraHepatitis Unit, National Center of Microbiology, Instituto de Salud Carlos III, Madrid Spain. Electronic address: Mcgarciagalera@gmail.com.
A AvellónHepatitis Unit, National Center of Microbiology, Instituto de Salud Carlos III, Madrid Spain. Electronic address: aavellon@isciii.es.
Instituto de Salud Carlos III · ESUniversidad de Salamanca · ESUniversidad Nacional de Colombia · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis E virus (HEV) genotype 3 produces zoonotic infection associated with the consumption of infected animals. HEV infections can become chronic in immunocompromised (IC) patients. The viral genome has three well defined open reading frames (ORF1, ORF2 and ORF3) within which various domains and functions have been described. This paper (i) describes a new method of complete sequencing of the HEV coding region through overlapping PCR systems, (ii) establishes a consensus sequence and polymorphic positions (PP) for each domain, and (iii) analyzes the complete coding sequence of an IC patient. With regard to the consensus, a high percentage of PP was observed in protease (PP=19%) and the X domain (PP=22%) within ORF1, the N-terminal region of the S domain (PP=22%) in ORF2, and the P1 (PP=35%) and P2 (PP=25%) domains in ORF3. In contrast, the ORF1 Y, ORF2 S, ORF2 M and ORF3 D1 domains were conserved in the reference sequences (0.40, 1, 0.70 and 0% of PP, respectively). The sequence from the IC patient had more mutations in the RpRp (D1235G, Q1242R, S1454T, V1480I, I1502 V, K1511R, G1373 V, E1442D, V1693 M), the terminal ORF2 S- domain (F10L, S26T, G36S, S70P, A105 V, I113 V), the X domain (T938 M, T856 V, S898A) and the helicase (S1014N, S975T, Q1133 K).

Indexed as

Genome, ViralGenomicsHepatitis EHepatitis E virusHumansMutationOpen Reading FramesComplete genomeHepatitis E virusHEVImmunocompromised

Identifiers

PMID26784284
PMCPMC7172825
OpenAlexW2294293192

What OpenQuestion holds

Textmetadata
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.